IronFeather's case (female, 25 years old)

[Hopeoneday]

About tachichardia, i discovered that is becuse of pois affect
nervous system( is this because norephiderphine spike in pois
, who knows) or because autoimune reaction that affect
ours nervous system and thus we hawe thouse symptomes.

Tachichardia in is not always the same, but i did
had  a lot of bad
pois episodes where my mucules is so stiffed( internal
muscules , esophagal swalowing , pelvis flore , neck..)
Thouse inhibition of muscules, largly inhibit my guts, then food
start to ferment and produce large amoung of gass(sibo)
wich put presure on my esophagal spitcher and then lungs
and that heart(vagus nerve tachichardia) eg the you get
heital hernia from all this.

This couse tachicardia in my case.(must lerned
this in a tuff way) no doctor will tell you this.

Try to notice do you hawe hiden air in top of yours stomac.
Beacause with pois atac and nerwous system
affected ,sensitivity  can produce tachichardias
(presure on spincher where dysfuntcional vagus
nerve send "wrong or write information" "to save you".
Uh, tired now  , maybe some words missing 

[Muon]

I’ve spoken to a woman who had colitis. She recovered with oral FMT capsules and snake venom. Sniffing the snake venom only once changed something inside her brain and since that moment her colitis was gone.

[Hopeoneday]

She sniff of her nose..



and baaam, colitis is gone

[IronFeather]

Hi Iron, what i forgot to ask you.. when you do high visual sexual
arousall , than lubricating fluids is start to producing, do you
feel eny inflamation or pain i yours reproductive organs?
Do you get eny pois symptomes from that or you need
"OF" to start pois cascade and symptomes?

For exemple i did some testings, visuall arousall on porpes for 20 min,
no masturbation , no ejac... in mans, lubricating fluids in cowpers
glands is starting to produce, olsou prostate and seminal vesicles
start producing semen products.. and after this i feell
inflamation around glands sometimes and slight pain..
and this will give me 30-50 % pois symptomes withouth "OF",
i am not always get pain in glands but this will hapen after
longer period of sexual abstinence on perpos.

Hi Hopeoneday! I should have replied to this much sooner, I'm sorry that I haven't participated much in the forum recently. For months I've been trying to adapt to the fact that I lost most of the things I loved because of POIS (sports and music), and honestly, I haven't been feeling very happy or motivated. But I'm doing my best to carry on and enjoy and value what I still have.

Before the drastic worsening that happened to me after I started using bleach to clean at home, I never experienced any symptoms from arousal apart from my acne worsening a bit, even if the arousal was very prolonged or intense. But now I do, even five minutes of arousal cause me days of sudden constipation, heart fluttering and extrasystoles, tension in the diaphragm and abdominal muscles, a random feeling of air hunger, brain fog and horrible irritability, diminished appetite, and a severe worsening of my usual acne. The symptom intensity is probably around 60% - 70% of what I usually get after orgasm.

However, I don't get any symptoms after a wet dream, nor do I produce any fluids, even if I experience what feels like very real arousal or even an orgasm in the dream. I think this isn't the norm, and that probably this absence of a physical reaction is the reason why the symptoms don't appear. It feels as if my body was completely disconnected from my brain during those dreams, does that happen to anyone else?

[IronFeather]

Can a MRI prove the changes before and after an O ? Pardon me if its already performed, I am not very updated with POIS Scan results

I haven't ever had an MRI scan, but I do remember that some forum member mentioned he had one and nothing was found. However, that's just a regular MRI scan performed at a random time, not before and after an O like you said. I do wonder if some physical changes would be observed if the second one is performed when the peak of the symptoms has been reached, like an enlarged pituitary gland, for example, in POISers who experience severe symptoms (I doubt anything could be seen in a scan like that in the initial stages of POIS, when the symptoms are mild). But I honestly have no idea.

[Prospero]

However, I don't get any symptoms after a wet dream, nor do I produce any fluids, even if I experience what feels like very real arousal or even an orgasm in the dream. I think this isn't the norm, and that probably this absence of a physical reaction is the reason why the symptoms don't appear. It feels as if my body was completely disconnected from my brain during those dreams, does that happen to anyone else?

Hi IronFeather. I believe that I can relate: with erotic dreams, in which I'm aroused to the point of orgasm, I've experienced two possible ends: either I ejaculate, and in this case my brain wakes up *during* the beginning of the ejaculation and triggers a *real* orgasm, until the end of the ejaculation - and I get classic POIS. Or something strange happens, which was the case in one or two occasions. In my dream I do begin to orgasm but it wakes me up just before the actual ejaculation happens (or just at the beginning, with only a little sperm as proof of the orgasm) and *I don't have a real orgasm* : waking up completely suppresses the orgasm and I realize I was only dreaming : I go from the middle of a dreamt orgasm to zero arousal instantaneously, my mind being as fresh and sober as if I was in the middle of a conversation with my grandmother. And I don't get POIS.

As for post-arousal symptoms, as I've narrated in my personal thread, I've just succeeded in suppressing them completely by taking zinc supplementation daily. It may not work for you, but for what it's worth...

[_kid]

If you try to would like to try to help her, don't waste your time... she knows what she has but she just doesn't want to hear it, so in case you want to pitty her I guess she'll be enjoy it but in case you would like to stay to help her.. stay away she just likes to be miserable

[IronFeather]

If you try to would like to try to help her, don't waste your time... she knows what she has but she just doesn't want to hear it, so in case you want to pitty her I guess she'll be enjoy it but in case you would like to stay to help her.. stay away she just likes to be miserable

Where on earth did you come from? Are you the same person than the user _kid who I was talking to before? I assume so, and that for some reason you have two usernames.

You are showing a very childish attitude here with your words, so I am not going to waste my time at all replying to you anymore. If you know what you have, what are you doing in this forum? The only person you are harming with this behavior is yourself, and I truly hope you will be able to improve in the future. You cannot tolerate that people are busy and not able to reply to you right away, so you have to delete your post where you were posing me questions (in a very aggressive and self-righteous way, I must say) and then say this about a person you don't know in the slightest? I have a life, and it's going to continue being that way, so if the fact that you and your theories are not the center of the world bothers you, and if you can't stand people contradicting you, please stay away from my thread until you have something constructive to say.

I'm not going to have MCAS just because it would support your little theory. You are interpreting everything I say in a skewed and biased way, and your ideas are simply incorrect and don't match at all the reality of the symptoms I experience. I don't have any allergic reaction during POIS and I don't have MCAS either.

Good luck, I hope you find a cure for yourself.

[Quantum]

If you try to would like to try to help her, don't waste your time... she knows what she has but she just doesn't want to hear it, so in case you want to pitty her I guess she'll be enjoy it but in case you would like to stay to help her.. stay away she just likes to be miserable

Hi, _kid,

One of the rules on this forum is to be nice and supportive.  This comment of yours is not.  Feel free to review the poiscenter.com rules at https://poiscenter.com/forums/index.php?topic=3774.0

There are a lot of hypotheses about the pathophysiology of POIS.  The similarity between POIS and MCAS is one hypothesis among hundreds of others.  Nothing has been proven yet about any hypothesis on POIS.  So, no one can say anything definitive about it. 

Moreover, we are not allowed to diagnose and give medical advice to others on the forum, which is another rule of poiscenter.com.  You can share what you think about your own case, and share what works for you, and that is as far as you can go. You can also present your hypothesis about POIS in general, with references, scientific explanations, and examples, and discuss this hypothesis with members interested in it. But, you cannot force your opinion on other members and have to respect their differing views.  What you wrote through your kid_, on MCAS, does not respect the forum rules any more than your last message as _kid.

 (note:  both accounts,  kid_ and  _kid, are the same user).

[Muon]

Look at her medical data, abnormal results. She had low urea (Should it not be high in Hyperammonia?). Acetone in urine was high 60 mg/dl (0-5). The latter can be elevated when you are on a ketodiet if I’m not mistaken. She also said she ate for two people. People complain of bad body odor, I wonder if these things are related. She is also skinny. Is the body unable to metabolize carbs properly leading to ketosis?

https://www.thehealthboard.com/what-can-cause-acetone-in-urine.htm

There are several other conditions that may contribute to the presence of ketones in a person's urine. Among them are pregnancy, breastfeeding, and sometimes even fever. Each of these conditions can temporarily raise a person’s metabolism. When this happens, a person either eats more to compensate for the body burning glucose at a faster rate, or goes into ketosis, with the accompanying presence of acetone in urine.

https://m.iliveok.com/health/smell-acetone-urine-causes-and-what-do_125852i15952.html

[demografx]

Do you believe…that [POIS] could have something to do with the refractory period…

Always have.

In my case, I believe refractory sluggishness is the culprit. Recently, my CPAP machine has improved my POIS enormously (and joyously!) I believe my newfound energy is speeding up the refractory process - - along with my TRT treatment.

But - - as Quantum indicates - - let’s wait a few months before declaring success.

I have been experimenting with Cialis:

“One 2017 meta-analysis found that taking PDE5 inhibitors like Viagra, Cialis, and Levitra boosted the number of motile sperm as well as normally shaped sperm.”

I think I see POIS improvement, perhaps my refractory sluggishness - - my POIS theory since 2007 - -  is speeding up?

[Muon]

Caffeine pills and exercise?
Cognition and Brain Activation in Response to Various Doses of Caffeine: A Near-Infrared Spectroscopy Study

[Muon]

Central Sensitization Syndrome could explain some of your triggers (chemical sensitivity, exercise intolerance, POIS?).

[Progecitor]

Further information pertaining to a possible link to hypochlorite hypersensitivity.
In your lab tests your neutrophils and leukocytes were often on the higher end, which is probably related.

In addition, environmental pollutants including formaldehyde, acetaldehyde, industrial isothiocyanate, hypochlorite, and acrolein (which is also produced during endogenous LPO processes), have been shown to cause irritation, coughing, and pain by stimulating TRPA1 through the same covalent binding mechanism.
https://www.mdpi.com/1422-0067/15/9/16430

Non-enzymatic lipid peroxidation induced by oxidants such as superoxide, hydrogen peroxide, hypochlorous acid and peroxynitrite generates reactive lipid species such as 4-hydroxynonenal (4-HNE) from polyunsaturated fatty acids (PUFA) of membrane lipid bilayers.
Experimental models of inflammatory diseases demonstrate that 4-HNE is produced by activated neutrophils which can serve as a potent chemoattractant for further leukocyte recruitment to the inflammatory foci.
https://www.sciencedirect.com/science/article/pii/S2213231716300490

Based on this it may be worthwhile to supplement plasmalogens and maybe to try some COX-2 inhibitors, which also helped several other people here.

Plasmalogens (Pls) are particularly susceptible to attack by ROS, while oxidative stress has been proposed as an additional mechanism for the Pls depletion in septic-related conditions, such as in COVID-19 severe cases. Of note, in sepsis, the Pls vinyl ether bond can be targeted by neutrophil-derived hypochlorous acid (a product of myeloperoxidase activity, highly increased in acute systemic infection in neutrophils) resulting in 2-chlorofatty aldehyde and 2-chlorofatty acid production. Increased 2-chlorofatty acid plasma levels associate with ARDS-induced mortality in human sepsis and several organ dysfunction in rats subjected to cecal slurry sepsis. In addition, in vitro and in vivo studies have shown that chlorinated lipids play an active role in the dysregulated host immune response in sepsis. For instance, 2-chlorofatty acid is a potent neutrophil chemotactic agent, which induces cyclooxygenase-2 (COX-2) expression in endothelial cells and lung alveolar cells, and disrupts the endothelial-blood barrier, including the BBB. Pls attacked by free radicals were proposed to generate precursors for chlorinated lipid production during sepsis with subsequent consequences on organ dysfunction, including in lung acute injury and ARDS.
https://www.sciencedirect.com/science/article/pii/S0361923023001272

More info on plasmalogens:
https://poiscenter.com/forums/index.php?topic=4321.msg47808#msg47808

Furthermore a probable reason for tachycardia is sepsis induced inflammation.

Patients with sepsis predispose cardiac arrhythmias because of excessive inflammation and circulating stress hormones. We identified that low mean arterial pressure, high body temperature and high procalcitonin levels were important factors in tachycardia etiology. According to our findings, there may be also a relationship between inflammation and tachycardia.
Hypotension in patients with sepsis results sympathetic nervous system activation and increase in heart rate.
It is stated that the sensitivity and specificity of procalcitonin are higher than many other mediators in defining the severe sepsis. Tachycardia is a result of endogenous mediators induced by inflammation like sepsis.
https://article.scholarena.com/Sepsis-and-Tachycardia-Etiologic-Factors-and-Effects-on-Prognosis.pdf

We show that exogenously added HOCl attacks the cellular plasmalogen pool and gives rise to the formation of 2-chlorohexadecanal (2-ClHDA). Reactive electrophile species (RES) are able to activate the cellular defense machinery, including the Keap1/Nrf2 antioxidant response, the unfolded protein response, or the heat shock response (HSR). Here, we show that 2-ClHDyA targets cytosolic and nuclear members of the HSR protein network. This is reminiscent of what has been reported for other prototypic RES like 15d-PGJ2, 4-hydroxynonenal (HNE), or acrolein that are potent inducers of the HSR.
Sepsis, a systemic inflammatory response that follows bacterial infection, is characterized by hypotension, ischemia, and multiple organ failure. Cardiac dysfunction is a consequence of sepsis and characterized by impaired contractility, diastolic dysfunction, and reduced ejection fraction.
Under septic conditions chemokine-, cytokine-, and tumor necrosis factor alpha (TNFa) release, alterations in nitric oxide (NO) production, dysfunctional Ca2+ homeostasis, activation of the complement and coagulation system, and impaired beta-adrenergic signaling contribute to organ dysfunction. As an additional culprit, myocardial metabolism shifts from fatty acid (FA) and glucose oxidation toward aerobic glycolysis and lactate production.
https://www.mdpi.com/1422-0067/21/23/9235


By the way have you by chance found any useful treatments in the meanwhile?

[Progecitor]

Additional HOCl scavengers:
It is well known that taurine removes hypochlorous acid (HOCl) by reacting with it to form chlorotaurine, and that HOCl stress impairs SOD activity. However, sulfur-containing amino acids such as cysteine or methionine can also scavenge HOCl.
https://www.researchgate.net/profile/Masato-Higuchi-2/publication/225041917_Taurine_plays_an_important_role_in_the_protection_of_spermatogonia_from_oxidative_stress/links/00b7d514a5c0763713000000/Taurine-plays-an-important-role-in-the-protection-of-spermatogonia-from-oxidative-stress.pdf