POIS treatment: theory & supplement stack

[swell]

Nana stack is interesting.   Many a vitamin are used in chronic fatigue syndrome.  Sam-e is excitory med it is not good for everyone if you have nerve overactivity or sensitivity.  I like Sam-e I need to begin again it takes fog away for me and make me happy.  BetaBlocker is good for you it is opposite to SAM.   Sam-e calms you but excite you, BetaBlocker calms you but do not energy you.

Hi Michael218. For me taking only 200mg SAMe lead me in horible state.
That mean this is not for me.
B vit not helping me at all, but I didnt try active b vitamines because cant get them in my country. I am ordered them to test because( kurtosis teory of genetics mutations).

My main problem is evan in apstineting period NERVE OVERSENSIBILITY, that mening evan touching and masaging lover back erea (wright up prostate erea) couse me heatrt palpilation, pelvis floar muscule cramps , asopagus muscule cramps... that afect my quality of life a lot(sewere breathing probl). This all X10 after eyaculation I barly surwive.
When I eksplane this to eny doctor, nowbody bolive me.
Only thing that help me to save my life in hard atacs are small dose of benzos.
All that lead me to i myabe hawe STIFF MAN SINDROME because good reaction on bezos. Stress and wory are bigg NO to our condition, bat that for me is imposible to manage, because i must earn mony for living.

[swell]

Nana1 I have inflammation visible in skin.  Your stack takes on neurology or brain symptom good only?.  So far what help me little is Progesterone, Niacin for inflammation in skin.  Sam-e in past help me very good on mood and mental things.   

The theory diagram below show the COX2, 5LOX and inflamation mediators but not inflamation sensors the Mastcell and Macrophages.  Where do they fit in diagram? or is it a separate pathway.

This post is about theory. Below is a diagram showing the central role that NF-kB (NF-kappaBeta) plays in inflammation. Don't worry about trying to understand all the complicated arrows.

• Region 1 (above the top dashed-line) shows initiators of inflammation (TNF, IL-1, bacterial antigen, virus, etc...).
• Region 2 (below the top dashed-line) shows the NF-kB activator (IKK-alpha, IKK-beta, IKK-gamma) (3 red rectangles).
• Region 3 shows a bunch of biochemistry with activated NF-kB.
• Region 4 (below the bottom dotted-line) shows the genetic up-regulation of Oxidative enzymes (COX, LOX, TDO, IDO, KMO, iNOS, etc...) by NF-kB.

Oxidative enzymes are responsible for inflammation (oxidative stress, allergy, depression, DNA damage, asthma, aging, and other inflammatory diseases). The oxidative enzymes are not shown in the below image.

In the above diagram (Region 1), IL-1 is just representative of the inflammatory class of cytokines (IL-6, IL-8, etc...). All of the inflammatory cytokines activate NF-kB. The anti-inflammatory cytokines (i.e. IL-10) inhibit NF-kB. This discussion fits into the POIS Cascade model in the following way:

[nanna1]

Hi swell,
  Immune cells (mast cell, white blood cell, etc...seen in the below diagram) strongly express NF-kB when activated (click the picture to expand it):

  Therefore, the diagram that I posted on Feb. 4, 2018 (NF-kB Signaling) can be viewed as showing the inside of an immune cell. The outer surface of the cell with its receptors is shown in Region 1. However, almost all cell types express NF-kB to some degree. So immune cells like mast cells and macrophages may not be the only cells involved in COX-2/5-LOX up-regulation.

Hi  rakeshbaasu,
  I noticed that your vitamin D3 supplement contains extra calcium. I would avoid supplementing calcium since free calcium ions in the blood can increase the release of arachidonic acid. Also, I didn't see a source of methyl groups (choline or betaine, etc...) or SAM-e in your stack. If you are having trouble finding all the methylation supplements, you may consider B complex since B complex usually contains some choline. However, be careful to monitor your daily B6 dosage (see original post).

[nanna1]

  In the thread "Muon's Case", one of the POIS Center members generously shared his blood test results showing elevated levels of human herpesvirus type 3 (HHV-3, Varicella zoster virus, chickenpox) and human herpesvirus 5 (HHV-5, cytomegalovirus). HHV-5 doesn't seem to be POIS related because it is very common and has few symptoms. However, HHV-3 has symptoms that are very similar to POIS. I also was infected with HHV-3 as a child. So, I did some reading recently on herpes viruses (herpes simplex virus, HSV) and (human herpesvirus, HHV) and just wanted to share. I assume the herpes HHV-(1,2,3,4,5,6) have similar in basic structure/function. HSV-1 and HSV-2 are also known as HHV-1 and HHV-2 respectively. So I referred to HHV and HSV interchangeably.

 HHV-3 infects and is stored in cells of the nervous system (neurons, astrocytes, etc...). Once herpes is activated, it starts to replicate and migrate through the nervous system in the dendrites. In these cells, HSV upregulates COX-2 in order to replicate [A1,A2,A3]. The upregulation of COX-2 by HSV occurs through JNK gene activation [J1,J2,J3]. HSV activation requires both JNK up-regulation and de-methylation of the herpes DNA [J2,J3]. The authors of this paper were able to stop herpes outbreaks by inhibiting the JNK gene alone [J1,J3]. I tried to summarize my current understanding of the papers [A1,A2,A3,J1,J2,J3] in the below diagram:

Prostaglandins activate JNK. JNK de-methylates viral DNA leading to viral symptoms. JNK also up-regulates COX-2 to produce more prostaglandins. This cycle requires a steady supply of arachidonic acid. (This diagram is greatly simplified. For example, PGE₂ upregulates IFN-y/TDO/IDO, but that is not shown here.)

Natural JNK inhibitors:

Taurine:
  During inflammation, taurine is converted into the anti-inflammatory molecule, Taurine chloramine (N-Chlorotaurine), inside of activated immune cells (neutrophil, macrophage, mast cells, etc...)[D1]. Taurine chloramine then selectively inhibits inflammatory enzymes such as COX-2 [E] and 5-LOX [F]. Taurine has been shown to inhibit HSV in vitro in human cells [K4] and inhibit JNK activation in vivo[K1,K2,K3] in animals.

PQQ:
  Pyrroloquinoline Quinone (PQQ) downregulates every known inflammatory pathway, including JNK, NF-kB, COX-2 and several cytokines [L1,L2]. However, PQQ is believed to have poor bioavailability. So it is not clear how much is actually absorbed in the body. Possible source

Methylators:
  The HSV virus replicates in a low methylation environment. There is already plenty of discussion of methyl donors in this thread. So I'll just refer to the below diagram. Purple arrows inserted by me:

(1)SAMe, (2)TMG (betaine) or choline, (3)B12, (4)B6, (5)B9 (metafolin)

COX-2 inhibitors:
  My neurologist once prescribed the COX-2 inhibitor, indomethacin, to me to treat orgasm induced headaches. I didn't take it at the time because indomethacin has longterm side effects on the stomach and liver. Recently, I tested indomethacin (~30 min prior to sex) without taking the POIS Cascade Stack for one-week. Indomethacin alone stopped 85% of my POIS symptoms. Their was some mild discomfort in my left ear and left side of forehead. This discomfort did not effect my productivity at work. I took a second dose of indomethacin the next day along with a Gen-1 H1-histamine receptor blocker, and all of my POIS symptoms were gone.

Gallic acid:
  Because of the side-effects of indomethacin, I find it unexceptable as a longterm treatment. One alternative could be Gallic acid. Gallic acid is a 10 times stronger COX-2 inhibitor than indomethacin, and it is also a strong mast cell stabilizer [G1]. Gallic acid is a moderate herpes simplex virus (HSV) inhibitor [H1,H2] although the anti-viral medicine Acyclovir was 100 times more effective than Gallic acid [H1]. Gallic acid is found in tea leaves, cocao and apple cider vinegar. More info here.

  I don't know if a herpes is a cause of POIS, but it seems interesting. Muon's blood test results also showed a possible candida infection. So there could be other infections. I hope this sparks some discussion and ideas of a cause.

References:
A1. Kaposi's sarcoma associated herpes virus (KSHV) induced COX-2: a key factor in latency, inflammation, angiogenesis, cell survival and invasion.
A2. COX-2 Induction during Murine Gammaherpesvirus 68 Infection Leads to Enhancement of Viral Gene Expression
A3. Cyclooxygenase-1 and -2 Are Required for Production of Infectious Pseudorabies Virus
A4. Activation of Monocyte Cyclooxygenase-2 Gene Expression by Human Herpesvirus 6: ROLE FOR CYCLIC AMP-RESPONSIVE ELEMENT-BINDING PROTEIN AND ACTIVATOR PROTEIN-1
D1. Taurine chloramine
E. Selective inhibition of cyclooxygenase 2-generated prostaglandin E2 synthesis in rheumatoid arthritis synoviocytes by taurine chloramine.
F. Influence of taurine and a substituted taurine on the respiratory burst pathway in the inflammatory response
G. Cost effective alternatives for omega-3: Gallic acid
H1. Anti-HSV-1 and anti-HIV-1 activity of gallic acid and pentyl gallate
H2. Evaluation of Anti-HSV-2 Activity of Gallic Acid and Pentyl Gallate
I1. Effects of caffeine and paracetamol alone or in combination with acetylsalicylic acid on prostaglandin E2 synthesis in rat microglial cells
I2. Caffeine Promotes Ultraviolet B-induced Apoptosis in Human Keratinocytes without Complete DNA Repair
J1. Discovery shows how herpes simplex virus reactivates in neurons to trigger disease
J2. JNK-mediated induction of cyclooxygenase 2 is required for neurodegeneration in a mouse model of Parkinson's disease
J3. Neuronal Stress Pathway Mediating a Histone Methyl/Phospho Switch Is Required for Herpes Simplex Virus Reactivation
K1. Taurine Protects Mouse Liver Against Arsenic-Induced Apoptosis Through JNK Pathway.
K2. Taurine reduces FK506-induced generation of ROS and activation of JNK and Bax in Madin Darby canine kidney cells.
K3. Taurine suppresses doxorubicin-triggered oxidative stress and cardiac apoptosis in rat via up-regulation of PI3-K/Akt and inhibition of p53, p38-JNK
K4. Activity of N-chlorotaurine against herpes simplex- and adenoviruses.
L1. Pyrroloquinoline Quinone (PQQ) Inhibits Lipopolysaccharide Induced Inflammation in Part via Downregulated NF-κB and p38/JNK Activation in Microglial and Attenuates Microglia Activation in Lipopolysaccharide Treatment Mice
L2. Pyrroloquinoline Quinone Decelerates Rheumatoid Arthritis Progression by Inhibiting Inflammatory Responses and Joint Destruction via Modulating NF-κB and MAPK Pathways.

[Hopeoneday]

Nana you might be reading my posts about hhv- http://poiscenter.com/forums/index.php?topic=2584.msg23205#msg23205

In those links resarch are discovered that hhv is inwolved ewan in undermetalation if i read corect.

Guys, lets chouse 2-3 poisers who are in usa, germany ...etc, i mean from countres who hawe ability to make prc dna virus tests and most adwanced tests.
Test from blod (they say) is only maybe relevant if infection is right now.

Nana, is Moun hawe elevated hhv 3 in pois or?

Conection -The girl name AJS (I put here girl on perpos) from naked forum say that only thing she kows is that her pois started after geting shingles.
And she say, that they found hi elevated levels of antibodies 3 diferent viruses.

lets check is there eny virus in our nerves, hhv6(this virus could be in our dna, geneticly) etc...

[nanna1]

Hi Hopeoneday,

Your post seems very relevant to this discussion. You are already ahead of me with some of this information. I didn't know about the vagus nerve infection hypothesis, but the link that you posted in (http://poiscenter.com/forums/index.php?topic=2584.msg23205#msg23205) is very informative. I will keep reading up on this. Thanks!

[Nas]

Hey Nanna,
To my understanding HHV-3 is basically VZV virus, which is chickenpox. Chickenpox in later stages does go dormant in the nerves. So in the case of Muon, did he experience chickenpox symptoms when he was a kid? Also aren't most of people around the developed world have chickenpox vaccinated ? I know I did personally. 

[nanna1]

Hi Nas,

  You are correct that human herpes virus-3 (HHV-3) is VZV, chickenpox, shingles. The HHV-3 vaccine is a live virus that has been weakened. But in some people, the vaccine can still infect the nervous system if the immune system does not eliminate it fast enough.

  Regarding herpes zoster, the US Centers for Disease Control states: "Chickenpox vaccines contain weakened live VZV, which may cause latent (dormant) infection. The vaccine-strain VZV can reactivate later in life and cause shingles. However, the risk of getting shingles from vaccine-strain VZV after chickenpox vaccination is much lower than getting shingles after natural infection with wild-type VZV."

  "Vaccines are less effective among high-risk patients, as well as being more dangerous because they contain attenuated live virus. In a study performed on children with an impaired immune system, 30% had lost the antibody after five years, and 8% had already caught wild chickenpox in that five-year period."

  I don't know if Muon was infected with HHV-3 as a child, but his virus test shows a HHV-3 (varicella-zoster) and HHV-5 (cytomegalovirus) infection. He does not have a HHV-6 infection. So if herpes is involved with POIS, HHV-6 is not required. But it could also be the case that different types of POIS come from different HHV viruses.

  Herpes viruses are not permanently latent (dormant). For HHV-1 and HHV-2, it was shown that stress (through JNK) triggers the activation of those viruses [J1,J3]. The shingles disease occurs when HHV-3 is reactivated when the immune system is compromised and can't fight it off. As long as the immune system is strong, the HHV can only dwell and spread through the nervous system in the neurons (and similar cells). It is very difficult for an immune cell to kill a neuron, because that would destroy memory. So HHV can hide in neurons. When a HHV tries to leave the nervous system it gets attacked and killed by immune cells. The immune system attack on the spreading HHV-3 is what may be causing POIS symptoms. That is the mechanism pictured below:

Prostaglandins activate JNK. JNK de-methylates viral DNA leading to viral symptoms. JNK also up-regulates COX-2 to produce more prostaglandins. This cycle requires a steady supply of arachidonic acid. (This diagram is greatly simplified. For example, PGE2 upregulates IFN-y/TDO/IDO, but that is not shown here.)

I obviously don't know anything for sure. But I thought it might be helpful to discuss the idea of an HHV infection.

Press release:
J1. Discovery shows how herpes simplex virus reactivates in neurons to trigger disease

Original research paper:
J3. Neuronal Stress Pathway Mediating a Histone Methyl/Phospho Switch Is Required for Herpes Simplex Virus Reactivation

[Nas]

Ok, so how does that possibly relate to POIS? How does an orgasm/ejaculation affect the HHV-3 trigger mechanics? I.e. how does stress trigger correlate with ejaculation? Also if that was the case, shouldn't we be having shingles when the Herpes start replicating?

I feel the infection theory could be a good one since I've always suffered from an inflamed urethra during POIS ( even inflamed anus but I don't know if that correlates ). The human body is a very complicated system you never know what can cause what.

[nanna1]

Hi Nas,

  Thanks for the interesting questions/comments. The shingles outbreak only occurs when the immune system is weak and cannot fight off the spread of the virus. The virus-POIS mechanism that I discussed earlier (March 11, March 12) assumes that the immune system is functioning properly. The virus is typically latent (dormant) within neurons and nervous system related cells. Once the stress trigger activates the virus, the virus spreads and causes the immune system to respond.

• Newly infected cells upregulate 5-LOX, IFN-gamma and other proteins to tell the immune system (T-cells, mast cells, white blood cells, etc...) where the virus is located.
• The immune cells attack the virus-infected cells with inflammation through neurotransmitters (histamine), cytokines (IL-8), and free radicals (hydrogen peroxide, nitric oxide).
• The inflammation kills the infected cells and the virus.
• The dead cells and viruses are "eaten" and cleared from the body (allergy).

  In the case of HHV-3, this attack on the virus would prevent a shingles outbreak by killing off the virus whenever it tries to escape the nervous system. Unfortunately, the attack (inflammation) and clearance (allergy) by the immune system of the pathogen (virus) can also make people feel very sick.

  As for the stress trigger that activates JNK and herpes, I don't know for sure since I am still learning about JNK. But I think there are three likely candidates:

1. The breakdown of cyclic AMP by PDE4.
2. A rise in cyclic GMP by NO production.
3. Increased PGE₂ (prostaglandin).

  cAMP and cGMP are both involved in penile erections. cGMP in the penis creates the erection, but it can also stimulate JNK and herpes replication. cAMP inhibits JNK and herpes replication.

  PGE₂ is produced whenever semen is produced and is usually found in high concentrations in the semen of healthy people. PGE₂ activates JNK. The word prostaglandin comes from two root words, prostate gland. It comes from arachidonic acid interacting with the COX-2 enzyme.

  Since COX-2 inhibitors (indomethacin) and PDE4 inhibitors (quercetin and curcumin) reduce POIS symptoms, the trigger could be a combination of 1. and 3. All of these molecules (cAMP, cGMP, PGE₂) are short ranged, meaning they don't travel very far from where they are created before being broken down. There are other stress related molecules that can trigger JNK, but that's all I know about stress triggers right now. I'm still reading about the potential virus-POIS link.

Thanks again Nas.

[Muon]

Yes I had chickenpox as a kid. Stress can trigger an attack of flares throughout my body in alternating fashion, taking turns. When one flare which takes a few seconds or less in duration fades out another one pops up somewhere else, it's like the body and something else playing a game of whack-a-mole where the body is one step behind. (mast cell attack, virus, cytokine release???)

So a virus can replicate itself without the body producing specific IgM? IgM has a relatively high half life. You may ask yourself if IFN-g is elevated in my case to suppress an infection. Also desenz treatment is able to reverse polarization from Th2 to Th1 in general. I suspect PGD2 acts on the CRTH2 of Th2 cells which decreases interferon gamma after orgasm and the body elevates IgG4 to dampen this Th2 response. My brother has POIS but doesn't have his IFN-g elevated, maybe this is potential latent infection which acts parallel next to POIS.

Maybe worth mentioning, I have used liquid H2O2 in the past (motivation was candida albicans). This improved a lot of symptoms in general but had not any influence on POIS. It only worked with water (250-300 ml water). IL-8 was tested positive 10 out of 10 times if you sum up the IL-8 tests of me and my brother. Perhaps this is a potential target for POIS research. If a majority of patients are postive for this parameter you can associate it with POIS, then we have something coupled to POIS, now we have nothing.

I'm in a proces getting these done: https://www.mastcellaction.org/assets/file?filePath=__/mast-cell-activation-markers-final-flyer.pdf

[Nas]

Very interesting Nanna. So is it possible to treat HHV-3 when it's dormant I wonder? 

I would also like to note since HHV-3 is a herpes virus, unsanitary masturbation ( since I'm a virgin ) could be possibly the place of infection for many of us. And I'm not sure about my urethra inflammation but its correlation with ejaculation makes me even a bigger believer of the viral theory. Will like to see further tests from Muon and other POISers in the future.

[nanna1]

Hi Muon,

  Thank you for sharing your personal experience and test results. I plan to get some detailed test results soon, but as you probably know these virus test are expensive. I agree with you that prostaglandins could be involved in how the immune system responds after orgasm since many POIS stacks seem to affect the arachidonic acid cascade. Your idea about PGD₂ and IFN-gamma is interesting especially considering your brother doesn't have elevated IFN-gamma. This information will help narrow down which test I need (or don't need to get).

  I express caution about using IgM test to determine herpes virus reactivation/replication. The herpes virus can replicate without the body producing IgM. In people with active shingles outbreak, it may be more common to have a negative IgM test than a positive one:

"IgM testing is considerably less sensitive than PCR testing of skin lesions. Commercial IgM assay may not be reliable and false negative IgM results are not uncommon." Center for Disease Control: Chickenpox (Varicella): Interpretation of Laboratory Tests for VZV: Laboratory Confirmation of Suspected Varicella

"Serum specimens drawn early during acute phase of infection or soon after vaccination may be negative for IgM- or IgG-class antibodies to this virus, respectively." Mayo Clinic: Varicella-Zoster Antibody, IgM and IgG (Separate Determinations), Serum: Caution

"A total of 62 patients were included in this study, and VZV IgM antibody was positive only in 23 patients (37%). The estimated antibody-positive period after HZ (herpes zoster, shingles) onset was 3.5 weeks (95% confidence interval 2.8–4.6 weeks)...The positive rate of VZV IgM antibody in HZ patients has been reported to range from 10% to 70% according to the test method, test period, and clinical symptoms of the patients." The positive duration of varicella zoster immunoglobulin M antibody test in herpes zoster

"The absence of an IgM antibody does not mean you do not have a active infection. Chronic infections in various tissues can persist with no evidence of IgM." HHV-6 Foundation: HHV-6A/B Testing: IgM test

"The HSV-1 IgM test result was negative despite the presence of a life-threatening acute infection, whereas the HSV-2 IgM test result was positive. False-positive results have been reported for both HSV and VZV (28, 29). Of note, IgM may not develop during active reactivation." Immunoglobulin M for Acute Infection: True or False?: (vii) Case 7: Comments.

  I agree, we need more POIS people tested for viral pathogens before clear conclusions can be drawn. But I'm curious, what would a mast cell activation test reveal? Many different things (virus, bacteria, poisons, food allergies, autoimmune disease) lead to mast cell activation. But maybe there is some new information in it? Thanks again Muon for sharing your test, experiences and knowledge on the immune system. It has sparked some discussion.

[nanna1]

Hi Nas

So far, I'm researching zinc, essential oils and Oleuropein (olive oil extract) as molecules that can kill dormant herpes viruses by disabling the outer coat.
PDE4 inhibitors (Theobromine, Theophylline, curcumin) can inhibit JNK and herpes virus replication.
Unfortunately, I don't think anything on the market has been shown to completely rid the body of the virus. That doesn't mean we can't see big benefits!

[Quantum]

NI nanna, Nas, Muon and HOD,

Very interesting discussion.

It makes me wonder what specificity would lead HSV/viral infections to finally cause POIS, because those infections are so frequent ( chickenpox was endemic when I was a child, no vaccine back then), and there are so few POIS cases.  I would be interest to see what specific genetic trait or specific metabolic default in immune system or else would finally lead from a frequent type of infection to a rare syndrome like POIS.

[Nas]

Hey Nanna,
I'm trying currently some typical anti-inflammation medications ( Cetrizin and Diphenhydramine ) You think they would be sufficient to stop the inflammation? I'm planning on a 2 months trial.

Hey Qunatum,
Yeah, very interesting indeed. There is a weird trigger mechanic at play here; we experience inflammation when we orgasm/ejaculate - I even felt POIS when I smoked cigarettes.

[nanna1]

Hi Nas,

  I don't take H1-histamine receptor blockers because long term use is associated with several brain diseases. See http://poiscenter.com/forums/index.php?topic=2502.msg21708;topicseen#msg21708
Any H1 blocker that makes you sleepy, does so by blocking acetylcholine receptors and temporarily shutting down portions of the brain.
Allegra (fexofenadine) is the only H1-histamine blocker that does not cause long term cognitive impairment. Allegra does not cross the blood-brain barrier or inhibit acetylcholine receptor. When doing a experiment recently to test if COX-2 was involved with POIS, I took the COX-2 inhibitor, indomethacin, and a H1 receptor blocker. But this was a one-time experiment focused on testing an idea about COX-2 and POIS. H1 blockers do stop histamine induced arachidonic acid (AA) cascades. But I am highly cautious against H1-histamine blockers for mental health reasons (except Allegra).

  I believe that part of reason I can get full relief from all POIS symptoms is that I have removed arachidonic acid (AA) from my diet. Plants don't make AA but animals do. So by not eating meat and dairy, I don't need to take H1 and a1 blockers with my stack in order to stop AA release. I realize that a AA free diet is hard to maintain. I have even tried to cheat on my AA intake (it doesn't work). So if the POIS Cascade Stack + low AA diet is not for you, COX/LOX inhibitors could be the next best option.

  In my opinion, COX-2 inhibitors and 5-LOX inhibitors are the only guaranteed ways to stop inflammation. The oxidative enzymes (COX-2, LOX, iNOS, TDO, IDO) are the last step before inflammation occurs. A list of natural COX/LOX inhibitors can be found here Cost effective alternatives for omega-3
Curcumin is a good 5-LOX inhibitor if you are not trying to have a baby (start a family). Otherwise, it may be better to take tumeric which has many health benefits beyond 5-LOX inhibition. I haven't seen many good natural options for blocking COX-2, but vitamin D3, the PDE4 inhibitor theobromine and a good mix of antioxidants can help.

[Nas]

Well I'm using Cetirizin which is far less likely to cross the blood brain barrier. But I'll also look into supplementation medication for safer use. And about eliminating AA by reducing meat is economically unsustainable for me because I live in Iraq and meat is a large factor in our every day cuisine. Not mentioning that meat here is far more efficient when it comes to energy per serving/cost compared to vegetarian options here.   

[jonny90]

I can confirm, that Alpha-GPC of this stack does work very well before and after O, so even if you did not take something before, Alpha-GPC does make it better.
I used it with N-Acetyl-Tyrosine together.
After O, our dopamine-system is blocked (prolaktine) and we can fix it faster with Alpha-GPC and N-Acetyl-Tyrosine

I think this stack will fix our brainfog a lot faster:

Alpha-GPC 500mg - 1g a Day
Omega 3 [High Quality] (500mg EPA, 350 DHA)
Uridine Monophosphate 150mg
N-Acetyl Tyrosine 350mg (alternative: mucuna pruriens)
Vitamin B-Komplex (low dose)

This stack does fix the dopamine problem

https://corpina.com/uridine-supplement-stacks-help-repair-dopamine-receptors/

[aswinpras06]

 I have a feeling that Pois basically weakens our immune system or make it to malfunction.  Many of the dormant infections(whether bacterial,fungal or viral) become active once the immune defence is interrupted by pois.

1.The healthy diet and supplements which work for many of us, some how prevents this immune system malfunction. 

2.Good refreshing sleep also works for many in reducing pois,  because it boosts the immune function.

3.Broad spectrum antibiotics like azithromycin also have helped a few of us in reducing pois.

4. Many of us have chickenpox and shingles more than the normal population. The chickenpox virus or other neural dormant infection may be the reason for some of us not tolerating hot or cold showers in the head or neck region.This  I think may make them active again.

I am now going to try some natural antibiotics{Neem leaves,virgin coconut oil,Garlic,nacetylcysteine} for next one month. Turmeric is not included as it is said to be bad for sperm health and we are planning for a child.

Will post if I find any improvement.