Author Topic: An introduction to Prospero's case  (Read 25763 times)

Prospero

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Re: An introduction to Prospero's case
« Reply #40 on: July 07, 2021, 03:05:18 PM »
Interesting, thank you.

Muon

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Re: An introduction to Prospero's case
« Reply #41 on: July 19, 2021, 05:06:24 AM »
I'm sure it is because of A) to retain potassium and waste sodium
https://en.wikipedia.org/wiki/Progesterone
"Moreover, progesterone is also known to be an antagonist of the sigma 1 receptor"

Yesterday, there were people saying they developed POIS after Finasteride use (see https://poiscenter.com/forums/index.php?topic=458.msg41283#msg41283). Finasteride is an inhibitor of 5alpha-reductase, which happens also to transform Progesterone in 5a-dhp and then allopregnanolone. It may be no coincidence. So low activity of 5a-reductase equal high progesterone, low allo and low dihydrotestosterone.

helllo,i sufferd from pois for 7 years,it was a nightmer my i had severe brain fog and itchy eyes,i lost a lot of opportunities because of brain fog,i tried a lot of doctors:urologist?Immunologist mostly,no results or little results
i thought it might be related to brain so i went to a neurosurgen and gave him the articles about pois he told me to visit his friend who was  on of the top Psychiatrist in the country,after some sessions with him,he told me that my pois is caused by imbalance in my brain biochemistry and its psychosomatic but "it has  physical roots in brain,he prescribed 80 miligrams of prozac and 20 miligram of bouspirion and after 3 months i had no brain fog or itchy eyes,i never felt this great in my life,guys find the best psychiatrist in your county and ask for his or her help,maybe your case is similar to mine or brain related

https://en.wikipedia.org/wiki/Fluoxetine#Pharmacodynamics

"Fluoxetine increases the concentration of circulating allopregnanolone, a potent GABAA receptor positive allosteric modulator, in the brain."

"In addition, fluoxetine has been found to act as an agonist of the sigma-1 receptor."
« Last Edit: July 19, 2021, 05:10:07 AM by Muon »

Prospero

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Re: An introduction to Prospero's case
« Reply #42 on: July 19, 2021, 04:25:26 PM »
Interesting findings, Muon, thanks.

As for sigma receptors, I'm a bit worried. When I read that "physiologic effects when the sigma-receptor is activated include hypertonia, tachycardia, tachypnea, antitussive effects, and mydriasis" (wiki), it resembles some of my symptoms. I also read that it increases glutamate release. But if I have high progesterone I would expect the opposite, excessive antagonism of sigma receptors. Or would extra progesterone be produced by the body to counter over-activation of sigma receptors?

I have new blood tests coming in a few days, I'll keep you updated.
« Last Edit: July 19, 2021, 04:27:37 PM by Prospero »

Muon

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Re: An introduction to Prospero's case
« Reply #43 on: July 20, 2021, 07:52:27 AM »
Or would extra progesterone be produced by the body to counter over-activation of sigma receptors?

IDK. takedrugstoletgo said that her menstrual cycle induces POIS like symptoms when progesterone rises plus she becomes more attracted to same sex in POIS mode. So this could be pointing in the direction of progesterone. The latter could perturb some kind of balance. If the sigma's are overactive then, you would say, a rise in progesterone would decrease the POIS symptoms but the opposite is true in the example above, that is, if changes in progesterone affects POIS symptoms at all. So does progesterone rise upon orgasm?

I've tried medication that targets P4 receptors but without any noticable effect. Same dose as in the 2nd POIS paper. The sigma-1 receptor modulates calcium signaling through the IP3 receptor. I don't have knowledge about these mechanics. I already mentioned in my thread that decreases of intracellular calcium could play a role in lymphocytes regarding the lab data. There are other hormones that bind to sigma's as well. Sigma 2 is involved in mTOR which is linked to cancer (and mast cell activation). High levels in men: High progesterone levels are associated with family history of premature coronary artery disease in young healthy adult men

https://en.wikipedia.org/wiki/Sigma-1_receptor
« Last Edit: July 20, 2021, 07:55:45 AM by Muon »

Prospero

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Re: An introduction to Prospero's case
« Reply #44 on: July 22, 2021, 03:28:32 PM »
Some new blood tests.

DHT: 0.69 ng/ml (RR: 0.33-1.20)
Aldosterone: 312 pg/ml (RR: 67-335)
Renin: 12.60 pg/ml (RR: 5-40)
Vit. B6: 89 nmol/l (RR: 42-145)

So it seems normal, though Aldosterone is quite high. But what is puzzling is the result for amino acids. They're almost all under the reference range. Extremely strange.

Alanine: 182 micromol/l (RR: 286-416)
Arginine: 48 micromol/l (RR: 61-103)
Asparagine: 42 micromol/l (RR: 45-72)
Aspartic acid: 2 micromol/l (RR: ?)
Citrulline: 17 micromol/l (RR: 20-34)
Cystine: 9 micromol/l (RR: 65-109)
Glutamic acid: 14 micromol/l (RR: 9-107)
Glutamin: 263 micromol/l (RR: 432-706)
Glycine: 132 micromol/l (RR: 181-293)
Histidine: 48 micromol/l (RR: 73-97)
Hydroxyproline: 8 micromol/l (RR: <37)
Isoleucine: 46 micromol/l (RR: 54-78)
Leucine: 82 micromol/l (RR: 109-153)
Lysine: 119 micromol/l (RR: 157-231)
Methionine: 17 micromol/l (RR: 21-35)
Ornithine: 37 micromol/l (RR: 50-100)
Phenylalanine: 33 micromol/l (RR: 43-65)
Proline: 96 micromol/l (RR: 150-224)
Serine: 76 micromol/l (RR: 98-174)
Taurine: 35 micromol/l (RR: 30-116)
Threonine: 77 micromol/l (RR: 97-197)
Tryptophan: 43 micromol/l
Tyrosine: 27 micromol/l (RR: 50-76)
Valine: 167 micromol/l (RR: 213-283)
1-Methylhistidine: 4 micromol/l
3-Methylhistidine: <10 micromol/l
AABA: 14 micromol/l
Argininosuccinic acid: 6 micromol/l
Homocitrullin: 2 micromol/l
Pipecolic acid: 4 micromol/l
Beta-alanine: 4 micromol/l
Ethanolamine: 6 micromol/l
Hydroxylysin: 1 micromol/l
Phosphoethanolamine: 4 micromol/l
Saccharopine: 8 micromol/l
Sarcosine: 1 micromol/l

Muon

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Re: An introduction to Prospero's case
« Reply #45 on: July 22, 2021, 03:41:10 PM »
Aminos Acids (No GABA detected and low in GABA precursors like Leucine, Glutamine, Valine, Serine)
_URINE AMINO ACIDS QUANTITATION_
Ref Range:
AMINO ACID Result (uM/mM Crea) Reference Range (uM/mM Crea)
~
Phosphoserine 4 Not Detected
Taurine 58 16-180
Phosphoethanolamine 3 Not Detected
Aspartic Acid 2 2-7
Hydroxyproline 1 <13
Threonine *6 7-29
Serine *16 21-50
Asparagine 4 <23
Glutamic Acid 1 <12
Glutamine 20 20-76
Sarcosine 0 Not Detected
Alpha Aminoadipic acid 1 Not Detected
Proline 0 <9
Glycine 46 43-173
Alanine 21 16-68
Citrulline 1 <4
Alpha Aminobutyric 0 <4
Valine 3 3-13
Cystine 3 3-17
Methionine *1 2-16
Isoleucine 1 <4
Leucine *1 2-11
Tyrosine 3 2-23
Phenylalanine 3 2-19
Beta Alanine 2 Not Detected
Beta Aminoisobutyric 2 <91
GABA 0 Not Detected
Ethanolamine 17 Not Detected
Tryptophan 0 Not Detected
Hydroxylysine 0 Not Detected
Ornithine 2 <5
Lysine 7 7-58
1-Methylhistidine 59 Not Detected
Histidine *25 26-153
3-Methylhistidine *14 19-47
Anserine 1 Not Detected
Carnosine 5 Not Detected
Arginine 1 <5
-
Creatinine 1469 mg/l

Lab Interpretation:
Aminoacids (U): Essentially normal urinary excretion of
physiological aminoacids. Excluded are cystinuria, Hartnup
disease, and lysinuric protein intolerance. No generalised
hyperaminoaciduria.

Muon

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Re: An introduction to Prospero's case
« Reply #46 on: July 22, 2021, 04:07:19 PM »
But what is puzzling is the result for amino acids. They're almost all under the reference range. Extremely strange.
Malabsorption?

Prospero

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Re: An introduction to Prospero's case
« Reply #47 on: July 22, 2021, 04:15:50 PM »
It's the first explanation I can think of, given that I'm underweight and have chronic constipation problems. Still, I have no deficiency for the vitamins I tested, nor iron etc., so it seems strange.
The lab made a little comment suggesting that empty stomach when I did the test was a possible explanation for low values (the body used the amino acids) but I had normal meals the days before, and I guess that everyone does the blood tests in the morning with empty stomach, so I'm a bit skeptic.

Iwillbeatthis

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Re: An introduction to Prospero's case
« Reply #48 on: July 22, 2021, 08:20:02 PM »
https://feelgoodbiochem.com/chapter-5/

"For low overall amino acids, either you are not eating enough protein and/or your GI tract is not absorbing them well. Consider appropriate diet and supplements to address amino acid support. Consider a CSA test and GI Test to address digestive issues. You can also consider running an Intestinal Permeability test and a Celiac test. Also consider a MAP test to look for ketosis. For low overall amino acids, consider Egg Protein Powder, AminoAssist capsules, and AminoAssist spray for three routes of administration of amino acids. Also, consider Bowel Support nucleotide blend, VitaOrgan, and Royal Jelly, if you have no bee allergies. Ora-Placenta may also be a help to support amino acids."

Copied from Amy Yasko (methyl cycle expert) biochemical test guide website, the products and tests mentioned are on https://www.holisticheal.com/. You can find more info on each specific amino acid on the first link I provided. The AminoAssist, egg protien powder, vitaorgan bowel support rna would be most helpful.

If you are gonna get a test like this again eg: hair mineral, gut tests I would recommend getting it through her website so you can get her suggestions specific to your results. She's seen tens of thousands of the same tests so she knows exactly what to suggest based on the levels of each amino acid etc. Which is better than just doing a test yourself somewhere and then not knowing how to fix it.



Muon

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Re: An introduction to Prospero's case
« Reply #50 on: July 24, 2021, 01:21:21 PM »
https://forums.phoenixrising.me/threads/channelopathy-in-cfs.84906/

@Prospero
Discussion about TRMP3, progesterone, pregnenolone, mu-opioid interaction. NK cells contain this channel as well. My IL-2 drops down and wonder whether it suppresses NK cell function which could tie into nanna's theory about viral replication (it sure affects Tregs). I haven't read everything.

Prospero

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Re: An introduction to Prospero's case
« Reply #51 on: July 29, 2021, 03:51:13 PM »
A quick update of my case: since approximately three months, the intensity of my POIS decreased significantly. Especially the permanent symptoms I was suffering from, which are much less violent and even perceptible (I had tachycardia absolutely all the time until April, in particular, and now much less and only in the hours following arousal). If I abstain from arousal for more than a day, I feel almost normal after the night, and showers systematically erase my post-arousal symptoms. As for the post-orgasmic symptoms, they're still there, but well controlled with Paracetamol, and they disappear after a day or two.
So this is for the "hard" symptoms, but I still do not feel like before my POIS become "permanent": I never feel perfectly healthy, physically or psychologically, and just a little arousal is enough to trigger the usual symptoms again. (There are often different symptoms according to the time, not the complete set each time: sometimes chills, sometimes pelvic pain, sometimes need to sleep, loss of appetite... though always nervousness, mood shift, weakness.)

What I've done concretely since April:
1/ stop taking Omega-3 (they were beneficial in the beginning, they calmed tachycardia, nervous and anxiety-related symptoms, but I felt that some other POIS problems were increased after a few months, like strange issues when falling asleep, and they ceased immediately after stopping Omega-3 ; and they were less efficient in the long run, tachycardia had returned after weeks or months and I was feeling generally unwell) ;
2/ taking artichoke+rosemary pills daily for 2 months, which are supposed to be good for the intestines and liver, and have choleretic properties: gut problems decreased markedly (no more constipation, although it returns if I stop the pills), I don't know if it's linked to the rest of the symptoms decrease ;
3/ eating more eggs, approximately every two days. (EDIT: + I also stopped milk and ate much less cheese.)
So I don't know precisely why, but after a few weeks, in May, I was really better and I still am. No change since then.

Next envisaged steps: I believe that I'll try a supplementation of amino acids to see if it changes anything, and I shall probably look for a few other blood tests (B1, B3, cortisol, ACTH come to my mind as for now). I may also see a gastroenterologist.
« Last Edit: July 30, 2021, 12:20:10 PM by Prospero »

Prospero

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Re: An introduction to Prospero's case
« Reply #52 on: October 03, 2021, 07:26:38 AM »
Bacterial analysis of sperm reveals the presence of Streptococcus anginosus.

Hopeoneday

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Re: An introduction to Prospero's case
« Reply #53 on: October 11, 2021, 04:09:16 PM »
Hi Prospero, this is intresting finding.
Do you hawe history of tooth root problems?
Can you be suspicios for hiden infection in root chhanel in your case?
« Last Edit: October 11, 2021, 04:41:14 PM by Hopeoneday »
Dr-pois.

Prospero

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Re: An introduction to Prospero's case
« Reply #54 on: October 11, 2021, 05:34:40 PM »
I have no particular reason to believe this - but who knows?

Prospero

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Re: An introduction to Prospero's case
« Reply #55 on: October 22, 2021, 01:35:13 PM »
New experience confirming what is already a known phenomenon among several Poisers : I have a cold these days, I tried to orgasm some time ago and - zero Pois, I feel completely normal.
To be honest I was quite sure I would get this result, as this morning I had noticed that I had no problem to wake up early in the morning, while usually it's horribly difficult as I'm in a state of unnatural torpor when I'm stretched out. It's one of the features of my Pois which have become permanent so far, with the weird feeling of sexual pleasure radiating in my head and along my spinal column at random moments (which is obviously connected, and was gone since the beginning of my cold too).

Prospero

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Re: An introduction to Prospero's case
« Reply #56 on: January 30, 2022, 04:51:48 PM »
Maybe not an uninteresting experience : after two weeks of abstinence and being a little constipated these days, when I defecated I had a slow runoff of sperm (only seminal fluid I guess?) - so, apparently from pressure on the prostate. I didn't get the slightest POIS symptom.
Arguably it means that my POIS isn't caused by seminal fluid or seminal fluid contact with the urethral tract, but either from semen itself or from the neurological processes of arousal, pleasure and orgasm. Or at least that another element linked to arousal and O is necessary to trigger symptoms.

Apart from this, I'm beginning an antibiotic treatment for my streptococcus infection, will post any result.

StrengththroughChrist

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Re: An introduction to Prospero's case
« Reply #57 on: February 04, 2022, 03:45:36 AM »
Brother pray to God and Jesus they will change your life forever and try antihistamines they made my pois go away when ever I have a nocturnal emission I take a Benadryl and it goes away

berlin1984

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Re: An introduction to Prospero's case
« Reply #58 on: February 04, 2022, 07:51:39 AM »
Welcome to the forum, StrengththroughChrist!

Please comment your Benadryl strength and dosage on https://poiscenter.com/forums/index.php?topic=31
What about non-nocturnal emission like sex or masturbation?
Especially also the timing, how long before/after orgasm do you take it?
Also please comment there (not here) which symptoms you have if you don't take Benadryl.

Thank you

Progecitor

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Re: An introduction to Prospero's case
« Reply #59 on: March 05, 2022, 02:44:45 PM »
S-adenosyl-L-methionine (SAMe) serves as an effective methyl donor while S-adenosyl-L-homocysteine (SAH) is a potent modulator of DNMTs and HNMTs activity. Dietary folic acid (200 mg/day) and vitamin B1 (0.8–1 mg/day) are essential for conversion of homocysteine (hyc) to methionine.
http://statics.drvoice.cn/uploadfile/2019/0217/20190217055754211.pdf

I saw you had a high homocysteine, while also a low methionine level. Although your folate level was all right, but it may be possible that you could still benefit from a vitamin B1 supplementation. Of course this may not solve every problem.
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.