Author Topic: Ideas on Herpes Induced POIS  (Read 9477 times)

nanna1

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Re: Ideas on Herpes Induced POIS
« Reply #60 on: July 11, 2018, 10:49:57 AM »
So what you are saying is that there is a second wave of vasodilation mediated by viral replication. Shouldn't vasoconstrictors/beta blockers work for POIS then? Prevent the first wave of vasodilation triggered by catecholamines to avoid viral replication.

Yes that is correct Muon, 2 phases vasodilation and blocking it should block POIS! I actual did a trial of Excedrin (migraine headache medicine) to test the vasoconstriction hypothesis I mentioned earlier before writing the above post.
So I am wonder if POIS requires:
1. vasodilation of a damaged blood vessel in the brain
2. a triggerable virus that induces systemic immune response/chemotaxis

Can someone disprove this hypothesis or show where it is lacking?
For example:
1. Can vasocontriction of blood vessels in the brain stop POIS?
2. Can inhibition of virus replication stop POIS?
I believe that orgasm releases vasodilators noradrenaline, adrenaline of the peripheral and central nervous system and also glutamate of the central nervous system. If the tissue that the virus infects is injured, there is an inflammatory stress response (NF-kB, COX, etc...) associated with the vasodilation (vascular stretching). In the second phase, the epithelia is reinjured by the immune system fighting the virus (vasodilation (histamine, NO) and chemotaxis (chemokines, IL-8, etc...)). In principle, Beta2-blockers could help block POIS in the periphery, but it would not stop glutamate induced vasodilation in the brain. Glutamate release is required for orgasm for all healthy individuals.

  Also, I have to add that HSV-1, VZV, and EBV could have different mechanisms with different symptoms. Because I don't have an HSV-1 infection, someone with HSV-1 could have additional symptoms and experiences that do not correlate with my own. But in all of the herpes viruses, herpes latency connects neurotransmitter receptors to the inflammatory cascades (NF-kB, COX, etc...).

NAS

I think coffee is a good option. It activates the central nervous system and is still a cholinesterase inhibitor. For some members of the forum green tea has worked, I believe it is due to the effect of caffeine.
For me, coffee greatly improves my mood, but I try to take it only in more extreme cases not to get too excited.
I tried caffeine as part of an Excedrin trial before writing the previous post.
« Last Edit: July 11, 2018, 10:20:05 PM by nanna1 »

Hopeoneday

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Re: Ideas on Herpes Induced POIS
« Reply #61 on: July 11, 2018, 04:51:17 PM »
Well i remeber times when i was in enormes stress, and i didnt know what stres is at all, andrenal fatigue and of course POIS. I thouse times aded 1 cup of cofee on all thouse body conditions was devastating on me. On hi adrenaline and cortisol you put cofee bevarages in and you will be crashed!
Today when my health is  big damaged from pois , cofee is good stuff from clearing fatigue and brain fog for couple of hours when i out of pois days.
But if you are damaged from pois, and ewan out of pois-hawing cofee on sewere stifed muscules, respiratory colapsing, impaired digestion, insomnia, pots etc- i do not think that is smart idea for cofee in those moments.

Guys, togedther we can beat this sxeaty illnes.
Nana thanks for your testing you done, that is the only whey and only our chance.
To focus more and more and focus as much is posible to eliminate posible couses one by one.
« Last Edit: July 11, 2018, 05:24:51 PM by Hopeoneday »
Dr-pois.

Muon

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Re: Ideas on Herpes Induced POIS
« Reply #62 on: July 11, 2018, 05:30:30 PM »
Hi nanna,

If (vascular/lymphatic) endothelial cells are being activated in this process then you could check for Weibel-Palade bodies in serum like IL-8, vWF, P-selectin etc. If you have high levels of these you could check for VEGF next: https://www.ncbi.nlm.nih.gov/pubmed/15345585

If there is mast cell activation present then endothelial cells will probably be affected, high concentrations are close to the endothelium.
This could explain (see figure 3 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217344/  )
-Your low neutrophil levels due to extravasation.
-My low CD57 NK cells due to the same mechanism.
-Decreased levels of leukocytes levels seen in members of my family
Activation of endothelial cells due to VEGF release of mast cells, could explain my IL-8
This could also explain elevated Lp-PLA2 levels seen in my brother http://circ.ahajournals.org/content/108/17/2041.full

So the point I want to make is that mast cells may be responsible for vascular problems. A Negative tryptase result does not rule out mast cell activation, it does rule out mastocytosis.
« Last Edit: July 11, 2018, 05:34:03 PM by Muon »

certainlypois2

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Re: Ideas on Herpes Induced POIS
« Reply #63 on: July 13, 2018, 04:32:27 PM »
is there  a way to block glutamate induced vasodilation. Based on this theory is msg a problem and how about exercise aerobics and weight lifting.
« Last Edit: July 13, 2018, 04:34:32 PM by certainlypois2 »

nanna1

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Re: Ideas on Herpes Induced POIS
« Reply #64 on: July 19, 2018, 10:35:59 PM »
Hi certainlypois2,

I wouldn't think MSG would be a problem. The amount of MSG in food is usually small compared to the amount of glutamate and glutamine. I added a Betaherpesvirinae stack. I tried to target the CMV/HHV-5 activation mechanism discussed in "Aspirin attenuates cytomegalovirus infectivity and gene expression mediated by cyclooxygenase-2 in coronary artery smooth muscle cells.". This stack only inhibits the norepinephrine induced vasodilation through COX/PGE2.

  Glutamate induces vasodilation through nitric oxide (NO) (Ref). Methylene blue can inhibit nitric oxide induced vasodilation. But I'm not sure what the best option is for reducing this effect. I haven't tested methylene blue for this purpose. Someone would have to make sure that methylene blue doesn't have some other effect that activates the virus independent of it's NMDA inhibiting effects. Maybe there is a better glutamate-induced NO inhibitor for this.
« Last Edit: July 20, 2018, 12:29:03 AM by nanna1 »

Quantum

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Re: Ideas on Herpes Induced POIS
« Reply #65 on: July 20, 2018, 09:31:52 AM »
  Glutamate induces vasodilation through nitric oxide (NO) (Ref). Methylene blue can inhibit nitric oxide induced vasodilation. But I'm not sure what the best option is for reducing this effect. I haven't tested methylene blue for this purpose. Someone would have to make sure that methylene blue doesn't have some other effect that activates the virus independent of it's NMDA inhibiting effects. Maybe there is a better glutamate-induced NO inhibitor for this.

Hi Nanna, and everyone,

Just a word of caution, here, about methylene blue.  Methylene blue is a very potent monoamine oxidase inhibitor.   This means that is has a high potential for severe drug interactions, in particular with antidepressant drugs.  Methylene blue also interact with tyramine containing food, just like the old MAOI antidepressant drugs.  Anyone willing to try methylene blue should consult with a health professional beforehand.

You can find more information in this thread:  http://poiscenter.com/forums/index.php?topic=1551.msg14569#msg14569 , and http://poiscenter.com/forums/index.php?topic=1551.msg14553#msg14553

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

nanna1

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Re: Ideas on Herpes Induced POIS
« Reply #66 on: July 20, 2018, 08:34:08 PM »
Thanks Quantum!  :)

Hi certainlypois2,

  I don't know how feasible a NMDA block will be because glutamate is required for orgasm and nitric oxide (NO) is require for erection (Ref). But it may not matter. The article on cytomegalovirus (HHV-5) CMV reactivation from vascular tissue (RefSE2) mentions that vascular stretching (i.e. vasodilation) of infected tissue is just one way to activate NF-kB and COX/PGE2. But ultimately, it is NF-kB and COX/PGE2 that cause the virus to reactivate. They inhibited CMV reactivation with COX inhibitors aspirin and indomethacin. This same research group in another study showed that anti-oxidants can inhibit NF-kB induced CMV reactivation.
Figure 5: "N-acetylcysteine (NAC) treatment decreases viral titer of infected coronary smooth muscle cells (SMC). The effect of NAC on viral titer is concentration dependent. Shown are virus yields per milliliter of a 10% SMC homogenate and cell counts from parallel cultures at 96 hours after infection (mean of three experiments)." from RefSE1
HCMV = human cytomegalovirus

   They found that anti-oxidants that decreased superoxide (O2-) and hydrogen peroxide (H2O2) also decreased the amount of CMV virus in a linear concentration fashion. So this could be a way of inhibiting viral reactivation even when there is vascular stretching. As long as the stretching of the infection-injured tissue does not activate NF-kB and produce prostaglandins, (1) the virus should not replicate and (2) the immune response should not induce POIS. The paper (RefSE1) is very thorough in demonstrating the first point (1).

  I remember Swell posted his glutathione stack which was effective for a while, but stopped working for him. That might be worth revisiting, and seeing how anti-oxidants with selenium might compare to N-acetylcysteine.
« Last Edit: July 23, 2018, 12:53:31 AM by nanna1 »

certainlypois2

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Re: Ideas on Herpes Induced POIS
« Reply #67 on: July 21, 2018, 01:31:09 AM »
Thanks.  Did you remove B1 from your stack because of CLA. It also blocks expression of transcription factors NF-kB and and monocytes adhesion to endothelial cells.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249497/


nanna1

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Re: Ideas on Herpes Induced POIS
« Reply #68 on: July 22, 2018, 06:52:50 PM »
Thanks.  Did you remove B1 from your stack because of CLA. It also blocks expression of transcription factors NF-kB and and monocytes adhesion to endothelial cells.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249497/
Hi Certainlypois2,

  You are correct that Benfotiamine (vitamin B1) downregulates the expression of inflammatory genes. About 2 to 3 years ago I remember people discussing on a forum how high-dose thiamine helped their POIS symptoms. So I tried thiamine then Benfotiamine. When I first started Benfotiamine, I believed that it produced a noticeable improvement in POIS symptoms. It was not an instant prepack improvement. It took a few days of constant supplementation.

 I lost my bottle of B1 a few months ago, but I noticed that I still don't have and POIS symptoms on my diet-stack. I broke my diet and my stack for blood test and supplement test several times. And when I resumed my diet-stack without B1 I still get full relief. This all occurred after I started taking CLA. I do still take some omega-3 (700mg not everyday) for general health, but not as much as I used to take for POIS. I think everyone should take omega-3 even if you don't have POIS because of the many health benefits. B1 is also good for general health, but I realize that many of us have spent a large amount of money on medical bills and trying supplements, so I try to reduce the number of supplements to the fewest possible to see POIS relief. But if others find that B1 is necessary then I will gladly add it back.

  But I'm not sure if CLA compensated of B1, or if B1 stopped working, or if something in my diet compensated for it, or if B1 ever did work (placebo?). I haven't properly tested all these scenarios but I suspect you are right about CLA. Good question Certainlypois2! If POIS is caused by herpes infections, then the effect of these stacks will be virus specific. CLA might be more effective against CMV than HSV-1, because CMV is dependent on long-chain fatty acids and CLA helps to burn fatty acids. Someone with a HSV-1 induced disease may not find CLA as effective as I do.

  Also, thanks for posting the link on Benfotiamine and NF-kB / arachidonic acid cascade. It has some good info.
« Last Edit: July 27, 2018, 05:11:07 AM by nanna1 »

swell

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Re: Ideas on Herpes Induced POIS
« Reply #69 on: July 23, 2018, 07:23:46 PM »
Nanna1 it would be helpful if you can take up the Glutathione GSH stack.  I am now convinced that my POIS is virus related.  My mental fog did not let me realize my Bells Palsy gets triggered with POIS and recovers in 7 days so directly correlates with POIS.  And bells palsy is known to be due to virus.   What I read is that only way to combat EBV/HPV etc is to strengthen immune system that there is no good medicine except anti-retrovirals which are not advisable?.  Now I realize that liposomal GSH is still helping me, maybe not fully as I like it to be.  It is known to strenghten a weak immune system that I think is its main function benefit.  My big POIS complaints are:

mental fog:  Adderall I take, beats the heck out of fog so I cannot include fog as a criteria, but listing it anyway.
skin growth all over body:  skin changes its characteristics as if there is systemic uticaria all over.   GSH is still managing it today somewhat maybe 30%. 
I feel as if some pointy growth in inside of eyelids:  I used to be in great discomfort constantly putting eye washes.  Eye lashes break and sit in eyes during pois period.  GSH is today managing it 80%.
very pale skin:  GSH is today managing it 30%
bells palsy:  GSH cured it for 2 months, but minimally effective now.
speech slurring: GSH again cured it for 2 months but mimimally effective now.
emotional symptoms:  GSH for 2 months worked but mimimally effective now. 

I think you and others with chemistry know how (not doctors) can tweak the stack, and maybe as you suggest that is the solution to POIS.

 

swell

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Re: Ideas on Herpes Induced POIS
« Reply #70 on: July 23, 2018, 09:08:39 PM »
So to date there is no systemic treatment for these viruses HPV/EBV etc.   I found one research which led me to:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5344427/

The medicine they point to:
https://www.buy-gene-eden.com/index.php

contains amazingly simple chemicals: quercetin 100 mg, green tea extract 150 mg, cinnamon extract 50 mg, selenium 100 mcg, and licorice extract 25 mg.  They talk about a patented delivery formula.  I suspect the delivery mechanism will be 'serrapeptase' enzyme, I think since that is only compound I know that can dissolve the protective films that virus built around them exposing them.  Any ideas on this one?

nanna1

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Re: Ideas on Herpes Induced POIS
« Reply #71 on: July 24, 2018, 02:01:41 AM »
Hi Swell,

  I agree that strengthening the immune system will benefit anyone with POIS. It seems that most of the supplements/herbs/vitamins/minerals that people take for POIS have immune boosting properties. I don't have all the answers on antioxidants, but I can share what I know and hopefully others will share what they know. I think that there are three rate limiting ingredients for glutathione production, selenomethionine, N-acetylcysteine (NAC), and glycine. Sorry I can't find the references. Selenomethionine is needed to produce all the glutathione recycling enzymes, glutathione peroxidase. And I guess you already know why N-acetylcysteine (NAC) is important glutathione production. But check out Table 1 from "N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action (2011)". This will give you a feel for the dosage of NAC you will need. In disease models, glycine increases glutathoine (RefRREH). Tri-methyl-glycine (TMG, betaine) has much higher bioavailability than L-glycine. Also, TMG may be less toxic to the brain.

  For herpes, I would not take glutamine since herpes viruses seem to like glutamine just as much as they like glucose. I haven't seen any evidence that glutamine increases glutathione production in humans. It doesn't seem to be rate-limiting. I'm not sure what type of glutathione you are taking, but I would compare it's bioavailability to that of NAC (Table 5).

Foods like garlic, onions, broccoli, cauliflower, and capers are good glutathione boosters.

  Also it might be good to think carefully about the redox cycle. Electrons flow from negative (NADH) to positive (oxygen) volts. Click below images to see full size.
Above figure from: Modulation of oxidative stress-induced changes in hypertension and atherosclerosis by antioxidants
 NADH (and NADPH) recycle glutathione levels.

Above figure from: Ascorbate and Glutathione: The Heart of the Redox Hub. Also see Figure 2 from Molecular Aspects of a-Tocotrienol Antioxidant Action and Cell Signalling.

  However, herpes viruses deplete NAD+ and NADH levels (RefGS, RefVR). If a virus is causing your POIS, low NADH levels in infected cells could prevent glutathione from working/recycling. A virus IgG test would help you know better what is going on. This is what I know about glutathione. Hopefully, others can contribute their knowledge.

  It may be worth looking into finding a xanthine oxidase (XO) inhibitor. I wrote about XO here. There is a cascade of inflammatory events:
1. Some herpes viruses (and influenza virus, and HIV) upregulate XO to increase superoxide (O2-).
2. Superoxide is then used by the other oxidative enzymes (COX-2, IDO, etc...) to oxidize substrates (arachidonic acid, tryptophan, etc...)
3. This produces (PGE2, kynurenine) and peroxide (H2O2)
4. H2O2 activates NF-kB
5. chronically elevated NF-kB causes problems
In other words, blocking the activity of XO and/or the production of superoxide will dramatically reduce the activity of all the other oxidative enzymes and NF-kB.

  Thanks Swell for sharing that link on permanent virus clearance. I'll look into it. I also have been working on a strategy to remove the virus permanently. See Intravenous Vitamin C trial at the bottom of the Potential NORD and NIH grant ideas post. The science behind this approach can be found here "Long-term herpes relief and permanent virus removal strategies".
« Last Edit: July 27, 2018, 05:10:37 AM by nanna1 »

POISse

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Re: Ideas on Herpes Induced POIS
« Reply #72 on: July 25, 2018, 02:48:15 PM »
Hi everyone,

I have been using indomethacin for more than a month and I wanted to share my experience.

I started researching about indomethacin after one of nanna1's post on this thread. Interrestingly, I had most of the symptoms related to emicrania continua right after O: unilateral pain, conjonctival injection, nasal congestion, ptosis (https://en.wikipedia.org/wiki/Hemicrania_continua).

I tried to take it at different time but the best results I had so far was between 2 to 3 hours before O. I am using 75mg indomethacin one time per day for 1 to 2 days after O.

Regarding the effects: I have less trouble speaking, my mind is clearer, general feeling is much better. I still have fatigue the day after O. I stopped using mytelase due to the bad side effetcs and good results with indometacin. It seems to be also efficient for CFS related symtoms. 

Note: I had bad side effects in the begining around the left ear and indomethacin can harm your eardrums and cause ulcers, ask your GP before using it,

Thank you nanna1 for your post.

Cheers,

POISse

Nas

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Re: Ideas on Herpes Induced POIS
« Reply #73 on: July 26, 2018, 09:28:57 PM »
Hey everyone,
So I just did another round of vasoconstrictor treatment, I tried: Propanolol 10mg, Indomethacin 50mg, Paracetamol 1000mg, Aspirin 100mg, Caffeine 30mg, Pseudoephedrine 30mg, Chloropheniramine Maleate 4mg. I masturbated after 30 minutes of intake. 
I'm currently writing with still brain fog and general cognitive symptoms, I just can't seem to get rid of them. I don't know about time to heal but it'll probably be reduced.
*sigh* If let's say I'm constricting my blood vessels to reduce permeability, it doesn't seem to be enough to guarantee that I won't have brain symptoms; what ever it is that is getting inside of my brain and causing this inflammatory reaction, I need to find a better way to stop it.

nanna1

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Re: Ideas on Herpes Induced POIS
« Reply #74 on: July 27, 2018, 05:05:48 AM »
Hi everyone,

I have been using indomethacin for more than a month and I wanted to share my experience.

I started researching about indomethacin after one of nanna1's post on this thread. Interrestingly, I had most of the symptoms related to emicrania continua right after O: unilateral pain, conjonctival injection, nasal congestion, ptosis (https://en.wikipedia.org/wiki/Hemicrania_continua).

I tried to take it at different time but the best results I had so far was between 2 to 3 hours before O. I am using 75mg indomethacin one time per day for 1 to 2 days after O.

Regarding the effects: I have less trouble speaking, my mind is clearer, general feeling is much better. I still have fatigue the day after O. I stopped using mytelase due to the bad side effetcs and good results with indometacin. It seems to be also efficient for CFS related symtoms. 

Note: I had bad side effects in the begining around the left ear and indomethacin can harm your eardrums and cause ulcers, ask your GP before using it,

Thank you nanna1 for your post.

Cheers,

POISse

  Thanks POISse for sharing your experience. I'm glad you were able to find some relief! I appreciate that you found out the pre-O timing for the dose. When I did my trial, I just took the doctor's word for the timing, but my doctor was wrong. After you posted this I went to look up the pharmakinetics, and here is what Merck says:
"Following single oral doses of Capsules INDOCIN 25 mg or 50 mg, indomethacin is readily absorbed,
attaining peak plasma concentrations of about 1 and 2 mcg/mL, respectively, at about 2 hours.
" (page 2, paragraph 7)

  As you mentioned, one of the side-effects of indomethacin is that with long-term daily use it can produce ulcers (due to being oxidized/broken-down in the stomach). However, I found some information on selenium and N-acetylcysteine that should help reduce the side-effects from daily indomethacin. One study found that selenium could help prevent and heal indomethacin ulcers "Curative effect of selenium against indomethacin-induced gastric ulcers in rats."

N-acetylcysteine also prevented indomethacin side-effects:
-N-acetylcysteine a possible protector against indomethacin-induced peptic ulcer: crosstalk between antioxidant, anti-inflammatory, and antiapoptotic mechanisms
-The Gastrprotective Effect of N-acetylcysteine and Genistein in Indomethacin-Induced Gastric Injury in Rats.

For an indomethacin dose of 50mg, that would translate to:
-selenomethionine: 100 micrograms (in Fig. 3 above: the 50 ug/kg bar)
-N-acetylcysteine (NAC): 600 mg

Please keep us updated on any other things you find out (successes, failures, tips, etc...).

  For anyone who is interested, my indomethacin trial is posted here http://poiscenter.com/forums/index.php?topic=2683.msg23773#msg23773
« Last Edit: July 27, 2018, 01:24:20 PM by nanna1 »