Author Topic: POIS treatment: theory & supplement stack  (Read 204521 times)

Eliasjoelrivera

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Re: POIS cure: theory & supplement stack
« Reply #500 on: December 06, 2019, 02:28:28 PM »
Very interesting to observe the inflammation process. Maybe I have a lot to do with pois. We would have to investigate. The vagus nerve is also implicit.



Inflamed neurons


The immune response of our body can accelerate memory loss in Alzheimer's disease.

Allison bond

age fotostock
The inflammation fulfills a possible exacerbating function of cardiovascular pathologies or tumors. It may be necessary to add another incrimination to the list: Alzheimer's disease.
According to a study published in Neurology, when an inflammation appears in the body, whether due to infection or injury, the immune response seems to accelerate memory loss in people with Alzheimer's. In that study the alterations of the cognitive faculties were examined in a period of six months; Alzheimer's patients suffering from chronic (and progressive) inflammation due to, for example, obesity or arthritis, experienced a memory loss four times greater than that of patients without such inflammation.
Those who suffered chronic inflammation, but had also experienced an acute immune response (short-lived, such as an infection) were even worse: their memory loss accelerated 10 times faster than that of patients without any medical condition.
"When we started the study, we thought that acute events would be important," explains Clive Holmes of the University of Southampton. "But we hadn't realized the weight that chronic inflammation was going to have."
Well, how is the brain injured by inflammation, either by a chronic disease or by an infection? The cause is the body's immune system, which launches an attack on invading pathogens; releases inflammatory proteins such as tumor necrosis factor, TNF. This molecule causes the vagus nerve, which extends from the brain to the abdomen and controls vital functions, such as the heartbeat, to send an electrical impulse to the brain, instructing it to release its own immune messengers.
In individuals with healthy brains, this chain of events has no greater consequence than some discomfort for a few days. But it is possible that the neurons in the brains of Alzheimer's patients are permanently in a state of attenuated inflammation. Thus, when they are exposed to the threat of a pathogen or a chronic disease, they can reach full inflammation, releasing compounds that end up being deadly to brain cells. It is not known for certain why these cells die, although Holmes suspects the annihilation of some neurons in his attempt to stop the spread of the virus, while others may die by accident in the fight to rid the body of invaders.
The results of the study could contribute to minimizing memory loss in Alzheimer's cases, suppressing chronic inflammation, for example, helping patients to lose excess weight. One could also point directly against the origin of the inflammation: "If the inflammation in the body is causing inflammation in the brain, and it is possible to dampen that signal, the blockage of the FNT would play a role in curbing Alzheimer's disease," says Holmes
« Last Edit: December 06, 2019, 02:32:03 PM by Eliasjoelrivera »

Eliasjoelrivera

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Re: POIS cure: theory & supplement stack
« Reply #501 on: December 06, 2019, 02:48:07 PM »
Treat brain inflammation in neurodegenerative diseases
Treat brain inflammation in neurodegenerative diseases
Inflammation of the brain plays an important role in the development of diseases such as acute brain trauma, strokes or chronic conditions such as Alzheimer's disease or sclerosis. Therefore, a possible therapeutic target for the treatment of the disease may be to block the causes of that neuroinflammation.


The work being carried out by the Mar?a Trinidad Herrero group of Program 1 of CIBERNED studies inflammation in neurodegeneration and in dementias. In this study we analyze the type of cells that overexpress CCL2 in various scenarios of T-cell infiltration in the brain, in three different species.


Lymphocyte infiltration is an important phenomenon in the inflammatory response in neurodegeneration. Brain tissue diseases such as brain tumors and viral or bacterial infections show subsets of infiltrated T cells. Therefore the control of blood cell entry may have clinical importance and therapeutic implications. Until now we knew that CCL2 is a chemokine that participates in brain inflammation, but we were not clear about its contribution to lymphocyte entry into the parenchyma.

The images obtained show that perivascular astrocytes are responsible for the expression of CCL2 in the three situations analyzed, in the three different species. The results show that the expression of CCL2 by astrocytes contributes to the entry of lymphocytes into the brain parenchyma. In the experiments carried out in mice, blocking CCL2 by a specific neutralizing antibody attenuated infiltration. On the other hand, the fact that the level of CCL2 correlates with the infiltration of T cells and not with the number of circulating lymphocytes suggests that the presence of CCL2 in astrocytes contributes to the lymphocyte extravasation process and plays an important role. at the cellular entrance.

From a therapeutic point of view, manipulation of CCL2 can have a beneficial effect on neurodegenerative diseases. The expression of CCL2 has been related to the aggressiveness of the glioma and, in fact, the use of CCL2 neutralizing antibodies has been suggested as a possible strategy for its treatment. However, CCL2 infiltration research has focused primarily on the function of tumor infiltrated macrophages, but not on other cell types. This work suggests that, like macrophages, CCL2 can also mediate lymphocyte infiltration into the glioma and contribute to the level of aggressiveness. This may be one of the therapeutic targets to control lymphocyte infiltration in brain tumors.

Consequently, in other neuroinflammatory processes, such as acute brain trauma, strokes or chronic conditions such as Alzheimer's disease or sclerosis, prolonged and sustained inflammation mediated by CCL2 may have cytotoxic effects, worsening the incidence and severity of the illness

lycopoulos

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Re: POIS cure: theory & supplement stack
« Reply #502 on: December 07, 2019, 07:38:36 PM »
Hi @eliasjoelriviera, thank you for your post about effects of inflammation on the brain. What does this mean for POIS suffers, is our destiny early onset of Alzheimer?s?

Eliasjoelrivera

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Re: POIS cure: theory & supplement stack
« Reply #503 on: December 07, 2019, 09:47:04 PM »
Share the article because there are many relationships. apart explains the mechanism of neuronal inflammation. It may serve to understand the mechanism of pois.

Eliasjoelrivera

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Re: POIS cure: theory & supplement stack
« Reply #504 on: December 09, 2019, 12:51:55 PM »

2. Stress.

 

Making a brief synopsis (see Figure 1), the classical stress pathways initially involve the Hypothalamus that integrates the information from the sensory and visceral pathways, the Hypothalamus would activate two parallel routes: the SAM axis (Sympathetic-Adreno-Medullary) and the HPA axis (Hypothalamic-Pituitary-Adrenal) (Sirera et al, 2006).

 

 



Figure 1

 

 

The SAM axis begins when the sympathetic preganglionic neurons of the spinal cord receive information from the hypothalamus by activating the Sympathetic Branch and inhibiting the Parasympathetic Branch, this activation generates changes aimed at preparing the body for sustained physical exertion and decision making. The activation of sympathetic postganglionic neurons produces the release of Noradrenaline that is secreted at the level of the adrenal medulla and in brain structures: hypothalamus, limbic system, hippocampus and cerebral cortex. On the other hand, the sympathetic preganglionic neurons activate the marrow of the adrenal glands, releasing the adrenaline circulation and, to a lesser extent, norepinephrine, generating an increase in the plasma glucose and fatty acid levels, the production of thyroxine is also increased, while It produces a decrease in insulin, estrogen and testosterone levels, and inhibition of prolactin secretion.

In parallel, the HPA Axis starts from the activation of the Paraventricular Nucleus of the Hypothalamus and aims to maintain the parameters of effort and attention. The neurons of the paraventricular nucleus secrete through the portal vessels to the adenohypophysis the Corticotropin-Releasing Hormone (CRH). CRH and other related hormones enter the circulatory system that joins the hypothalamus with the anterior pituitary, and by activating the pituitary, corticotropin (ACTH) is released and to a lesser extent β-endorphin.

On the other hand, the activation of the Neurohypophysis by the magnocellular neurons of the hypothalamus generates the segregation of Vasopressin and Oxytocin that will enhance the effect of CRH. Once Corticotropin is secreted in the bloodstream, it stimulates the production and release of Glucocorticoids (cortisol and corticosterone) and mineralocorticoids by the Adrenal Glands. The effects of high levels of glucorticoids (especially cortisol) in the medium / long term on health are really harmful: increase in blood pressure, damage to muscle tissue ... so there are feedback circuits that try to maintain their levels blood within defined parameters.

 Immune system activation (Hansen-Grant et al, 1998; Reiche et al, 2004) by the SAM and HPA axes occurs through two different mechanisms, on the one hand the binding of hormones to their cognitive receptors and on the other indirectly through the deregulation of the balance that has to prevail in the production of pro-inflammatory cytokines (Sirera et al, 2006b; Maes et al, 1998). Proinflammatory cytokines are soluble mediators that promote and mediate inflammatory processes, the following stand out: interleukin 1 (IL-1) is involved in the regulation of the immune process and inflammation; interleukin 6 (IL-6) which also serves as a link between the endocrine system and the immune system; and Tumor Necrosis Factor (TNF) that has the ability to destroy certain cell lines and initiates the cascade of proinflammatory cytokines and other mediators. There are data that in addition to the endocrine system, the cytokines IL-1, IL-6 and TNFα interact with the Noradrenergic, Serotonergic, and Dopaminergic systems (Kronfol & Remick, 2000


 Inflammation

 

Inflammation is a biochemical process that can be caused by numerous endogenous or exogenous factors, in fact any immunological phenomenon capable of affecting the stability of the system can be considered as a stressor and the process may be referred to as inflammatory stress. The Immune System has the function of recognizing and destroying both external and internal pathogens. To do this, it has two intercommunicated systems: innate or nonspecific immunity and acquired or specific immunity that is usually subdivided into two complementary groups: cellular immunity and humoral immunity. It is the nonspecific system cells (neutrophils, macrophages and dendritic) that initiate the immune response through phagocytosis and inflammation. Non-specific immunity induces specific immunity, and as a result a specialized response is generated and we could say with memory. The intensity, duration and peculiar characteristics of the inflammations will depend on the affected area, the previous state and the cause that causes it.

Chronic inflammation occurs as a result of the presence of an infectious agent, antigen or for a long time due to an immune system disorder. More and more data are available that suggest that inflammation may contribute to the development of diseases such as Alzheimer's (Tan et al, 2007), cancer (Pikarsky et al, 2004), atherosclerosis (Pi?on & Kaski, 2006), and diabetes (Rosado and Mendoza, 2007), in addition to those where inflammatory processes are the same basis of the disease as Crohn or rheumatoid arthritis. Chronic inflammation is characterized by the formation of fibrous tissue and that the cell infiltrate is mainly composed of macrophages, lymphocytes and plasma cells. Among the mediators of inflammation we must highlight the role of cytokines, especially IL-1β and TNFα, capable of activating numerous humoral cascades of mediators that perpetuate the activation of the system. Cytokines (see Table 1) form an important group of proteins that act as mediators of communication between living cells. In order to understand the role of cytokines, it is necessary to understand their mechanisms of action that are both local and general, several non-exclusive ones have been postulated: passive transport to the circumventricular zone, union to the vascular endothelium and subsequent release by other agents (prostaglandins, nitric oxide) inside the brain, active transport across the blood brain barrier and peripheral activation of nerve endings where release has occurred (Watkins al, 1995
IL-1β and TNFα are present from the beginning in the sequence of activities that seek the release and use of glucose for tissue repair or elevation of body temperature, inducing the production of a second wave of cytokines, IL -1, IL-6, IL-8 and Macrophage Chemotactic Protein, derivatives of arachidonic acid or eicosanoids, platelet activating factor (PAF), free radical release and nitric oxide (NO) production, also anti-inflammatory cytokines (IL-4 and IL-10) and the release of other inflammatory mediators (Nonaka, 2001) such as bradykinins, histamine ... IL-1 and IL-6 act on the HPA axis (Chrousos, 1995) increasing ACTH and cortisol secretion. The regulatory-suppressive function of the immune response will then depend on the balance between the synthesis of different cytokines with different actions. If the inflammation is prolonged, other systems will be activated: the Endocrine, the Noradrenergic, the Serotonergic and the Dopaminergic (Kronfol & Remick, 2000).

Inflammatory stress is immunomodulator, in this sense the existence of a possible pattern of inhibition of cellular immune response (Th1) has been hypothesized while increasing humoral immunity (Th2) or vice versa (Singh et al, 1999; Agarwal & Marshall, 1998). Th1 produce (IFN-γ, TNF-β) macrophage activators, in contrast Th2 produce IL-4, IL-5, IL-10, and IL-13 activators of antibody response, other models could also exist . However, the results observed in clinical processes such as systemic Lupus erythomatous (Chang et al, 2002) or in prostate cancer (Filella et al, 2000) have been described as ambiguous. We accumulate data that suggest that proinflammatory cytokines are capable of: activating both the HPA Axis and the Locus Coeruleus - Norepinephrine system of the SAM Axis. Stimulate plasma glucocorticoid concentrations, altering the activity of hypothalamic noradrenergic neurons, reducing norepinephrine in the spleen. Glucocorticoids in turn inhibit the secretion of IL-2, IFNγ and IL-12 while increasing the secretion of IL-4 and IL-10. The chronic or intermittent inflammation that is generated by the presence of an infectious focus can thus be associated with stress, being able to initiate the cascade of biochemical processes that make it formally indistinguishable from the psychobiological process itself.

 

4. Depression

 

Depression is a syndrome or mood disorder characterized by the criterial presence of a set of symptoms: sadness, anhedonia, asthenia or lassitude, decreased attention and concentration, loss of self-confidence, pessimism, ideation of death or suicide, insomnia, anorexia? In the classic model that emerged in the 1960s, the Serotonin system and the Noradrenergic System were basically involved in the development of the syndrome (Ressler & Nemeroff, 2000; Mongeau et al, 1997; Nemeroff. 2002). However, in recent years various biochemical processes capable of generating changes in mood have been studied in depth. Among them we can highlight inflammation, ischemia, necrosis, apoptosis ... Of all of them it is probably the most studied inflammation and in which we have more data that suggest the relationship between the course of depression and that of inflammation (Licinio & Wong, 1999)
The theoretical bridge to relate inflammation and depression, as well as stress (both psychological and physical), is made up of cytokines (Connor & Leonard, 1998 and more specifically by interleukins, especially proinflammatory ones. Proinflammatory interleukins interact with Endocrine, Noradrenergic, Serotonergic and Dopaminergic Systems (Kronfol & Remick, 2000) In the most current two-way models, it is considered that both stress and depression and inflammation are capable of activating and modifying the cytokine balance and vice versa. As an example, an increase in pro-inflammatory interleukins (IL-1, IL-6, TNFα) regardless of their origin can be related to increases in norepinephrine, serotonin, dopamine, cortisol, corticotropin CRH releasing hormone, and ACTH corticotropin, together with a decrease in Gonadotropin GnRH Liberating Hormone and Natural Killer activity cells (Kronfol & Remick, 2000).

The strongest evidence of the role of cytokines in depression comes from the clinical observation of animals (Felger et al, 2007) and patients treated with interferons (Asnis & La Garza, 2005). Thus the administration of interferon-α (Gleason & Yates, 1999) (in Hepatitis C or Melanoma), of interferon-β (in Multiple Sclerosis), interferon-γ (Kaposi's Sarcoma or in Chronic Granulomatous Disease) or of interleukin -2 (in Metastatic Cancer), are associated with affective and behavioral changes that include the development of depressive episodes. Other evidence that suggests the role of the immune system in the development and consolidation of depression includes observations that depressed patients show: high levels of IL-6 (Chrousos, 1995; Maes et al, 1993); high levels of acute phase reactants and activation markers of immune cells, as well as impaired immune function (Maes et al, 1993). Cytokines appear to exert a depressive effect, directly through activation of corticotropin-releasing hormone, or indirectly causing resistance to glucorticoid receptors, which causes hyperactivity of the hypothalamic-pituitary-adrenal axis, due to inhibition of the normal feedback mechanism. . Intracranial administration of proinflammatory cytokines causes the same disease effects as their systemic administration. Therefore, proinflammatory cytokines have two places where they can exert their distinct action, in the same place of inflammation and in the CNS.
Stress, whether physical or psychological, plays an important role in triggering and evolving depressive disorders. In addition, depression has shown the existence of a biochemical profile at the endocrine and immunological level similar to that observed in stress. Glucocorticoids (Burke et al, 2005) are among the main mediators of the immunosuppressive effects generated by stressors. Among the effects described in humans we find lymphocytopenia (for example after widowing), monocytopenia, and neutropenia. Also glucocorticoids seem to be involved in reducing the production of certain cytokines (IL-1, IL-2, IL-6, IL-8, TNF) or in the increments of others such as IgA, IgE, IgG or IgM . In addition, glucocorticoids also exert their action in the brain by crossing the blood brain barrier. In this sense, mineralcorticoid receptors have been found among other locations in the pyramidal and granular neurons of the hippocampus, the olfactory nucleus, the amygdala, the striatum and the septum. Glucocorticoid receptors are present in a high proportion in the hippocampus and in the hypothalamus, we also find them in the frontal, parietal and entorhinal cortex among others. Consequently glucocorticoids can modulate various processes in the central nervous system.

In recent years, the dopaminergic system is acquiring a specific weight (Dunlop & Nemeroff, 2007) in the pathophysiology of depression. The excitatory function of Dopamine in the neurons of the Paraventricular Nucleus, where the activation of the D1 and D2 dopaminergic receptors stimulates the HPA axis and promotes corticosterone secretion, establishing a positive feedback system. And also the relationships that are being found between neurons with D2 receptors and PAR-4 proteins (Gurumurthy et al, 2005; Park et al, 2005; Mattson & Gleichmann, 2005)
« Last Edit: December 09, 2019, 12:58:15 PM by Eliasjoelrivera »

nanna1

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Re: POIS cure: theory & supplement stack
« Reply #505 on: January 15, 2020, 01:07:24 AM »
Hi All,
  It was brought to my attention that I included citrulline malate in the POIS Cascade stack. It was only supposed to be listed in the Betaherpesvirinae stack. This was a mistake on my part. Citrulline (or arginine) should only be taken with an arginase inhibitor (see post). I apologize for this mistake.
-------------------------------

On a different topic: There has been a recent POIS paper which is relevant to the stacks (and model) discussed in this thread. In the paper, the researcher tested several treatments:
  1. anti-histamines (centirizine and diphenhydramine)
  2. alpha-blockers (terazosin and alfuzosin)

Anti-histamines were not effective:
"The patient was initially started on a trial of cetirizine, and instructed to orgasm weekly. After 4 weeks, the patient reported a significant improvement in abdominal cramping and reduction of diarrhea to once per week, but experienced no change in the remainder of his symptoms. Diphenhydramine had no effect on his symptoms..."
-Postorgasmic illness syndrome: potential new treatment options for a rare disorder (2019)

Alpha-blockers were effective:
"At this time, we suspected his symptoms could be in part secondary to an increased autonomic response, and he was started on a trial of terazosin, followed by several months of alfuzosin. He reported significant improvement of all symptoms on both alpha-blockers. Following ejaculation, bowel movements normalized within two days, with no cramping and only one loose stool. He denied needing prolonged sleep and reported elimination of muscle soreness. His eye dryness and redness improved significantly..."
-Postorgasmic illness syndrome: potential new treatment options for a rare disorder (2019)

  These alpha-blockers (terazosin and alfuzosin) inhibit the alpha1-adrenergic receptor (a receptor for epinephrine and norepinephrine). The alpha-blocker treatment appears to be at least as effective as the COX-inhibitor treatment in Ashby and Goldmeier (2010). In this case study, these results seem to confirm that epinephrine and norepinephrine are the chemical triggers for Post Orgasmic Illness Syndrome.

« Last Edit: September 25, 2020, 09:44:18 AM by nanna1 »
POIS clusters: 1,3,4,5,7
POIS criteria: 1,2,3,4,5
2 stacks that give me complete relief of POIS symptoms are listed here: POIS cure: theory & supplement stack
Find medical test: https://www.findlabtest.com/

Nas

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Re: POIS cure: theory & supplement stack
« Reply #506 on: January 15, 2020, 02:30:14 AM »
Nanna, I tried terazosin an hour before ejaculation and it did cause a refractory ejaculation however it was POIS as usual. Does it mention regular use? Alpha blockers are also terrible with their side effects as one time I nearly fainted on one of them.

hapl

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Re: POIS cure: theory & supplement stack
« Reply #507 on: January 16, 2020, 11:00:45 AM »
Are there natural compounds that would have similar effects to the alpha blockers?

nanna1

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Re: POIS cure: theory & supplement stack
« Reply #508 on: January 21, 2020, 06:24:21 PM »
Nanna, I tried terazosin an hour before ejaculation and it did cause a refractory  however it was POIS as usual. Does it mention regular use? Alpha blockers are also terrible with their side effects as one time I nearly fainted on one of them.
  It might be beneficial to check the pharmacokinetics for terazosin. That drug takes several days before the full therapeutic effect is reached. In the paper, they did not time the dose, so you should assume it was taken daily/regularly. They also mentioned that there were side-effects (i.e. dizziness) that made the POIS patient have to stop treatment. The key finding from the paper is that they verified that the alpha1-adrenergic receptor can trigger POIS. The trigger is not the same thing as the cause for the disease. It just means that the cascade of symptoms in POIS do not occur until there is a rise in adrenaline and noradrenaline (epinephrine and norepinephrine) levels. This is the same receptor that is responsible for ejaculation contractions. But these alpha-blockers do not seem to be safe treatment options for POIS.

Are there natural compounds that would have similar effects to the alpha blockers?
Hi hapl,
  Adenylyl cyclase inhibitors might have a similar effect by inhibiting some adrenergic stimulation. But the model in the original post shows ways of hacking the adrenergic receptors.
« Last Edit: January 22, 2020, 10:19:36 PM by nanna1 »
POIS clusters: 1,3,4,5,7
POIS criteria: 1,2,3,4,5
2 stacks that give me complete relief of POIS symptoms are listed here: POIS cure: theory & supplement stack
Find medical test: https://www.findlabtest.com/

kingfisher

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Re: POIS cure: theory & supplement stack
« Reply #509 on: February 02, 2020, 09:21:28 AM »
Nanna1, thanks a lot for your research. I could not read the Cornell study fully as I did not have access. However, it seems to be a report on a single POIS patient, not a statistical study with multiple participants.

A few folks in this forum have tried alpha blockers before - Flomax(tamsulosin), Silidosin etc. but these don't seem to have worked for POIS. Maybe I did not take these drugs right from a dosage or timing standpoint. What was the dosage and timing mentioned in the study?

I personally tried 0.4 mg of tamsulosin every day for many months.  I also tried alfuzosin 10 mg for a few weeks but gave it up as I could not tolerate the side effects.
« Last Edit: February 02, 2020, 12:42:06 PM by kingfisher »

Spartak

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Re: POIS cure: theory & supplement stack
« Reply #510 on: February 07, 2020, 02:30:43 AM »
My unsupported theory is that in my case the worst part of the POIS is somehow dopamine related.
I do not experience these physical symptoms like some other members do, or I do not notice these symptoms, everything in my case is mainly psychological and cognitive.  I did have in the past some complications due some supplements, which caused me some physical symptoms, like from Magnesium or Zinc which caused me burning sensations inside which leaded to uncontrolled mini Os, but these are not my usual symptoms.

Sure I get headaches, low energy, weakness and so.. but I feel like, if I could only boost dopamine I would feel more satisfied and would not lose that feel of reward after doing things, which would I think make my POIS very tolerable. Could be wrong though.

Too bad in my country DRI supplements are really hard to find, I spoke with a doctor and so far seems only some for "nicotine addiction" dopamine inhibitors are available, I might give a try if doctor decide it is worth of trying.
But it is still in all in the air.
« Last Edit: February 07, 2020, 05:00:34 PM by Spartak »
no sugar diet helps me a tiny bit, also makes my mind much calmer in general. Sugar is definitely something my body does not handle well. Also I noticed that other inflammations like a hangover are better since I quit sugar. I avoid sweet fruits as well.

drop247

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Re: POIS cure: theory & supplement stack
« Reply #511 on: February 09, 2020, 07:01:46 AM »
these results seem to confirm that epinephrine and norepinephrine are the chemical triggers for Post Orgasmic Illness Syndrome.

I concur that epinephrine and norepinephrine seem to be tied to POIS. I realize I can get POIS symptoms without orgasm in periods of acute stress. I also realize I have a major problem dealing with stress and anxiety. I'm starting a course of Alfuzosin prescribed by my doctor. I don't believe it is the solution for me but it will be an interesting test. I also have some urinary symptoms it may help like having to urinate often and leakage after I go.

yesyesyes

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Re: POIS cure: theory & supplement stack
« Reply #512 on: February 16, 2020, 03:47:41 PM »
For me personally an enzyme, called Phosphodiesterase 4 (PDE4) might be to blame for POIS symptoms as an OTC pill that's a PDE4 inhibitor (against spasms) makes me feel less moody/weird after sex. Maybe people with POIS have a defect in some or more of the PDE4 enzymes?

Just putting this out there as it could help others, too. :) It took me like 19 years to find this little and inexpensive pill that works on my POIS symptoms. I've tried all ADs, herbs, niacin, NSAIDs, you name it out there to no help.

dizzy

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Re: POIS cure: theory & supplement stack
« Reply #513 on: February 16, 2020, 06:19:29 PM »
an OTC pill that's a PDE4 inhibitor (against spasms) makes me feel less moody/weird after sex

Interesting. What is the active compound name, and what dose do you use?
Male, INTJ. POIS symptoms: red eyes, ear-pain, anxiety, speech problems, pale/ugly skin, stiff neck, double chin, tinnitus, light sensitivity. POIS even after stimulation without O.

yesyesyes

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Re: POIS cure: theory & supplement stack
« Reply #514 on: February 16, 2020, 06:30:24 PM »
The compound is called Drotaverine.
I discuss more of my story and that drug here: https://poiscenter.com/forums/index.php?topic=3220.0

nanna1

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Re: POIS cure: theory & supplement stack
« Reply #515 on: February 17, 2020, 07:16:30 PM »
Hi yesyesyes,

I'm excited that you found something that works for you! Keep sharing your good news. Caffeine and caffeine metabolites (xanthine, paraxanthine, pentoxifylline, theobromine, and theophylline) are used in medical literature to produce pharmaceutical grade phosphodiesterase 4 (PDE4) inhibition.
caffeine phosphodiesterase inhibitor

It is well know that PDE4 inhibitors like caffeine help stimulate an increase in beta-endorphin release.
Caffeine stimulates beta-endorphin release in blood but not in cerebrospinal fluid (1982)
One case study hypothesized that POIS is related to a dysfunction in the mu-opioid receptor and beta-endorphin signaling.
Basically, I think that the POIS hypothesis in the following paper is correct but incomplete:
"Postorgasmic Illness Syndrome (POIS) in a Chinese Man: No Proof for IgE‐Mediated Allergy to Semen" (Jia Yin, et al, 2015)

  In that Jia Yin et. al. paper, they focus mostly on showing that IgE allergy is not involved in the POIS of one patient. However, towards the end of the paper, they suggest that POIS could be caused by low beta-endorphin signaling (low endorphins or low mu-opioid receptors).
But caffeine (and its xanthine metabolites) are non-selective phosphodiesterase inhibitors meaning that it inhibits PDE1, PDE3, PDE4 and PDE5. So it has multiple benefits for the immune system, it is all-natural and has a proven safety record (especially when taken with taurine or theanine, but not coffee). The timing and dosing information for caffeine can be found in either of these three post (Post1, Post2, Post3).

It may be helpful to look at other ways to increase beta-endorphin levels naturally (laughing, meditaion, social activity with the opposite sex, etc...).
« Last Edit: February 17, 2020, 09:12:09 PM by nanna1 »
POIS clusters: 1,3,4,5,7
POIS criteria: 1,2,3,4,5
2 stacks that give me complete relief of POIS symptoms are listed here: POIS cure: theory & supplement stack
Find medical test: https://www.findlabtest.com/

drop247

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Re: POIS cure: theory & supplement stack
« Reply #516 on: February 17, 2020, 07:38:06 PM »
I'm starting a course of Alfuzosin prescribed by my doctor.

Just an update on this. I took Alfuzosin for 4 days and had the side effects that are common, dizziness upon standing and fatigue. I didn't even try having an O since I thought 4 days wasn't long enough to give it a real trial. I may try again when I have an extended holiday and won't mind the side effects.

yesyesyes

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Re: POIS cure: theory & supplement stack
« Reply #517 on: February 18, 2020, 06:05:21 AM »
nanna1, hi. :)
Unfortunately I'm caffeine intolerant - it makes me jittery and makes my bp too high. Even green tea does. I also have a light connective tissue disorder (often goes with MCAS). Anyone else?

Muon

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Re: POIS cure: theory & supplement stack
« Reply #518 on: February 18, 2020, 11:17:03 AM »
PGE2 is a mast cell mediator, see table 3: Mast Cell Biology at Molecular Level: a Comprehensive Review

nanna1

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Re: POIS cure: theory & supplement stack
« Reply #519 on: February 20, 2020, 11:05:01 PM »
  I understand that some have had bad experiences with caffeine overdosing. In many cases, a bad experience is enough to avoid future experiences. I understand that reasoning. Please listen to your body!

  But for those who are experimenting with phosphodiesterase inhibitors, caffeine has the best safety reputation and is the most effective phosphodiesterase (PDE) inhibitor available. Caffeine is also broad spectrum, meaning it inhibits multiple PDEs (PDE1, PDE3, PDE4, PDE5). It has low financial cost, high bioavailability and is readily available from healthy food sources.

  I personally would not consume caffeinated beverages (or any drug based PDE inhibitor) on a regular basis. They are more effective at boosting endorphin levels and blocking arginase when taken as part of a complete pre-pack stack and or taken with food.

  Caffeine jitters come from glutamate/dopamine imbalance. When glutamate is high and dopamine is low, too much caffeine will cause muscle shakes. The best solution is to consume caffeinated beverages with or after a meal. Food will slow the absorption and provide more dopamine production to prevent jitters. Another solution is to consume theanine and alpha-GPC with the caffeine. This has a general affect of lowering glutamate and increasing the release of dopamine.

  All PDE inhibitors (including PDE4 inhibitors) change blood pressure and heart-rate at their effective dose. If you have chronic blood pressure issues, please check with your physician to see if you are healthy enough to take these drugs.

  Other ways of naturally boosting endorphins includes social interaction, laughing, meditation, etc...
« Last Edit: February 20, 2020, 11:25:24 PM by nanna1 »
POIS clusters: 1,3,4,5,7
POIS criteria: 1,2,3,4,5
2 stacks that give me complete relief of POIS symptoms are listed here: POIS cure: theory & supplement stack
Find medical test: https://www.findlabtest.com/