Author Topic: Mucoviscidose (fibrose kystique) Reverse POIS?  (Read 485 times)

Alanboy

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Mucoviscidose (fibrose kystique) Reverse POIS?
« on: December 29, 2021, 05:10:53 PM »
Hello, Alan there 29yo, from france

I follow POISCENTER since like 10 years.

Like a lot of peoples my POIS start around 13-14 yo, i have 29 now. I saw a lot of subject about allergy of your own sperm, but with my desease, i dont have canal deferent, that mean, my sperm stays in my testicles when i "o". I have of course normal orgasme but it's only seminal fluid, not sperm. Maybe that information can help the progress of POIS

I wanted to talk about my POIS life, cause today i have big problems. I renember my first POIS syndrome it was classic symptoms , ( brain fog, congestion nose, eyes red, social problem, muscle weakness, and more)

The problem now, my POIS completly evolved, now my symptoms look like Myathenia Gravis ( i know some peoples got a cholinergic type) the problem i cant use
anticholinesterases drugs due to their side effect of breath, my "Mucoviscidose" is very stable, and atypique i got luck. But i dont want take this risk for the moment. (i tried Lecithin soy)

I didnt respect the POIS rules, last year i had one or two "o" every day. And now when i wait 2 week or more without having an "o" i feel so bad (Myasthenia gravis symtom) I know it's strange, POIS basicaly it's after "o" not if you did nothing 2 week. I have like a "Reverse POIS" since few months, the only thing i changed few months ago, it was Milnacipran drugs, not very bad result but i had premature ejaculation with that drug. I stopped it since few months, but still have night ejaculation... If any have an idea for that problem?

I know some peoples just said you got lucky you feel bad only without having sex, it's not true, i still have the classic Symptom POIS after "o"

And to be honest since this milnacipran, my brain fog stay for ever now, even if i stop having sex.

Another problem discover last years 10 September 2020 i taked Vitamin called "Biotine" B8. for few months no problem, but now if i take just ONE tablet, i have Myasthenia attack very hard. How explain that? what the first time i took like 3 months biotine without problem?

and no more Myasthenia attack SINCE i tried el famoso 5 September 2021 "CBD" make my life worst like never. CBD evolved my POIS i think, i took sublingual form, 5% only, but since that CBD( i stopped it of course), i have myasthenia gravis symptoms

The question is :

-What to do about my nocturnal ejaculations, while i sleep ( Cause "Milnacipran" ) i stopped it, the problem still there
-Biotine = Myasthenia attack, why? due to POIS? CBD = same effect. 1 tablet Biotine = Myasthenia symptoms few days or weeks.
-Reverse POIS possible? (If i wait 15 days without ejaculating and i do = Myasthenia attack)
-Currently the bigest problem it's the brain fog no stop since months with, or without "o"
-excitement, also gives me small symptoms
-How counter that myasthenia gravis  symptom?













Quantum

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #1 on: December 29, 2021, 11:27:17 PM »
Hi Alan,
I have found this webpage about myasthenia gravis and biotin:  https://www.ehealthme.com/ds/biotin/myasthenia-gravis/

It seems to be a rare effect and no explanation yet for the mechanism.
You are 100% responsible for what you do with anything I post on this forum and of any consequence it could have for you.  Forum rule: ""Do not use POISCenter as a substitute for, or to give, medical advice" Read the remaining part at http://poiscenter.com/forums/index.php?topic=1.msg10259#msg10259

hurray

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #2 on: December 30, 2021, 05:51:33 AM »
Hi Alan,

Sorry to hear about your negative experience which you think may be linked to milnacipran. I've taken it "on demand" for almost 2 years.

With regards to nocturnal emissions, I haven't had one since I started taking milnacipran - I rarely had them before I started taking milnacipran either. My experience with premature ejaculation is the opposite to yours - if I've taken milnacipran recently, I can usually "keep things going" for as long as I need to. It's a well-documented side-effect of serotonin reuptake inhibitors, the drug "Priligy" is a short-lasting SSRI that is made specifically for extending premature ejaculation.

One other thing, I almost never go more than 10 days without an O - if I tried to go 2 weeks or more, I strongly suspect that noctural emissions would become a problem. After a week without an O I get very irritable and "horny". I would have really struggled in my 20s to abstain for a week.


Alanboy

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #3 on: December 30, 2021, 08:24:15 AM »
Maybe i can't stand being normal anymore, because i was on POIS H24 last years.

I got good effect from Milnacipran aswell, but, premature ejaculation side effect for me, not good combo with POIS ^^ I heard about that drug too "Priligy"
Thanks Quantum for link, very interesting. I'll try diet without biotine, it is very difficult to find foods that do not contain biotin



hurray

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #4 on: December 30, 2021, 01:45:31 PM »

The problem now, my POIS completly evolved, now my symptoms look like Myathenia Gravis ( i know some peoples got a cholinergic type) the problem i cant use
anticholinesterases drugs due to their side effect of breath, my "Mucoviscidose" is very stable, and atypique i got luck. But i dont want take this risk for the moment. (i tried Lecithin soy)


I went through a period of experimenting with Cholinesterase inhibitors to treat my POIS. I bought a supply of donepezil, galantamine, pyridostigmine and rivastigmine. Donepezil was the most effective of the 4 in reducing my POIS symptoms, but it was nowhere near being 100% effective - 50% at best, perhaps. It has been several years since I tried Donepezil.

I should point out that I do not suffer from any of the symptoms of Myathenia Gravis, and I am just relating my experiences rather than recommending that you take any medicines. On this forum, we always advise that any prescription medicines should be taken only with the advice and supervision of a doctor. Your own experiences are a good illustration of why prescription medicines can be dangerous.

Hopeoneday

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #5 on: January 01, 2022, 07:28:18 AM »
Intresting, how you react on small dosing off coffee?
Dr-pois.

Progecitor

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #6 on: January 08, 2022, 02:57:55 PM »
I am practically the only one here who has had a really terrible experience with biotin. It is true though that I had it from the very first time I took it. Of course it hits me less severely in chronic POIS, but very badly when I am already in an ill state. It is like having a consecutive O and the most noticeable change is that I develop heavily bloodshot eyes. I suspect biotin as the main reason I had a bad experience with complex vitamins B. Maybe you could refer to my treatment methods that I have been building in the past year, but you should also note that this list is not exactly accurate and you should refer to other sources as well. I also don't have MG to the best of my knowledge.
https://poiscenter.com/forums/index.php?topic=3798.0
(ctrl+f: alfalfa)

The positive effects of biotin were mostly discussed here:
https://poiscenter.com/forums/index.php?topic=2192.100
https://poiscenter.com/forums/index.php?topic=2763.msg42272#msg42272

The positive effects of biotin are probably related to PPARG agonism which leads to NF-kB inhibition a known inflammatory factor.
https://en.wikipedia.org/wiki/NF-%CE%BAB

One possible reason for biotin being detrimental is the downregulation of PGC-1a.
https://poiscenter.com/forums/index.php?topic=3986.msg42923#msg42923
(ctrl+f: biotin)

PGC-1a downregulation may be involved in Myasthenia Gravis, although its endogenous regulators (Sirt1 and irisin) are differentially expressed in MG, so a definite conclusion has yet to be made. If you consider testing supplements based on this, please keep in mind the possible implications for COVID-19 as well.
(ctrl+f: Myasthenia)

And some members also have Biotinidase deficiency, but I am not exactly sure how it relates to all of this.
https://poiscenter.com/forums/index.php?topic=3694.msg42218#msg42218

Alanboy

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #7 on: March 25, 2022, 06:43:36 AM »
Thanks Progrecitor for that rich information.

May i ask you which effect you have from biotin? When i take it i literally have a crisis of myasthenia.

I wanted to update my situation, the only thing currently that manages to partially calm my crises it's "Choline Bitartrate" that proove my type of POIS is "Cholinergic"

I am currently in discussion with my neurologists who take seriously the "POIS" syndrome Doctor Miget Gabriel from PARIS. They will doing a "Mestinon" test soon, it's an anticholinesterase, to prevent the breakdown of acetylcholine

Unfortunately my POIS is present even when i abstain, since the Milnacipran that i suspect to have caused me a seminal leak that cause a constant POIS

Alan


Cursed

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #8 on: April 07, 2022, 11:28:01 AM »
Alanboy, whay do you mean your symptoms look like Myasthenia gravis? What symptoms do you get? Have you been diagnosed with it? Have you had any blood tests?

I also had a negative experience wity biotin and don't take it for that reason. It makes me very horny and sensitive, and increases brain fog, etc, strange effect.

Progecitor

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Re: Mucoviscidose (fibrose kystique) Reverse POIS?
« Reply #9 on: May 12, 2022, 12:42:21 PM »
Thanks Progrecitor for that rich information.

May i ask you which effect you have from biotin? When i take it i literally have a crisis of myasthenia.

I wanted to update my situation, the only thing currently that manages to partially calm my crises it's "Choline Bitartrate" that proove my type of POIS is "Cholinergic"

I am currently in discussion with my neurologists who take seriously the "POIS" syndrome Doctor Miget Gabriel from PARIS. They will doing a "Mestinon" test soon, it's an anticholinesterase, to prevent the breakdown of acetylcholine

Unfortunately my POIS is present even when i abstain, since the Milnacipran that i suspect to have caused me a seminal leak that cause a constant POIS

Alan

Hi Alanboy!

I haven’t tested biotin that much, but its effect feels much like having an O. About 2 hours after intake the eyes become more bloodshot and I also feel myself awful. It is like gradually developing a blood poisoning similarly to POIS onset. It may also do something to the kidneys as the urine didn’t burn as usual, but I would need to confirm this with more testing, however I am not too keen in testing things that make me feel worse. The same is true for choline. Interestingly direct choline supplementation seems to make me worse, however many supplements that help me are actually considered acetylcholinesterase inhibitors, which should increase acetylcholine levels. I don’t know if there is a connection between biotin and acetylcholine, but they are probably only parts of the greater picture. For example PGC-1a, estrogens and anandamide also modulate cholinergic activity. Actually biotin decreases PGC-1a, which could be a possible link to acetylcholine receptors.
I hope your Mestinon test was informative if you have already had that, but there are some other AchEI supplements that could be tested for a similar purpose. Most of these were beneficial for me and some even had an anti-depressive effect, namely drotaverine, L-theanine, lungwort, saffron, Polygonum multiflorum.

Acetylcholinesterase levels were significantly decreased dose dependently with drotaverine and decline in AchE levels might be due to the indirect acting cholinergic effect of drotaverine; increasing acetylcholine levels by inhibition of actylcholinesterase.
https://sci-hub.se/https://link.springer.com/article/10.1007/s11064-021-03327-9

Consistent with these traditional uses, Muira puama (P. olacoides) ethanol root extract has shown memory retrieval improvement in young and aging mice in-vitro acetylcholine esterase inhibitory activity and prevention of stress-induced hypothalamic-pituitary-adrenal hyperactivity. In addition, Muira puama formulations have demonstrated efficacy in treating male erectile dysfunction and low libido and low sex drive in women.
https://link.springer.com/article/10.1186/s40203-015-0008-z

Rhodiola has beneficial effects on learning and memory in neonatal rats, through modulation of acetylcholine levels and MAO inhibitory activity.
https://link.springer.com/article/10.1186/s13020-019-0246-9

Astaxanthin showed neuroprotective effect in male albino rats treated with combination of astaxanthin (25 mg/kg/week) and doxorubicin (2 mg/kg/week). Particularly, it restored hippocampal function and cholinesterase activity and reduced ROS and proinflammatory cytokines production.
https://sci-hub.se/https://www.sciencedirect.com/science/article/abs/pii/S1043661819327367

The effects of L-theanine on Abeta and AGE generation were investigated in this study. Decreased AGEs and Abeta1-42 levels were reflected by increased acetylcholine (ACh) concentration and acetylcholinesterase (AChE) activity inhibition compared to model rats.
https://downloads.hindawi.com/journals/omcl/2021/8850112.pdf

The water extract of the fruit rind of G. cambogia produced significant anticholinesterase activity by inhibiting cholinesterase by 30% and 67% at a concentration of 500 and 1000 ug/mL, respectively.
https://sci-hub.se/https://pubmed.ncbi.nlm.nih.gov/25732350/

Random googlings because somewhere in forum it was mentioned that acetylcholinesterase inhibiton (and choline supplementation?) helps, someone with more science knowledge please confirm if relevant:

Pulmonariae officinalis (Lungwort) (Apparantely there are multiple lungworts, so NOT Lobaria pulmonaria)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910643/
The P. officinalis extracts showed slightly lower acetylcholinesterase inhibitory effects – 87.7%, tyrosinase inhibitory effects – 73.69%,

Saffron
https://pubs.acs.org/doi/10.1021/jf300589c
Saffron extract showed moderate AChE inhibitory activity (up to 30%),

The extraction of new substances with AChEI activity from plants has been a very effective method to develop new anti-AD drugs. Galantamine is the only naturally occurring drug on the market, and it consists of alkaloids extracted from Amaryllidaceae. Huperzine A is also a common AChEI developed and marketed independently in China. Huperzine A can alleviate neuroinflammation and oxidative stress and improve cognitive function after repeated traumatic brain injury. The traditional Chinese medicine Yinhuang oral liquid also has significant inhibitory activity against AChE. Zhang et al. identified the following potent AChEIs in Yinhuang oral liquid by using high-performance liquid chromatography-electrospray ionization mass spectrometry (ESI-MS): chlorogenic acid, cryptorchidic acid, baicalin, baicalein, etc. Among the plant extracts reported in other studies, an extract of T. chebula and the aerial part of Amygdalus scoparia (50% inhibition at 300 µg/mL) not only have acetylcholinesterase inhibitory activity but also have antioxidant activity. Palmatine, fluoroureone B, ginseng stem and leaf saponins (GSLS), two kinds of maleimides and macarubiginosin C, and the monoterpene latifolia have been proven to have AChE inhibitory activity and are all potential AChEI candidates.
In addition, (-)-pterin N, coumestrol, and the citrus flavanone hesperidin are all multifunctional inhibitors that have been extracted from nature, showing good inhibition against BACE1, AChE and BchE.
In addition to the dual effect cholinesterase inhibition properties, the leaves of Elatostema papillosum (EPL), Polygonum multiflortan
(mistype?: multiflorum) and Spatholobus suberectus also exhibit potent antioxidant activity.
Recent studies have shown that the extracts of both Cassia tora and Morinda officinalis can effectively inhibit the activity of cholinesterase. Through ITC analysis, Budryn et al. found that active substances in coffee, ferulic acid and dihydrocaffeic acid, could interact strongly with BChE, indicating the potential therapeutic effects of coffee.

https://www.researchgate.net/profile/Xin-Cao-11/publication/337748759_Progress_in_Target_Drug_Molecules_for_Alzheimer%27s_Disease/links/5ef1dc7192851ce9e7fce0f0/Progress-in-Target-Drug-Molecules-for-Alzheimers-Disease.pdf

In the peripheral nervous system, PGC-1a has been shown to regulate gene expression at the neuromuscular junction and influences expression of acetylcholine receptors in muscle fibers. In addition, elevated PGC-1a levels protect neural cells in culture from cell death caused by oxidative-stressor through its induction of antioxidant genes.
https://academic.oup.com/abbs/article/43/4/248/884?login=true

Thymol and carvacrol and their derivatives thymoquinone and thymohydroquinone, terpinen, p-Cymen inhibit the activity of acetylcholinesterase AchE.
Estrogen plays an important role in memory function. In the body, estrogen gives effect through its interaction with estrogen receptor, estrogen alfa receptor (RE-a) and beta (RE-B). Memory function regulation including cholinergic system is through RE-a, while RE-B modulates RE-a activity. The decrease in choline acetyltransferase (ChAT) activity in the hippocampus causes the production of acetylcholine (ACh) in the hippocampus to fall, this may be marked by the decrease of several cholinergic markers, including AChE levels. Estrogen induces ChAT, prevents decreased affinity of up-take choline and ChAT activity in the frontal cortex and hippocampus, influences the transport of neurotropin factor (NGF, BDNF).

https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Black+Cummin+Extract+%28Nigella+sativa+Linn%29+on+Spatial+Memory+Performance+in+Menopausal+Model+of+Rat&btnG=

We conclude that anandamide inhibits the evoked acetylcholine release via stimulation of a receptor that is different from the CB1 and CB2 receptor. Furthermore, anandamide increases basal acetylcholine release via stimulation of vanilloid receptors located at primary afferent fibres. Stimulation of the vanilloid receptor by capsaicin causes an increase in basal acetylcholine release from myenteric neurons and smooth muscle contraction. These excitatory effects of capsaicin are inhibited by the combined blockade of NK1 and NK3 tachykinin receptors, which suggests that the stimulation of vanilloid receptors induces a release of tachykinins which, in turn, cause release of acetylcholine via activation of NK1 and NK3 receptors on cholinergic myenteric motoneurones.
The present study shows that the endocannabinoid anandamide has opposite effects on basal and evoked release of acetylcholine which are mediated by different mechanisms.
Anandamide increased basal acetylcholine release from the myenteric plexus-longitudinal muscle preparation via stimulation of vanilloid receptors. This effect involves the release of tachykinins from afferent nerves. In addition, anandamide inhibited the electrically-evoked release of acetylcholine and longitudinal muscle contraction.  We therefore conclude that anandamide inhibits the evoked acetylcholine release from guinea-pig myenteric neurones via a non-CB1 receptor.

https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1038/sj.bjp.0704220