Hypersensitive neural pathways to orgasm causing neuroinflammation (pois attack)

[hosamitaha]

5/3 update: instances of bipolar II patients developing pois like symptoms during the depressive phase of bipolar II disorder and milnacipran anti-epileptic role are added to the post.

A member here told me that a combination of carbamazepine 200 mg and amirtriptyline 25 mg taken every night was 100% effective in preventing symptoms. He said that he still got pois when he tried amitriptyline alone but didn?t report any POIS on carbamazepine alone. This effect has been consistent for over a year of treatment till now given that he masturbates not more than once every three days or else he would get POIS.

So I looked up on POIS centre, subreddit and FB group for any evidence on anti-epileptics which are also mood stabilisers: 1-carbamazepine. 2-valproic acid. and found no data on carbamazepine except for one recommending it because levetiracetam (a novel anti-epileptic drug with very close mode of action but isn't first line for epilepsy and not a strong mood stabiliser like valproic and carbamazepine) worked for them. another on reddit said levetiracetam worked but isn?t clear to what extent. One on POIS centre said that 3 months of valproic acid worked

This article proposes a model mechanism for the etiology of Chronic fatigue syndrome (a condition I believe is very much like POIS but in POIS the trigger is evident and measurable)

https://pmc.ncbi.nlm.nih.gov/articles/PMC3166239/

it postulates that our neuronal pathways are abnormally sensitive to the point orgasm can trigger an electrical ?i.e seizure-like? activity in the brain and we know in medicine that in epilepsy, the patient has a ?hypersensitivity to stimulation mechanism? and that seizures cause neuronal excitotoxicity which the neurons can?t handle ultimately leading to neuroinflammation. Neuroinflammation is what also causes the stopping of brain and body functions we see in POIS symptoms.

Holy fuck if POIS is actually a rare type of seizure-like illness all along leading to neuroinflammation and chronic fatigue attack symptoms. We need to embark that road more. These drugs can increase the threshold for stimulation targeting that very etiology.

Just a clarification for those who don't know, seizure doesn?t always mean the dramatic rhythmic muscular contraction and presents as non-motor forms as well. This is the medical definition of seizure: A seizure is a sudden, brief disruption of brain activity caused by abnormal, excessive, or synchronous neuronal firing. Depending on the regions of the brain involved, seizures can lead to changes in movement, sensation, behavior, awareness, or consciousness. Symptoms vary widely.

Also I believe that those who get symptoms with bare sexual stimulation without orgasm may have the most hypersensitive neural pathways of us all

This may also be part of why many report decreases of symptoms with being in a state ketosis. It is known that ketosis helps epileptic patients too. Also, this might be why a lot report migraines during POIS which are known to have a pathophysiology of abnormal sensitivity and excitotoxicity too.

Milnacipran reported to be effective in preventing pois with many partially because it raises threshold for stimulation

https://pubmed.ncbi.nlm.nih.gov/19841905/

Many people with POIS, experience worsening of symptoms with glutamine supplementation which is also the case with epilepsy and bipolar disorder!

https://pmc.ncbi.nlm.nih.gov/articles/PMC8970572/

https://pubmed.ncbi.nlm.nih.gov/34233236/

https://www.nature.com/articles/npp20092

https://www.reddit.com/r/Nootropics/comments/jx5his/hypomania_from_lglutamine_discontinue_or_just/

https://www.webmd.com/vitamins/ai/ingredientmono-878/glutamine#:~:text=Bipolar%20disorder%3A%20Glutamine%20might%20increase,body%20converts%20glutamine%20to%20glutamate.

Multiple report of pois like symptoms during depression phase of bipolar 2 disorder

https://www.reddit.com/r/bipolar2/s/Y6sooLk8AA

https://www.reddit.com/r/bipolar2/s/DAvQHgHWta

https://www.reddit.com/r/bipolar2/s/9Tx2LfgihT

https://www.reddit.com/r/bipolar2/s/NVw4B1SlsK

report of depression phase of bipolar 2 resolving by getting a flu which also happens in pois

https://www.reddit.com/r/bipolar/s/AVB9gjs3XM

Finally, I want to add that I feel very good on prolonged abstinence with exercise and healthy lifestyle like some sort of hypomania but when pois ensues during that it becomes a living hell of melancholy and suicidality worse than normal pois attacks (text book major depression maybe?). Like all my good progress was multiplied by -1. This extremely big difference doesn?t happen when I regularly masturbate and don?t care for my life that much.

POIS may be an undocumented form of a mood lability ending in cfs-attack due to hypersensitive neural pathways

[Quantum]

Thanks for sharing your hypothesis, Hosamitaha.
I see POIS as a group of related ailments having the same triggers and causing similar symptoms, and it is clear that many POIS types have a strong neurological component.

I, too, think that many POIS symptoms are similar to what we see in CFS/ME, and in long COVID, and it has been discussed here, on the forum.  I also think the exotoxicity has a central role, that is why I use TDO and IDO inhibitors in order to control my POIS symptoms, among other things.
Somw years ago, I also created a thread here about the similarities between a POIS attack, and encephalitis.  Inflammation in the brain sure seems to be an important aspect of POIS. 

Carbamazepine had been mentioned before on the forum, There is even a thread from a member who eliminated his POIS with carbamazepine and/or levetiracetam, while taking those for temporal epilepsy ( see https://poiscenter.com/forums/index.php?topic=4583.msg49301#msg49301).  But, as usual with POIS, this solution will work only for a certain proportion of POIS sufferers, and not for the others.
Some POIS types seem to be more systemic than just affecting the brain, like those who have strong allergy symptoms, joint aches, intense flu-like symptoms, dermatologic problems, and so on.  But extreme fatigue, mood swings, difficulty concentrating, etc, are very often present, and point to neuroinflammation in the brain, just like you discuss in your hypothesis.
I am not surprised to read that this member has to limit his sexual activity in order for his control method to stay effective.  I experiment quite the same with my own pre-pack method.  If too many repetitions in a short time period, it will not contain my POIS symptoms anymore.

[hosamitaha]

I appreciate yours sharing this knowledge with us, Quantum.

Encephalitis usually refers to life-threatening inflammation of brain that doctors undergraduate curriculum covers up well.

What doctors curriculum doesn?t teach is the concept of functional diseases (i.e. neuroinflammation) or non life-threatening inflammation of central nervous system (brain and spinal cord). Doctors are unexposed to those kind of diseases and are most of times resistant to education on this part too.

The systemic symptoms as allergy, aside from neuroinflammation, are interesting because we don?t know if they occur (1) downstream from nervous pathology or if (2) they share a common origin with neuroinflammation or (3) totally have another distinct origin. Three possibilities. Yet I believe fixing the neurological component is of utmost importance.

In epilepsy, we know that valproic acid is more broad-spectrum for all kinds of brain hypersensitivity problems, more stronger on the neuroinflammation part and can induce long term changes. Carbamazepine is golden too in some other kinds of epilepsy and has some neuroinflammatory modulating properties but has the advantage of being more tolerable. However, despite both being safe, they require some follow-up investigations every while to make sure the few unlucky who get side effects are detected early.

I believe I read that someone here said depakene (valproic acid) taken for three months completely resolved their pois but this was recent. Let?s ask them if the effect persisted!

Thanks for sharing your hypothesis, Hosamitaha.
I see POIS as a group of related ailments having the same triggers and causing similar symptoms, and it is clear that many POIS types have a strong neurological component.

I, too, think that many POIS symptoms are similar to what we see in CFS/ME, and in long COVID, and it has been discussed here, on the forum.  I also think the exotoxicity has a central role, that is why I use TDO and IDO inhibitors in order to control my POIS symptoms, among other things.
Somw years ago, I also created a thread here about the similarities between a POIS attack, and encephalitis.  Inflammation in the brain sure seems to be an important aspect of POIS. 

Carbamazepine had been mentioned before on the forum, There is even a thread from a member who eliminated his POIS with carbamazepine and/or levetiracetam, while taking those for temporal epilepsy ( see https://poiscenter.com/forums/index.php?topic=4583.msg49301#msg49301).  But, as usual with POIS, this solution will work only for a certain proportion of POIS sufferers, and not for the others.
Some POIS types seem to be more systemic than just affecting the brain, like those who have strong allergy symptoms, joint aches, intense flu-like symptoms, dermatologic problems, and so on.  But extreme fatigue, mood swings, difficulty concentrating, etc, are very often present, and point to neuroinflammation in the brain, just like you discuss in your hypothesis.
I am not surprised to read that this member has to limit his sexual activity in order for his control method to stay effective.  I experiment quite the same with my own pre-pack method.  If too many repetitions in a short time period, it will not contain my POIS symptoms anymore.

[Quantum]

I appreciate yours sharing this knowledge with us, Quantum.

Encephalitis usually refers to life-threatening inflammation of brain that doctors undergraduate curriculum covers up well.

What doctors curriculum doesn?t teach is the concept of functional diseases (i.e. neuroinflammation) or non life-threatening inflammation of central nervous system (brain and spinal cord). Doctors are unexposed to those kind of diseases and are most of times resistant to education on this part too.

The systemic symptoms as allergy, aside from neuroinflammation, are interesting because we don?t know if they occur (1) downstream from nervous pathology or if (2) they share a common origin with neuroinflammation or (3) totally have another distinct origin. Three possibilities. Yet I believe fixing the neurological component is of utmost importance.

In epilepsy, we know that valproic acid is more broad-spectrum for all kinds of brain hypersensitivity problems, more stronger on the neuroinflammation part and can induce long term changes. Carbamazepine is golden too in some other kinds of epilepsy and has some neuroinflammatory modulating properties but has the advantage of being more tolerable. However, despite both being safe, they require some follow-up investigations every while to make sure the few unlucky who get side effects are detected early.

I believe I read that someone here said depakene (valproic acid) taken for three months completely resolved their pois but this was recent. Let?s ask them if the effect persisted!

Thanks for sharing your hypothesis, Hosamitaha.
I see POIS as a group of related ailments having the same triggers and causing similar symptoms, and it is clear that many POIS types have a strong neurological component.

I, too, think that many POIS symptoms are similar to what we see in CFS/ME, and in long COVID, and it has been discussed here, on the forum.  I also think the exotoxicity has a central role, that is why I use TDO and IDO inhibitors in order to control my POIS symptoms, among other things.
Somw years ago, I also created a thread here about the similarities between a POIS attack, and encephalitis.  Inflammation in the brain sure seems to be an important aspect of POIS. 

Carbamazepine had been mentioned before on the forum, There is even a thread from a member who eliminated his POIS with carbamazepine and/or levetiracetam, while taking those for temporal epilepsy ( see https://poiscenter.com/forums/index.php?topic=4583.msg49301#msg49301).  But, as usual with POIS, this solution will work only for a certain proportion of POIS sufferers, and not for the others.
Some POIS types seem to be more systemic than just affecting the brain, like those who have strong allergy symptoms, joint aches, intense flu-like symptoms, dermatologic problems, and so on.  But extreme fatigue, mood swings, difficulty concentrating, etc, are very often present, and point to neuroinflammation in the brain, just like you discuss in your hypothesis.
I am not surprised to read that this member has to limit his sexual activity in order for his control method to stay effective.  I experiment quite the same with my own pre-pack method.  If too many repetitions in a short time period, it will not contain my POIS symptoms anymore.

Let us know of the resutls if you try carbamazepine.

[hosamitaha]

Disclaimer: zero words or theories in this post or the first one were written or generated by chatgpt.

Following up on my theory on hypersensitive neural pathways to stimulation leading to neuronal excitotoxicity and subsequent neuroinflammation (pois attack or chronic fatigue-like symptoms).

While epilepsy and bipolar stem from this pathophysiology, less attention in my first post was given to ?migraine?. Migraine shares this same pathophysiology.

POIS similarity in origin to migraine answers a lot of questions and raises also new important ones.

Both are a form of neuronal excitotoxicity and cortical spreading depression. However, the case in POIS is more silent, unlike migraine, and I believe many of you report the infamous ?tingling in the head? during orgasm if not tension or even tension headache after orgasm. Migrainers experience "pain" so they seek treatment early in the course of the disease before it becomes cognitively and physically debilitating. We don't experience pain when pois comes to our lives in the first years so pois increases everytime causing more vicious neuroinflammation attacks over the years.

A small medical background about migraine: Migraine was previously explained as the occurence of initial vasoconstriction followed by vasodilation. This theory was later proven to be only a part of the picture and not the main pathology, vasoconstriction occurs only secondary to neuronal excitotoxicity and cortical spreading depression. Nonetheless, stopping this vasoconstriction is part of an effective treatment in reducing both symptoms of migraine and POIS.

That explains a lot!! like why "Niacin" a vasodilator works for some in decreasing symptoms by preventing this initial vasoconstriction. A previous post in the pois subreddit was dedicated to nitroglycerin which is also a vasodilator. In addition, a lot report that the infamous Cialis (scientific name: tadalafil) taken 1 hour before O is very effective in reducing symptoms due to targeting this initial vasoconstriction.

However, vasoconstriction as I said is secondary to neuronal excitation, so we need also to prevent the electrical brain activity from happening in the first place.

I previously talked about possible roles of valproate and carbamazepine. I also talked about how amitriptyline 25mg + carbamazepine 200mg daily reduced the symptoms for one fellow poiser (who is a medical student by the way) to 1 hour of mild symptoms if any symptoms at all. He recently added that he tried using carbamazepine 200mg alone and said it was effective in reducing symptoms from 3 days to 12 hours in their case implying both drugs played a role in prevention.

Going back to migraine. Below is a list of medically proven drugs by evidence used to prevent migraine with their details and some associations I made to POIS.

.

Approved first line drugs for migraine prevention:

1-The insufficiently trialed Valproic acid by POISers (other names include: divalproex or valproate or valproate sodium or depakene or depakote). The beast for prevention of migraine, epilepsy and bipolar attacks. This one I believe has the biggest potential due to its established effect for all these conditions. Some extra data about its role in migraine: ?They are particularly useful for prolonged and atypical migraines.?

2-Beta-blockers especially propranolol, metoprolol and timolol. Evidence supports medical use as first line for migraine prevention. However, there is a take here. Building up those drugs in a dose of 40mg up to 320mg for 8-12 weeks is crucial. Poiscenter has only one trial with the correct buildup dose who said his symptoms were reduced by at least 75%. The other people who tried beta-blocker only taken once before orgasm reported no benefit, that?s not a complete dose and no wonder why it didn?t help!

3- Topiramate or Topamax. A first line drug for migraine prevention and one that wasn?t trialed by any POISer. More data on its role in migraine: ?Topamax is another drug used as a first-line treatment option for migraine prophylaxis.\[15\] Topamax has comparable efficacy to propranolol for preventing migraine headaches. It should be started at a low dose of 25 mg daily and slowly titrated up to 100 mg twice daily. Patients should continue treatment for at least 2 to 3 months before the treatment efficacy is evaluated.?

.

Approved second line drugs for migraine.

1-Amitriptyline trialed by our friend. When amitriptyline was used by many POISers (especially alone and in lower doses less than or equal to 25mg), it only cushioned POIS symptoms but POIS was still there by increasing all important neurotransmitters like norepinephrine, dopamine and serotonin. But wait! I said we want the ?prevent the whole attack? effect not the ?raise my neurotransmitters solve my symptoms after neuroinflammation already ensued? effect. For amitriptyline to completely prevent migraine the following needs to be taken into consideration: "Amitriptyline is shown to be beneficial in migraine prevention.\[19\] It may be more effective than propranolol in mixed migraine-tension types of headaches. Response to treatment can be seen in up to 4 weeks and is more rapid than with beta-blockers. The daily dosing is 25 to 150 mg daily.?

2- Venlafaxine, or as we call it (life?s free trial without POIS). Sadly the effect goes away after 4-6 week and POIS comes back as was reported by many POISers.

.

Possibly effective drugs by medical evidence for migraine.

1-Carbamazepine which worked for our friend and targets bipolar and epilepsy very effectively. Sadly it has less evidence regarding its use in migraine prevention. But I believe we need to try it.

2-Candesartan (an angio-tensin receptor blocker originally for treating hypertension). It has vasodilatory effects.

3-Lisinopril (an ACE inhibitor) similar to angio-tensin receptor blockers.

4-Nebivolol a beta blocker.

5-Nicardipine a calcium channel blocker and a vasodilator.

.

Ineffective drugs for migraine prevention and also ineffective for POIS (coincidence?)

1-SSRIs whose role in POIS is a more of cushioning of symptoms and not prevention of the attack. it might help by delaying ejaculation and decreasing overstimulation which is problematic in our case.

2-Gabapentin which in my opinion is an extreme medication and doesn't benefit either migraine or epilepsy or bipolar (or POIS according to many)

3-Lamotrigine which despite, being a Popular mood stabilizer and anti-epileptic, is ineffective in migraine prevention by research evidence.

.

Other effective meds by POISers and their correlation to this theory.

1-the notorious milnacipran: milnacipran is effective (for some) in prevention of the attack

As it raises the threshold for stimulation as evidenced here: [https://pubmed.ncbi.nlm.nih.gov/19841905/](https://pubmed.ncbi.nlm.nih.gov/19841905/)

It was reported to be effective in preventing migraines in a study: [https://pubmed.ncbi.nlm.nih.gov/24030685/](https://pubmed.ncbi.nlm.nih.gov/24030685/)

And post coital headache and premature ejaculation in another: [https://journals.lww.com/americantherapeutics/fulltext/2019/10000/milnacipran\_for\_postcoital\_cephalgia\_and\_premature.37.aspx](https://journals.lww.com/americantherapeutics/fulltext/2019/10000/milnacipran_for_postcoital_cephalgia_and_premature.37.aspx)

2- testosterone replacement therapy raises the threshold for stimulation and protects from migraine in many studies. Many migrainers suffer from low testosterone.

3- L-citrulline acts as vasodilator by stopping the initial vasoconstriction secondary to neuroexcitability just like niacin.

4-taurine: many many migrainers were helped by taurine, surprise, many poisers too and it is in the POIS chart.

5-there is weak evidence and anecdotes that fenugreek helps migraines

6-pre-pack with IDO/TDO/NMDAr blockers whose main mechanism are preventing hyperstimulation worked for a some poisers

7-ketosis: migrainers report cure from keto and cutting gluten. Poisers report a lot of help from this.

8-some migrainers report benefit from antihistamines in preventing their attacks but this is somewhat uncommon. Some poisers symptoms are prevented by antihistamines but this also is not the case for many..

[demografx]

Disclaimer: zero words or theories in this post or the first one were written or generated by chatgpt.Following up on my theory on hypersensitive neural pathways to stimulation leading to neuronal excitotoxicity and subsequent neuroinflammation (pois attack or chronic fatigue-like symptoms).While epilepsy and bipolar stem from this pathophysiology, less attention in my first post was given to ?migraine?. Migraine shares this same pathophysiology.POIS similarity in origin to migraine answers a lot of questions and raises also new important ones.Both are a form of neuronal excitotoxicity and cortical spreading depression. However, the case in POIS is more silent, unlike migraine, and I believe many of you report the infamous ?tingling in the head? during orgasm if not tension or even tension headache after orgasm. Migrainers experience "pain" so they seek treatment early in the course of the disease before it becomes cognitively and physically debilitating. We don't experience pain when pois comes to our lives in the first years so pois increases everytime causing more vicious neuroinflammation attacks over the years.A small medical background about migraine: Migraine was previously explained as the occurence of initial vasoconstriction followed by vasodilation. This theory was later proven to be only a part of the picture and not the main pathology, vasoconstriction occurs only secondary to neuronal excitotoxicity and cortical spreading depression. Nonetheless, stopping this vasoconstriction is part of an effective treatment in reducing both symptoms of migraine and POIS.That explains a lot!! like why "Niacin" a vasodilator works for some in decreasing symptoms by preventing this initial vasoconstriction. A previous post in the pois subreddit was dedicated to nitroglycerin which is also a vasodilator. In addition, a lot report that the infamous Cialis (scientific name: tadalafil) taken 1 hour before O is very effective in reducing symptoms due to targeting this initial vasoconstriction.However, vasoconstriction as I said is secondary to neuronal excitation, so we need also to prevent the electrical brain activity from happening in the first place.I previously talked about possible roles of valproate and carbamazepine. I also talked about how amitriptyline 25mg + carbamazepine 200mg daily reduced the symptoms for one fellow poiser (who is a medical student by the way) to 1 hour of mild symptoms if any symptoms at all. He recently added that he tried using carbamazepine 200mg alone and said it was effective in reducing symptoms from 3 days to 12 hours in their case implying both drugs played a role in prevention.Going back to migraine. Below is a list of medically proven drugs by evidence used to prevent migraine with their details and someassociations I made to POISApproved first line drugs for migraine prevention:1-The insufficiently trialed Valproic acid by POISers (other names include: divalproex or valproate or valproate sodium or depakene or depakote). The beast for prevention of migraine, epilepsy and bipolar attacks. This one I believe has the biggest potential due to its established effect for all these conditions. Some extra data about its role in migraine: ?They are particularly useful for prolonged and atypical migraines.?2-Beta-blockers especially propranolol, metoprolol and timolol. Evidence supports medical use as first line for migraine prevention. However, there is a take here. Building up those drugs in a dose of 40mg up to 320mg for 8-12 weeks is crucial.Poiscenter has only one trial with the correct buildup dose who said his symptoms were reduced by at least 75%. The other people who tried beta-blocker only taken once before orgasm reported no benefit, that?s not a complete dose and no wonder why it didn?t help!3- Topiramate or Topamax. A first line drug for migraine prevention and one that wasn?t trialed by any POISer. More data on its role in migraine: ?Topamax is another drug used as a first-line treatment option for migraine prophylaxis.\[15\] Topamax has comparable efficacy to propranolol for preventing migraine headaches. It should be started at a low dose of 25 mg daily and slowly titrated up to 100 mg twice daily. Patients should continue treatment for at least 2 to 3 months before the treatment efficacy is evaluated.?Approved second line drugs for migraine.1-Amitriptyline trialed by our friend. When amitriptyline was used by many POISers (especially alone and in lower doses less than or equal to 25mg), it only cushioned POIS symptoms but POIS was still there by increasing all important neurotransmitters like norepinephrine, dopamine and serotonin. But wait! I said we want the ?prevent the whole attack? effect not the ?raise my neurotransmitters solve my symptoms after neuroinflammation already ensued? effect. For amitriptyline to completely prevent migraine the following needs to be taken into consideration: "Amitriptyline is shown to be beneficial in migraine prevention.\[19\] It may be more effective than propranolol in mixed migraine-tension types of headaches. Response to treatment can be seen in up to 4 weeks and is more rapid than with beta-blockers. The daily dosing is 25 to 150 mg daily.?2- Venlafaxine, or as we call it (life?s free trial without POIS). Sadly the effect goes away after 4-6 week and POIS comes back as was reported by many POISers.Possibly effective drugs by medical evidence for migraine.1-Carbamazepine which worked for our friend and targets bipolar and epilepsy very effectively. Sadly it has less evidence regarding its use in migraine prevention. But I believe we need to try it.2-Candesartan (an angio-tensin receptor blocker originally for treating hypertension). It has vasodilatory effects.3-Lisinopril (an ACE inhibitor) similar to angio-tensin receptor blockers.4-Nebivolol a beta blocker.5-Nicardipine a calcium channel blocker and a vasodilator.Ineffective drugs for migraine prevention and also ineffective for POIS (coincidence?)1-SSRIs whose role in POIS is a more of cushioning of symptoms and not prevention of the attack. it might help by delaying ejaculation and decreasing overstimulation which is problematic in our case.2-Gabapentin which in my opinion is an extreme medication and doesn't benefit either migraine or epilepsy or bipolar (or POIS according to many)3-Lamotrigine which despite, being a Popular mood stabilizer and anti-epileptic, is ineffective in migraine prevention by research evidence.Other effective meds by POISers and their correlation to this theory.1-the notorious milnacipran: milnacipran is effective (for some) in prevention of the attackAs it raises the threshold for stimulation as evidenced here[https://pubmed.ncbi.nlm.nih.gov/19841905/](https://pubmed.ncbi.nlm.nih.gov/19841905/)It was reported to be effective in preventing migraines in a study: [https://pubmed.ncbi.nlm.nih.gov/24030685/](https://pubmed.ncbi.nlm.nih.gov/24030685/)And post coital headache and premature ejaculation in another: [https://journals.lww.com/americantherapeutics/fulltext/2019/10000/milnacipran\_for\_postcoital\_cephalgia\_and\_premature.37.aspx(https://journals.lww.com/americantherapeutics/fulltext/2019/10000/milnacipran_for_postcoital_cephalgia_and_premature.37.aspx)2- testosterone replacement therapy raises the threshold for stimulation and protects from migraine in many studies. Many migrainers suffer from low testosterone.3- L-citrulline acts as vasodilator by stopping the initial vasoconstriction secondary to neuroexcitability just like niacin.4-taurine: many many migrainers were helped by taurine, surprise, many poisers too and it is in the POIS chart.5-there is weak evidence and anecdotes that fenugreek helps migraines6-pre-pack with IDO/TDO/NMDAr blockers whose main mechanism are preventing hyperstimulation worked for a some poisers :)7-ketosis: migrainers report cure from keto and cutting gluten. Poisers report a lot of help from this.8-some migrainers report benefit from antihistamines in preventing their attacks but this is somewhat uncommon. Some poisers symptoms are prevented by antihistamines but this also is not the case for many..

hosamitaha, I am not singling you out.

To better highlight my points below, I have even reduced your post to 1/3 of our normal text size. To  show its length in perspective.

This has been posted before:

EVERYONE: for good
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Why Lengthy Posts Are Discouraged
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By keeping your posts concise and engaging, you contribute positively to the forum environment, making it enjoyable for everyone involved.

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