[Chaos]

1) Welcome Sohail! We're very happy that you found this forum. We really think and hope 2013 is the year that we can finally get some good research and solve this POIS problem once and for all!

Thank U. i hope 2.

Hi,
We had a big discussion about histamine receptors over on poiscenter.
There's some stuff here newbielink:http://poiscenter.com/forums/index.php?topic=795.30 [nonactive].
I think it's best not to post about new theories over there (as it's against the rules) but you could read the posts if you want. The h3 idea isn't new. H3 blockers aren't widely available. Alternatives are mast cell stabilisers.

Just so you know, everyone releases histamine when there's an erection. When h2 blockers are given to someone, it impedes them getting an erection.
That doesn't mean there's not an immunological reaction going on here but the question is why are POIS sufferers different rather than why do POIS sufferers have histamine release upon an O.

Hi, Thanks 4 the link. I read a couple of posts there.
Yes clobenpropit is one of them and sadly that's not available(like other h3 A.H.). I take Lorazepam if i get extremely depressed. but i usually only take loratadine because lorazepam is harmful.
I'm not sure if i understand your view. Histamine has many functions in the body. Pois is not related to erection/histamine realese for erection. I don't get depressed or numb because of erection. our symptoms seems like an allergy(allergy to seminal fluid). Probably histamine release for erection is local and little. But allergy to seminal fluid releases lots of histamine in whole body.
Allergy theory is not new. I'm not sure but I remember that was Dr waldinger's theory.  anyway
It seems there are different kinds of pois. Probably...

[Chaos]

I'm 21 and still there is no beard on my cheeks. is that related to POIS?

[GDRTW]

Great to see all this new information coming out. A couple of power plays from me as my biggest issue is with sensitivity to light. Feels like a very weak retina that makes me lethargic and very easily tired. I found Huperzine to be a big help and I have also discovered that passionfruit seeds (need to be bitten and chewed on) can help alleviate as well. I am in Taiwan where teas are readily available around the corner. I go for a passionfruit green tea in times of need.

[acronym]

"Most people  are  with low ceruplasmin,  some people  are with high ferritin/ The  major  imbalances seen ,   low dopamine/ serotonin  ratio.    High RT3 ratio which points to copper overload."
Gbolduev...so low ceruplasmin. means no carrier for copper in the body...and you say copper overload. why because it accumulates in the wrong places? With low ceruplasmin I thought this would result in copper deficiency symptoms, not copper overload. If any of us have low ceruplasmin, then taking extra copper in a supplement would be a waste wouldn't it because it is not going to get picked up.
I have been taking fairly high doses of zinc for a number of years as part of a treatment for Pyroluria. I wonder if I have screwed up my Cu levels because of this. I had hair mineral test a number of years ago (prior to the Pyroluria diagnosis) and most metals showed up in the normal range except titanium.

[Chaos]

@kurtosis I'm so happy I found you're an INTJ. I'm really interested in personality psychology stuff.
I'm an INTP-big5:RLUAI-enneagram:5.
Do you think asking other members to take personality test is a good idea?
I'm really curious if there is any correlation between personality type and pois.

[Gbolduev]

ACRONYМ,

What happened to me  that I was stressed  and  for some stupid reason I started to take zinc also, and took it for a while.   that is when my Pois started.    it sped my  thyroid  relative to  adrenal gland, and my  dopamine which is  associated with adrenal  became  lower than   serotonin   which was associated with  thyroid.    Basically the gap between  dopamine and serotonin increased//   To tell you the truth from the blood work that I  saw , this is the imbalance  in 90% cases/    So the cure for this imbalance  is to  lower your thyroid, and at the  same time increase your methylation.

[kurtosis]

@kurtosis I'm so happy I found you're an INTJ. I'm really interested in personality psychology stuff.
I'm an INTP-big5:RLUAI-enneagram:5.
Do you think asking other members to take personality test is a good idea?
I'm really curious if there is any correlation between personality type and pois.

Daveman on poiscenter was also an INTJ. Not sure about the others.
Several POIS sufferers experience POIS symptoms upon erection. Histamine release on orgasm is greater. In response to Vincent M, H1 do not appear to be responsible for maintaining an erection. The h2 receptors in the penis are effected but histamine levels increase. Arguably not a problem for most people but it makes me itchy, sneezy and brings about something that feels like a headache that never quite develops.
See http://www.ncbi.nlm.nih.gov/pubmed/7850330
for a description of histamine's role in sexual function.

These results indicate that histamine may play a role in human penile erection. The erection-promoting action of histamine is probably due to H2 receptor activation, although another histamine receptor, possibly H3, also seems to be involved. This study suggests that histamine could be a valuable tool in the diagnosis of erectile dysfunction.

The results appear conclusive but scientists are supposed to be cautious in what they say. This is generally considered a good thing
There are other articles on ncbi about this also.
http://www.ncbi.nlm.nih.gov/pubmed/3133686

While the H2 antagonists do not always have strong behavioural effects when administered peripherally, there is evidence that cimetidine has a depressant effect on sexual function

Women have been known to get a "sex flush" reaction following an orgasm and some of them experience sneezing and mild symptoms associated with an allergic reaction. I spoke with my doctor, an allergist, about this and she said that it was not thought to be an allergy but rather a result of increased histamine levels.
It's an interesting phenomenon. http://en.wikipedia.org/wiki/Flushing_(physiology)#Sex_flush
but doesn't lead to headaches or confusion in most sufferers.

There are some reports of people developing POIS like symptoms following taking propecia. I think this was discussed on poiscenter but I haven't time to look it up now.

One reason the flush might lead to confusion and nausea is an overloaded calcium channel. As Yasko is fond of saying "glutamate is the gun and calcium is the trigger" when discussing excitotoxins and seizures in autistic kids.
http://www.dramyyasko.com/resources/autism-pathways-to-recovery/chapter-4/
But you don't have to trust Yasko on this. She's just collecting a "well known" set of facts about glutamate and Ca ion interaction. See http://en.wikipedia.org/wiki/Glutamate_receptor#Excitotoxicity

Overstimulation of glutamate receptors causes neurodegeneration and neuronal damage through a process called excitotoxicity. Excessive glutamate, or excitotoxins acting on the same glutamate receptors, overactivate glutamate receptors (specifically NMDARs), causing high levels of calcium ions (Ca2+) to influx into the postsynaptic cell.[34]
High Ca2+ concentrations activate a cascade of cell degradation processes involving proteases, lipases, nitric oxide synthase, and a number of enzymes that damage cell structures often to the point of cell death.[35] Ingestion of or exposure to excitotoxins that act on glutamate receptors can induce excitotoxicity and cause toxic effects on the central nervous system.[36] This becomes a problem for cells, as it feeds into a cycle of positive feedback cell death.

[FinalPanic]

ACRONYМ,

What happened to me  that I was stressed  and  for some stupid reason I started to take zinc also, and took it for a while.   that is when my Pois started.    it sped my  thyroid  relative to  adrenal gland, and my  dopamine which is  associated with adrenal  became  lower than   serotonin   which was associated with  thyroid.    Basically the gap between  dopamine and serotonin increased//   To tell you the truth from the blood work that I  saw , this is the imbalance  in 90% cases/    So the cure for this imbalance  is to  lower your thyroid, and at the  same time increase your methylation.

Hi Gbolduev - how do you go about re-balancing these factors - this is of interest to me, thank you. My POIS started over 30 years ago after a bout of stress and terrible insomnia and anxiety - it all just kicked off and the condition has stayed with me ever since, lasting anything from two days to two weeks after O.

[Vincent M]

In response to Vincent M, H1 do not appear to be responsible for maintaining an erection. The h2 receptors in the penis are effected but histamine levels increase. Arguably not a problem for most people but it makes me itchy, sneezy and brings about something that feels like a headache that never quite develops.
See http://www.ncbi.nlm.nih.gov/pubmed/7850330
for a description of histamine's role in sexual function.

These results indicate that histamine may play a role in human penile erection. The erection-promoting action of histamine is probably due to H2 receptor activation, although another histamine receptor, possibly H3, also seems to be involved. This study suggests that histamine could be a valuable tool in the diagnosis of erectile dysfunction.

The results appear conclusive but scientists are supposed to be cautious in what they say. This is generally considered a good thing
There are other articles on ncbi about this also.
http://www.ncbi.nlm.nih.gov/pubmed/3133686

While the H2 antagonists do not always have strong behavioural effects when administered peripherally, there is evidence that cimetidine has a depressant effect on sexual function

Interesting. I have taken ranitidine, an H2 receptor inverse agonist, with no effect on my erections. Perhaps I'd need something for the H3 receptor as well.

[nathan123]

@ German:  I have one interesting factor for my POIS.  What I always observe is if I take new medicine for the first time, it will decreae the POIS symtoms.  Later this will not works for reducing the POIS pain.  I experienced this for SSRI, Sodium tablet, all herbal (around 10 to 15 varities) and other medicines.  What is the reason behind this.  We are not able to find the solution to this problem.  Please clarify.
Further I will get my test results after 20th.  In my town some of the test you mentioned is not avialble and I required to go to another big city for this and I am planning to go on 15th.  On 20th I will update all the test you require. 

thanks for the your help. 
with regards,

Nathan.

[Gbolduev]

Nathan, 

it is hard to say ,  since you were taking all kind of  stuff...but I can  guess, that   when you take  something  to increase  serotonin  lets say ,  then it  spikes and then crashes, and the actual effect might be  the decrease,  but if you  take it all the time , may be  it  starts  building up , and thus your ratio stays  impaired, I mean  dopamine serotonin  ratio.  That is why  when you smoke all the time and then quit  you find yourself with really  low serotonin  levels , since smoking  was providing  constant serotonin boost and  the methylation of  serotonin  adjusted.

[Gbolduev]

To me , lets say with  the niacin,   it releases serotonin in the flush,  so  the actual ratio  might  go up , I mean  dopamine  to serotonin , since  niacin has released some of  the serotonin.  after orgasm , your dopamine   goes up and then crashes,  and serotonin  goes up.  So  if you have   low  dopamine / serotonin ratio  from the getgo, I mean before the orgasm,  then after naicin   it goes up   and then  after orgasm  becomes normal, that is why may be some people feel normal after naicin.   Since the  ration of dopamine and serotonin   tells you  about the state,  either  infection or inflammation..   high  or low  is bad.

[kurtosis]

In response to Vincent M, H1 do not appear to be responsible for maintaining an erection. The h2 receptors in the penis are effected but histamine levels increase. Arguably not a problem for most people but it makes me itchy, sneezy and brings about something that feels like a headache that never quite develops.
See http://www.ncbi.nlm.nih.gov/pubmed/7850330
for a description of histamine's role in sexual function.

These results indicate that histamine may play a role in human penile erection. The erection-promoting action of histamine is probably due to H2 receptor activation, although another histamine receptor, possibly H3, also seems to be involved. This study suggests that histamine could be a valuable tool in the diagnosis of erectile dysfunction.

The results appear conclusive but scientists are supposed to be cautious in what they say. This is generally considered a good thing
There are other articles on ncbi about this also.
http://www.ncbi.nlm.nih.gov/pubmed/3133686

While the H2 antagonists do not always have strong behavioural effects when administered peripherally, there is evidence that cimetidine has a depressant effect on sexual function

Interesting. I have taken ranitidine, an H2 receptor inverse agonist, with no effect on my erections. Perhaps I'd need something for the H3 receptor as well.

The theory is that those people with less active mast cells may need less rantidine to reduce libido.  It is a noted side effect of the drug but it doesn't appear to affect everyone & I think the reason is base histamine levels.
http://www.drugs.com/sfx/ranitidine-side-effects.html
h3 receptor inverse agonists are viewed as a potential treatment for ADHD as they may promote attention. See http://en.wikipedia.org/wiki/Ciproxifan
Again, this is all very new. The classic ADHD drugs are still amphetamines and it's possible that there will be new insights into the role of mast cells and histamine levels in attention related disorders. Similar to those anecdotal reports of kids with autism being more likely to suffer from allergies.
Stuff is related but figuring out how is the problem. I don't know how long it will take medical researchers to integrate their knowledge but a condition like POIS is interesting as it appears to have symptoms from multiple physiological systems which are viewed as different specialities now. I.e. immunology, psychiatry, neurology and endocrinology. So in one respect, solving POIS may yield new light on other illnesses but in another it appears to be a rare disease with limited economic value from curing it...

Great value to us of course

[Gbolduev]

so basiciallly    in    the normal POIS,   thyroid  makes your  adrenal  pump harder.  And   cortisol is usually high ,  since cortisol  is pumped to  create RT3 hormone to stop   the thryoid affect... This  the  ratio of dopamine/serotonin is   not right and also  conversion  of noradrenaline  into  adrenaline.    That is why  naicin works,   it grabs methyl   and  inhibits conversion of noradrenaline to adrenaline.

Herman

[kurtosis]

We allowed to post here if we keep it scientific. Keeping it scientific means providing evidence.
If you did not just come up with this theory out of nowhere then you should past evidence you can easily provide.
nobody is competing or trying to attack you, we just want evidence.

I'm not even sure there's a moderator any more. Like Elvis, they may have left the building

[Gbolduev]

http://www.medical-library.net/reverse_t3_dominance_syndrome.html

[Gbolduev]

http://fatnews.com/index.php/weblog/comments/1151/

[Vincent M]

Interesting, Kurtosis. I have read a bit about H3 receptor inverse agonists and they do seem to have a lot of potential. It'd be interesting to see how they'll do when they hit the market.

[Gbolduev]

Norepinephrine
Also known as:   NE;  Noradrenaline;  Levarterenol
Description
Catecholamine Stimulatory Neurotransmitter that is chemically similar to Adrenaline.
Beneficial Biological Functions of Norepinephrine
Norepinephrine possesses Life Extension potential:
-   A high ratio of Serotonin/NE accelerates the Aging Process.
-   A low ratio of Serotonin/NE slows down the Aging Process.
Immune System
NE stimulates the release of Hormones that provide the Thymus Gland with correct instructions.
Metabolism
NE alleviates Obesity (by stimulating the body's Brown Adipose Tissue to utilize other Adipose Tissue in the production of Energy).
Nervous System
Norepinephrine is produced and secreted by the Adrenal Medulla.
   Norepinephrine controls the Adrenergic Nervous System (a component of the Autonomic Nervous System).
   Age related decline in NE levels are associated with Age Related Memory Decline.
   Persons afflicted with Alzheimer's Disease usually have insufficient Norepinephrine in their Brains [scientific research - humans].
NE depletion can cause Apathy.
   NE suppresses Appetite.
   NE stimulates Beta-1 Adrenergic Receptors.
   NE stimulates Beta-2 Adrenergic Receptors (although NE has less affinity with these Receptors than does Adrenaline).
NE is involved in Moods (due to its central role in the excitatory drives associated with mood and Emotion).
   NE deficiency is a major cause of Depression.
   NE enhances Learning.
   NE enhances Memory.
Norepinephrine helps to minimize the sensation of Pain:
-   Norepinephrine travels via a descending pathway that originates in the Locus Coeruleus of the Medulla of the Brain and terminates in the Dorsal Horn of the Spinal Cord to inhibit the release of Substance P (the Neuropeptide that initiates Nerve Impulses relating to Pain).
Sexual System
NE increases Sexual Desire.
Norepinephrine Enhances the Function of these Substances
Hormones
NE is the immediate precursor of Adrenaline:
NE is required for the release of human Growth Hormone (hGH).
   Norepinephrine stimulates the release of Luteinising Hormone Releasing Hormone (LHRH) from the Hypothalamus.
   The nightly production of Melatonin occurs primarily as a result of NE release from postganglionic sympathetic Neurons that terminate in the Pineal Gland:
-   Following its release from these Neurons, Norepinephrine interacts with Adrenergic Receptors which (via a specific G-Protein) in turn activate Adenyl Cyclase in the Membrane of Pinealocytes (Cells of the Pineal Gland).
-   Activation of Adenyl Cyclase in the Pineal Gland increases the intracellular production of Cyclic AMP (cAMP) which then activates the N-
acetyl Transferase (NAT) enzyme (a precursor for Melatonin synthesis from N-acetyl Serotonin).
-   Approximately 85% of Melatonin produced in the Pineal Gland occurs as a result of Norepinephrine activating Beta-Adrenergic Receptors and approximately 15% occurs as a result of activation of Alpha-Adrenergic Receptors.
These Substances Enhance the Production or Release of Norepinephrine
Coenzymes - Electron Transport System
Nicotinamide Adenine Dinucleotide (NAD) is essential for maintaining proper levels of Norepinephrine in the Synapses of Neurons:
-   After Norepinephrine crosses the Neuron's Synapses it loses one electron to form oxidized Norepinephrine.  In the presence of NAD, this oxidized Norepinephrine then re-converts back to active Norepinephrine.  If there is a deficiency of NAD, the oxidized Norepinephrine loses another electron to irreversibly form Noradrenochrome.
-   NADH increases the production of Norepinephrine within the Brain.
Enzymes
Decarboxylases are required for the manufacture of NE.
Alkaloids
Yohimbine increases blood levels of Norepinephrine [scientific research - Yohimbine increases serum NE levels by up to 66%].
Amino Acids
Phenylalanine is a precursor for the endogenous production of Norepinephrine.
   Tyrosine is a precursor for the endogenous production of Norepinephrine.
Environmental Factors
Regular Exercise increases the production of Norepinephrine.
Methylxanthines
Caffeine increases Norepinephrine synthesis and release within the Brain [scientific research - animals].
Minerals
Calcium affects the function of NE.
   Copper is a cofactor for the Dopamine Beta-Hydroxylase enzyme (that catalyzes the conversion of Dopamine to Norepinephrine).
Organic Acids
Fumaric Acid stimulates the activity of the Dopamine Beta-Hydroxylase (that catalyzes the conversion of Dopamine to Norepinephrine).
Pharmaceutical Drugs
Many Tricyclic Antidepressants (including Amitryptiline, Desipramine and Imipramine) increase Norepinephrine levels within the Brain by blocking the reuptake of Norepinephrine into Alpha-1 Adrenergic Receptors (i.e. by functioning as Norepinephrine Reuptake Inhibitors), thereby increasing the availability and effects of NE [caution:  Tricyclic Antidepressants have numerous potentially toxic side-effects and contraindications].
Sibutramine inhibits the reuptake of Norepinephrine.
   Venlafaxine (a relatively new type of Pharmaceutical Antidepressant) inhibits the reuptake of Norepinephrine into Neurons.
Smart Drugs
Deprenyl totally inhibits the destruction of Norepinephrine by Monoamine Oxidase Type B (MAO-B):
-   Deprenyl blocks the re-uptake of NE from the Synapses between Neurons into the Storage Sites within Neurons (thereby increasing the level of Norepinephrine in its active state within the Synapes) - Deprenyl could therefore be described as a Norepinephrine Re-Uptake Inhibitor.
Idebenone enhances the endogenous production of Norepinephrine (by facilitating the cellular uptake of Tyrosine).
   Vinpocetine increases the Brain's turnover of Norepinephrine.
Vitamins
Vitamin C is a cofactor for the conversion of Dopamine to Norepinephrine by Dopamine Beta-Hydroxylase (it is converted to its Dehydroascorbic Acid form during this metabolic process).
These Herbs Enhance the Function of Norepinephrine
Ginkgo biloba stimulates the release of Norepinephrine within the body [scientific research].
   Ginsengs increase the body's Norepinephrine production when the body is under Stress [scientific research].
These Substances Interfere with or Block Norepinephrine
Enzymes
Monoamine Oxidase Type A (MAO-A) causes the breakdown (oxidation) of Norepinephrine to Dihydroxymendalic Acid [this activity is essential to keep Norepinephrine levels in check, however excessive MAO production can over-deplete Norepinephrine].
Flavoproteins
If Nicotinamide Adenine Dinucleotide (NAD) deficiency exists, Norepinephrine is oxidized to irreversibly form Noradrenochrome.
Neurotoxins
DSP-4 causes long-lasting depletion of Norepinephrine by damaging Noradrenergic Neurons.
Neurotransmitters
Gamma Aminobutyric Acid (GABA) inhibits the release of Norepinephrine (by binding to and activating GABAb Receptors).
Alkaloids
Cocaine causes depletion of Norepinephrine due to its over-stimulation of the Central Nervous System causing the sudden release and non-replacement of the body's reserves of NE.



Amino Acids
Tyramine causes over-stimulation of the Adrenal Glands, resulting in depletion of the body's Norepinephrine reserves.
Pharmaceutical Drugs - Amphetamine Derivatives
GABAb Receptor Agonists inhibit the release of Norepinephrine (by binding to and activating GABAb Receptors).
   Ritalin causes the sudden release of stores of NE and subsequent depletion and deficiency.
Recreational Drugs
Amphetamine causes the Brain to release NE and to block the recycling of NE, resulting in the high concentration of NE in the Synapses between Neurons that is responsible for the stimulatory effects of Amphetamine [however long term or excessive usage of Amphetamine causes NE depletion due to the large amounts of NE that are released but not replaced].
These Ailments Cause the Depletion of Norepinephrine
Adrenal Glands
Continual Stress causes the over-production of NE and its subsequent depletion.
Aging Process
The body's supplies of Norepinephrine decline in tandem with the Aging Process:
-   The number of Neuron Receptors for NE decline with the progression of the Aging Process.
-   The conversion of nutrients into NE declines with Age.
Metabolism
Hypoglycaemia causes NE deficiency.
Toxic Effects of Excessive NE Production
Cardiovascular System
Chronically elevated Norepinephrine levels can induce abnormal Blood Clotting (increasing the possibility of Thrombosis and Heart Attack).
Nervous System
Excessive NE production causes Schizophrenia.

Copyright 1997 In-Tele-Health

[Gbolduev]

Kurtosis, notice the ratio of  serotonin to  noradernaline.