Author Topic: POIS treatment: theory & supplement stack  (Read 204614 times)


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Re: POIS treatment: theory & supplement stack
« Reply #560 on: January 05, 2021, 09:47:21 AM »
Interesting, I always thought DHA was a good thing. I have all the classic constant CFS symptoms in addition to POIS / MCAS / etc. I'll have to check into that. Any particular pure EPA brands you recommend? - I buy mine from here and they explain why they use no DHA in the article, Puri also said that pure epa will get the body to start making its own DHA

I found the best dose for me is just one capsule before meals if I take two I don't get the same effect, however Proffessor Puri uses much higher doses in his ME patients of like 2000mg a day he also uses Vegepa instead from amazon which I have not tried but they seem similar.

Nanna's reasoning on EPA and DHA : "About Omega-3: Because of the way that EPA is metabolised in the body, it does not have any toxicity in the body. So, the more the merrier! DHA has a theoretical toxicity, but this has never been demonstrated in vivo"

I noticed healing in my brain instantly from the first capsule, my speech improved drastically also, reactions to showers became much less and no rashes anymore. I've spent thousands of pounds on different supplements and this has definitely been the best one. I must add that I've used four fish oils with DHA in the past and I end up feeling worse.

I think this oil is a must try option if you have any of these aspergers symptoms, chronic fatigue, depression, mcas, lyme disease, feeling inflamed in your brain the whole time, viral infections.

I had a bad O so POIS interrupted the healing process of the EPA for a few days but afterwards I started to feel the nice healing feeling in the brain again.

I also had a bad reaction to TDCS where autistic symptoms and speech became much worse, I assume it was because of calcium channel signalling issues, and I stopped feeling the effects of the EPA for weeks. But this has nothing to do with the EPA itself, I wouldn't recommend TDCS so much as it's really hit and miss for me - a lot of the times I end up feeling worse. Voltage gated calcium channels could be the issue. I want to try verapamil the calcium channel blocker mentioned in this article about Arachidonic Acid and autism. Verapamil is also a mast cell stabiliser and this article says it has fixed people's gut issues.
« Last Edit: January 05, 2021, 09:51:37 AM by Iwillbeatthis »


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Re: POIS treatment: theory & supplement stack
« Reply #561 on: January 29, 2021, 03:04:22 PM »
I had 2 Os in the morning today for the first time in weeks and I am feeling the bad effects a lot more than I normally have been recently. I'm feeling pretty nauseous as well.

In the last few Os before this, a strange thing started happening where I would get a serotonin/endorphin boost and feel really good straight after the O, now I don't know if that was because I was taking the pure EPA or because of the Brain gain supplement but I did run out of the brain gain supplement for a few weeks now as I wasn't sure whether I should continue it. Today I didn't get that "feel good" boost after O at all. And in the times before this I was mainly getting the symptoms the day after the O however I was only doing one O and usually in the evening.

Anyway I'm going to order the flavonoid/folinic acid brain gain supplement again to see if it was that, I'm also going to buy cystoprotek as I want my bladder to heal.

Bob Morane

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Re: POIS treatment: theory & supplement stack
« Reply #562 on: September 04, 2021, 07:29:55 PM »
Interesting, I always thought DHA was a good thing. I have all the classic constant CFS symptoms in addition to POIS / MCAS / etc. I'll have to check into that. Any particular pure EPA brands you recommend?

This is the brand Professor Puri recommends
I have not tried it. I am just answering your question.


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Re: POIS treatment: theory & supplement stack
« Reply #563 on: November 21, 2021, 03:59:01 PM »
Hello guys, I read the first page and it's seem very interesting so thanks you for that!

Can you tell me if we got possitve feeback about this and what are the news after 4 years? If I want to try can you tell me what should I buy and how should I do it? Sorry but I'm reading so many different think about pois and I'm a little bit confused and lost right now but this stuff seems very promising.


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    • a Chinese man's case and situation of all the POISers undergoing desenz in China
Re: POIS treatment: theory & supplement stack
« Reply #564 on: February 28, 2022, 07:19:09 AM »
  After over a decade, I believe I have cured my POIS. I wanted to open source my supplement stack to get feedback/improvemnets and to help others going through what I went through.

  During orgasm there is a transient increase in norepinephrine release [1] (see Neuroendocrine responses to arousal and orgasm).
  Postorgasmic illness syndrome (POIS) occurs when there is an overexpression of the ?1-adrenergic (a1A) receptor and a subsequent over-stimulation of a1A by rising norepinephrine levels [2]. Part of the effect of ?1-adrenergic , a1A, stimulation is to obtain methyl groups (choline) from the phospholipid bilayer stored in the form of phosphatidylcholine (PC) [3]. a1A stimulation upregulates the enzymes Phospholipase A2 and C, which remove a PC-arachidonic acid molecule from the cell wall (lipid bilayer) and separates PC from arachidonic acid (omega-6 fatty acid, AA) [4]. PC is now free to produce choline and replenish the pool of methyl groups consumed in both semen and neurotransmitter production.

  However, the release of arachidonic acid, or AA, is problematic since it is a key substrate for the production of inflammatory hormones by the enzymes 5-LOX, COX-2 and the CYP450 group [4]. It is the rapid release of AA and mass production of inflammatory hormones (such as prostaglandin E2) that triggers sickness associated with POIS.

  During normal sexual activity, histamine is not elevated (Becker et. al. 2011). However, POIS-like symptoms could be stimulated by non-coital external allergens (food, pollution, etc...), by replacing norepinephrine with either histamine or glutamate, and replacing a1A receptor with either the h1-histaminergic (h1H) or NMDA (NR2B) receptor. For example, histamine stimulation of h1H upregulates the enzyme Phospholipase A2, leading to the same release of PC and AA as discussed above [5, 6].
  Blocking both of the processes represented by red arrows in the figure above would, according to this theory, stop POIS. In other words, each red path is a required step for the disease to manifest. And the upregulation of NF-kB (NF-kappa Beta) by reactive oxygen species (ROS) is a required step for the increased production of COX-2 and inflammation.
  We can refer to the cascade of events, starting with simulation of the a1A, h1H, NR2B receptors and ending with the production of inflammatory prostaglandins, as the POIS Cascade. To stop POIS, you have to modify the POIS Cascade by inhibiting three key events:
1.   ?1-adrenergic and h1-histamine receptor overexpression
2.   NF-kB upregulation and inflammatory cytokine production
3.   arachidonic acid production and release from the PC-arachidonic acid complex

  (1) a1A receptor expression is down regulated by the universal methyl group donor S-adenosyl-methionine (SAM-e) by donating its methyl group through methyltransferase enzymes [7]. In this way, SAM-e prevents the breakdown of the phospholipid bilayer [8] and the subsequent metabolism of AA [9]. h1H receptor expression is down regulated by Protein Kinase C (PKC) inhibition [10]. PKC is potently inhibited by thiamine diphosphate, the active form of vitamin B1 [11]. Moreover, thiamine supplementation reduces median histamine levels [12].
  (2) Vitamin D3 is a strong inhibitor of NF-kB and COX-2 production [Ref link]. D3 accomplishes this by inhibiting the production of inflammatory cytokines such as TNF-a, IL-1B, IL-6, etc... [schematic diagram]
  (3) In the absence of dietary AA, omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) can reduce AA incorporation into the phospholipid bilayer and decrease the production of inflammatory prostaglandins such as PGE2 [4, 13]. Moreover, EPA directly competes with AA for access to enzymes 5-LOX and COX-2 [4]. And unlike AA, the metabolic products of EPA interaction with these enzymes are anti-inflammatory (link).

For a literature review of POIS related research see POIS literature review:

  Below I provide two separate supplement stacks that have given me complete relief of POIS symptoms. "The Betaherpesvirinae stack" is a prepack that targets a specific reactivation mechanism of cytomegalovirus (CMV, HHV-5) and herpes virus 6 (HHV-6) involving suppression of NF-kB and COX activity (see RefSE1, RefSE2). More details on how herpes viruses may initiate POIS can be found here (link). "The POIS Cascade stack" is the general daily health supplement (and vegan diet) regime that I use to treat my POIS, NE, and reduce exercise induced DOMS. These are two separate stacks which are not meant to be taken together. The below quantities for each stack are listed per dose.

The POIS Cascade stack:
On an empty stomach with water or juice, twice daily (water soluble):
---SAM-e (enteric coated)(200mg) [terminal methyl donor, a1A downregulator]
---Pyridoxal-5-phosphate, P-5-P vitamin B6 (2mg - 25mg) [homocysteine regulator]
---Metafolin or folinic acid, vitamin B9 (less than 200mcg) [methyl group cycler]
---cyanocobalamin, vitamin B12 (>50mcg, sublingual) [methyl group cycler]

nannan1, thank you for your post, I want to ask what kind of Vitamin B12 should I take, you said cyanocobalamin should be taken, but the url you shows that it is methylcobalamin. and could you help me to know, the vitamin B9 you recommended is the same as the methylfolate@now as this . thank you!
A Chinese man undergoing desenz from 2021.8 to 2022.2, it became worse from 1.5 to 4.5 days, do not know it is spontaneous deterioration or by desenz. Believe POIS is a kind of immune diseases. My case:


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Re: POIS treatment: theory & supplement stack
« Reply #565 on: March 06, 2022, 05:56:13 PM »
Would it be possible or helpful to combine this stack with the transient immune suppression stack? And if we're not trying to minimize cost, does adding extra 5-LOX like boswellia or COX-2 inhibiting herbs potentially add to the efficacy?

I've found some of this helpful for CFS-like symptoms in general, but I haven't yet found the right 'combo'. Taking copper before meals gives me some nausea, so I assume that means it's doing something. Taking Alpha GPC, SAMe, Methyl B, etc seems to improve my headaches, brain fog, etc - but maybe I need to raise the dosage. Right now taking 300mg Alpha GPC x 2, 500mg TMG x 1, 200mg SAMe x 2, a couple lecithin capsules, one Jarrow Methyl B (split in half, so taken twice a day). And some 150mg benfotiamine, etc.

Anyways, mainly curious thoughts (especially nanna1 if he checks in) on combining this stack with the Transient Immune stack.



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Re: POIS cure: theory & supplement stack
« Reply #566 on: April 26, 2022, 01:54:27 PM »
If this could explain parts of the POIS-trigger, I still would have a few questions:
  • Where is the vascular/balloon injury located?
  • What caused the original injury?
  • Why does the injury not heal now?
In terms of question 1, POIS symptoms are top-bottom asymmetric in everyone but also left-right asymmetric in some. So the inability to heal properly would have to be localized to specific vessels in the body, while not affecting healing in other blood vessel locations. I suspect that the answers to questions 2 and 3 are the same. Whatever would cause the original injury is also probably keeping it from healing, unless the original injury was a random event.

If you have any corrections or other thoughts, please share. That was interesting!

Piezo and CGRP?


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Re: POIS treatment: theory & supplement stack
« Reply #567 on: May 14, 2022, 02:41:40 AM »
Dear nanna1,

thank you for sharing this cascade model to explain POIS with the overexpression or overstimulation of the a1A receptor. This post actually helped me the most and I am struck by the captivating clarity of model and conclusions.
   You mention in one of the responses that Benfotiamime was one of the first things you started with which got you on the right track and I guess that the same is true for me among other important components. I was actually triggered by your post! Now I see that Benfotiamine was recently crossed out in your original post and you explained this with the relatively high costs in one of your later responses. Since the motivation to take it out in the stack is not mentioned in your original post as far as I can see, and there is a strong relevance for the a1A receptor, I would like to ask you to include it again in your stack and instead make clear that one could consider skipping it if the budget is limited. I am writing this since I am convinced about its relevance for me. It can also be possible that - since benfotiamine is fat soluble - a regular continuous intake of such a high dosis is not required to have an effect and maybe one could reduce the dosis after a while.
   Another comment I would like to make is that I am thinking of a connection of POIS with the COMT polymorphism which can be a potential genetic explanation for an overstimulation of the a1A receptor. This would also explain why the intellectual level of posts in this forum is far above average. The COMT polymorphism is associated with high senitivity and intellectual giftedness. ;-)

All the best!