Author Topic: Muon's Case  (Read 169886 times)


Muon

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Re: Muon's Case
« Reply #221 on: April 14, 2022, 06:01:45 PM »
I did experience these, they seem to come from the middle of my head. A couple of sequential clicks with short pauzes inbetween them (Induced by orgasm/ejaculation).
 
Case report; click sound from head if translation is correct: https://revistasacademicas.cl/Upload/ArticulosPdf/schu_20210819142132_baa6f065-d151-4644-8c52-af22c8ce431e.pdf

Muon

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Re: Muon's Case
« Reply #222 on: April 14, 2022, 07:20:38 PM »
Something is going on near the brainstem (pons/medulla?)
The nucleus of the Cranial nerve VII (bell's palsy) is located at the lower part of the pons. https://en.wikipedia.org/wiki/Facial_motor_nucleus
https://en.wikipedia.org/wiki/Vasomotor_center

IronFeather

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Re: Muon's Case
« Reply #223 on: April 19, 2022, 11:28:05 AM »
I can't remember now if I asked you this question before, but do you experience a sort of vibration when you tense a muscle? For example, if you extend your arm in front of you, palm down, and press your fingers against your palm, do your fingers and wrist vibrate, as in, being unable to keep a steady contraction? The same thing that usually happens to anyone after absolute exertion to the limit, but all the time and with just light/moderate contraction of the muscles? And if so, did this symptom appear at the same time than your exercise intolerance?
26-year-old Spanish woman with POIS symptoms for the last 13 years.
Suffering from exercise intolerance since April 2020.
My case thread, with medical tests results.

Muon

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Re: Muon's Case
« Reply #224 on: April 23, 2022, 08:33:13 AM »
I can't remember now if I asked you this question before, but do you experience a sort of vibration when you tense a muscle? For example, if you extend your arm in front of you, palm down, and press your fingers against your palm, do your fingers and wrist vibrate, as in, being unable to keep a steady contraction? The same thing that usually happens to anyone after absolute exertion to the limit, but all the time and with just light/moderate contraction of the muscles? And if so, did this symptom appear at the same time than your exercise intolerance?

No but the body in general isn't able to maintain or adjust tension optimally. The Bridge exercise is one of the worst, unable to keep steady contraction properly, takes a huge toll on my body afterwards. Even sitting in a chair gives me problems; lack of support to muscles (get impression that it originates from brain) in lower back leading to stress in centre of head which leads to stiffening of muscles elsewhere especially in the back. I get the impression that the centre of my head isn't able to deliver proper supply to the rest of the body. Exercising during altered tension (?) or inflammatory states (?) leads to trembling afterwards. Going over exertion limit leads to trembling and weakness. I get the impression that exerting any force puts a strain on my brain. It started with chronic general fatigue followed by some kind of "injury" on the inside of my leg/groin area which left me unable to play soccer (i wonder if that is tension/FM related as well). Sexual triggers make everything worse. At one point I was also doing weight lifting exercises 3 times a week aside from playing soccer, I wonder if that led me into a downward spiral.

Btw when my brother left psychiatric hospital (including complete isolation) my mom asked him what he felt during his stay. He told her that his brain felt drained.
« Last Edit: April 23, 2022, 08:48:18 AM by Muon »

Muon

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Re: Muon's Case
« Reply #225 on: April 23, 2022, 08:45:46 AM »
Interleukin-8 produced by T cells is under the control of dopamine signaling (IL-8 chronically elevated in me and brother).
 
"Human PBMC react to exposure to Candida albicans Ag through Th1/17 responses. Therefore, IL-8 production might be high under such conditions".

"Neutrophilic inflammation in chronic inflammatory diseases, such as asthma, rheumatoid arthritis, ulcerative colitis and multiple sclerosis, might be suppressed by dopamine D2-like receptor agonists"


Btw when my brother left psychiatric hospital (including complete isolation) my mom asked him what he felt during his stay. He told her that his brain felt drained.

First article talks about D2 receptor. D2 can be involved in psychosis (related to quote).

Premature ejaculation:
Stimulation of dopamine autoreceptors elicits "premature ejaculation" in rats

The Role of D2-Autoreceptors in Regulating Dopamine Neuron Activity and Transmission

"Autoreceptors on dopamine neurons are comprised of the D2-subtype of dopamine receptors."

=============================================================
==============================================================

If premature ejaculation is triggered by stimulation of D2 autoreceptors, does dopamine peaks too much or is there a high expression of D2 present on dopamine neurons. Are dopamine levels low and could this upregulate D2? What about the rate of transmission? What about D2 expression on immune cells?
« Last Edit: April 23, 2022, 10:06:13 AM by Muon »

Muon

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Re: Muon's Case
« Reply #226 on: May 04, 2022, 09:20:27 AM »
Blood pressure measurement May 4th, 2022, 16:00h:
Sys: 86
Dia: 54
HR: 68

Exercise intolerance prevents me from raising BP by exercising sufficiently.

I get the impression that the body isn’t able to cover optimal demand of blood supply to body parts when needed.

Another Trigger based phenomena: https://en.wikipedia.org/wiki/Reflex_syncope#Pathophysiology
« Last Edit: May 04, 2022, 11:46:02 AM by Muon »

Muon

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Re: Muon's Case
« Reply #227 on: May 08, 2022, 08:12:41 PM »
A spontaneous erection of the penis when waking up gives 0 symptoms. https://en.wikipedia.org/wiki/Nocturnal_penile_tumescence

Muon

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Re: Muon's Case
« Reply #228 on: May 12, 2022, 12:28:31 PM »

Muon

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Re: Muon's Case
« Reply #229 on: May 17, 2022, 08:46:56 AM »
Applying cold to groin area after O helps local soreness.

Edit: There seems to be different kinds of fatigue (maybe they are the same but they feel different), at least one from which I assume is accumulation of body tissue inflammation (seems to be proportional in intensity to body inflammation dynamics). The other one, I get the impression, is deep focal fatigue (peak behavior with relative high intensity) stemming from middle of the head. The latter can be partially countered by deep sleep/nap (resting doesn't work). Prior to desens the 2nd one often peaked during the tipping point from full POIS mode to recovery mode, day ~ 4-5.
« Last Edit: May 17, 2022, 10:11:12 AM by Muon »

Muon

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Re: Muon's Case
« Reply #230 on: June 07, 2022, 10:28:14 AM »
I can tolerate 1 mg nicotine gum. 2 mg chewing gum is too much, it heats up my body, I begin to sweat and get nauseous. My brain feels different on the stuff, slightly sedative. Awful stuff when >1mg.

Muon

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Re: Muon's Case
« Reply #231 on: June 08, 2022, 01:46:32 PM »
Abrupt emotion:
Had to break up a fight between two strangers on the street. Could feel my brain and legs were weak as in rubber. Pressure on lower part spine.

Surprised about something: pressure in middle part brain gone but altered sensation in right half of face. Waterbed effect.

Jumped by loud noise, made feel good.

Very angry made me feel good as well.

Bad posture with poor lower back support: stiff groin area, penis becomes sensitive. Friction on penis edge leads to weak rubbery legs: i trigger something in lowest part of spine.
« Last Edit: June 08, 2022, 01:52:36 PM by Muon »

Muon

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Re: Muon's Case
« Reply #232 on: June 10, 2022, 07:12:42 PM »
Yea this could be a contender for explaining a set of my symptoms: https://www.reddit.com/r/POIS/comments/v9hxa4/finally_diagnosed_with_something_concrete/
https://en.wikipedia.org/wiki/Myofascial_pain_syndrome

Asymmetric Chronic local tension problems, hardening muscles, weakness in those parts, poor posture making it worse. Can lead to breathing problems and more inflammation. I think it's connective tissue.

Progecitor

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Re: Muon's Case
« Reply #233 on: June 13, 2022, 07:53:50 AM »
Interleukin-8 produced by T cells is under the control of dopamine signaling (IL-8 chronically elevated in me and brother).
 
"Human PBMC react to exposure to Candida albicans Ag through Th1/17 responses. Therefore, IL-8 production might be high under such conditions".

"Neutrophilic inflammation in chronic inflammatory diseases, such as asthma, rheumatoid arthritis, ulcerative colitis and multiple sclerosis, might be suppressed by dopamine D2-like receptor agonists"


Have you never thought about trying to specifically suppress IL-8? This may not solve the underlying issue, however it may ameliorate the cytokine cascade and inflammation regardless of the cause. As most of the following supplements work for me and other POISers, I have to believe that IL-8 is involved in more than your cases only.

Some supplements that specifically inhibit IL-8:

- EGCG and caffeic acid
https://sci-hub.se/https://www.ingentaconnect.com/content/ben/cmc/2011/00000018/00000031/art00009
- EPA and DHA
https://www.sciencedirect.com/science/article/pii/S2352289520300126
- Saffron:
https://sci-hub.se/https://www.sciencedirect.com/science/article/pii/S0753332218335753
- L-theanine:
https://link.springer.com/article/10.1007/s00726-011-0847-9
- Curcumin:
https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.10812
- Imatinib:
https://onlinelibrary.wiley.com/doi/abs/10.1002/jcp.23029
- Astaxanthin
https://hrjournal.net/article/view/3990
- Resveratrol
https://sci-hub.se/https://www.tandfonline.com/doi/abs/10.1517/13543776.2013.834888
- Honokiol
https://sci-hub.se/https://www.sciencedirect.com/science/article/abs/pii/S0006295205005344

- PDE4 inhibitors
In vitro studies show that PDE4 inhibitors inhibit the release of cytokines such as tumor necrosis factor-a (TNF-a) and interleukin-8 (IL-8). The p38 MAP kinase pathway is activated by cellular stress and regulates the expression of inflammatory cytokines, including IL-8, TNF-a, and MMPs. p38 MAP kinase inhibitors have several effects relevant to asthma and COPD. They appear to have a preferential inhibitory effect on synthesis of Th2 compared with Th1 cytokines, indicating their potential application in the treatment of atopic diseases. c-Jun-NH2-terminal kinase phosphorylates Jun, a component of the transcription factor AP-1 that regulates many inflammatory genes and is therefore a target for inhibition in inflammatory diseases.
https://sci-hub.se/https://www.sciencedirect.com/science/article/abs/pii/S0163725805001737

- protein tyrosine kinase (PTK) inhibitors and protein kinase C (PKC) inhibitors
Production of interleukin-8 (IL-8) by gastric epithelial cells may play an important role in H. pylori-induced mucosal injury. The aim of this study was to evaluate physico-chemical factors and signal pathway regulating H. pylori-induced IL-8 production. The IL-8 production induced by TNF and H. pylori was also inhibited by protein tyrosine kinase (PTK) inhibitors and protein kinase C (PKC) inhibitors.
https://www.koreamed.org/SearchBasic.php?RID=2240437

- PPAR agonists (not specified)
PPAR agonists were reported to decrease local production of IL-6 in the intestine as well as IL-8 production. IL-8 is a key chemokine for neutrophil trafficking and broadly expressed by a multitude of cell types, including macrophages, and induced by a variety of inflammatory stimuli.
https://sci-hub.se/https://onlinelibrary.wiley.com/doi/10.1002/ptr.6625

Factors that may increase IL-8 release:

The p38/MAPK pathway has been found to control SASP secretion, which can be activated by phosphorylation in a few minutes after a stimulus. This pathway can also upregulate multiple cytokines, for instance, TNF-a, IL-6, and IL-8.
https://www.sciencedirect.com/science/article/pii/S0753332221001128

When deregulated, either by overexpression or downregulation, AP-1 factors promote tumourigenesis depending on the cellular context. Furthermore, elevated levels of pro-inflammatory cytokines and chemokines, such as IL-6, a pro-inflammatory cytokine involved in haematopoiesis, and CXCL8, a chemokine responsible for the recruitment and activation of immune cells, maintain malignant proliferation. Additionally, continuous production of IL-6 and CXCL8 results in the enhanced survival of lymphocytes, which further increases serum cytokine/chemokine levels. Finally, the identification of both AP-1 and NF-kB binding sites in the promoter region of IL-6 and CXCL8 cemented the NF-kB/AP-1/IL-6/CXCL8 axis. In addition, NF-kB and AP-1 TFs share common mechanisms of activation as they appear to be simultaneously activated by the same stimuli. For example, JNK activation via inflammatory or stress-related cytokines results in the phosphorylation of JUN and the nuclear translocation of NF-kB.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5923348/

Another study further suggested that oxidative stress and inflammation are interrelated as oxidative stress resulting from high ROS can precipitate the formation of inflammation by increasing the gene expression coding for inflammatory proteins, including NF-kB, peroxisome proliferator activator receptor gamma (PPARG), and activator protein 1 (AP-1). Consequently, inflammatory chemokines and cytokines are produced to induce inflammation.
https://www.mdpi.com/2079-7737/10/4/287/htm

Shortly after the discovery that cytokines like IL-1 and TNF-a could induce IL-8/CXCL8 in monocytes, laboratories, including the laboratory of coauthor Dr. Steven L. Kunkel, began to realize that structural cells, such as fibroblasts, endothelial cells, and hepatocytes, could release IL-8/CXCL8. It was quickly shown that IL-8/CXCL8 could contribute to host defense but also to inflammatory diseases and neutrophil-mediated tissue damage. Indeed, IL-8/CXCL8 had angiogenic activity on endothelial cells as well; the angiogenic activity was mediated by the amino acid motif of glutamic acid, leucine, and arginine (ELR) within the N terminus of the CXC family of chemokines, whereas ELR-negative CXC chemokines were actually angiostatic. Development of Abs against IL-8/CXCL8 allowed for studies using human disease samples, and it became clear that this chemokine was overexpressed in multiple forms of cancer, respiratory diseases, and tissue fibrosis.
https://www.jimmunol.org/content/202/1/3

Both LPO and ROS induced cytokine (TGF-B, TNF-a, IL-8) release may contribute to the development of nonalchohlic steatohepatitis.
https://www.researchgate.net/profile/Ankit-Gupta-23/publication/276293748_Hepatoprotective_Activities_of_Triphala_and_Its_Constituents/links/5556442908ae6943a8733a18/Hepatoprotective-Activities-of-Triphala-and-Its-Constituents.pdf

MERS-CoV induces higher expression of IL-12, IFNg, interferon gamma-induced protein 10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1 alpha (MIP-1a), and IL-8 than SARS-CoV.
https://onlinelibrary.wiley.com/doi/full/10.1002/rmv.2290

Multiple studies shown that pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-a), IL17, IL-1B, IL-6 and IL-8 are upregulated in IBS patients, while the concentration of anti-inflammatory cytokines like IL-10 decreases. It has also been reported that IL-17 is a crucial factor in IBS pathogenesis through activation of NF-kB, mitogen-activated protein kinase MAP kinase (MAPK), and TLRs pathway. IL-17 modulates inflammatory process and increases the pro-inflammatory cytokines production. Activated TLR4 enhances the production of pro-inflammatory cytokines such as IL-1B, IL-6, IL-8 and TNF-a in IBS patients.
https://sci-hub.se/https://www.sciencedirect.com/science/article/abs/pii/S0024320520308547
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.

Muon

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Re: Muon's Case
« Reply #234 on: June 13, 2022, 07:50:05 PM »
Yes I had a list with these things but I lost it. Doctor's don't cooperate with IL-8 suppression. I'm aware of ~75% what you have written. I would measure that cytokine in seminal plasma for other POISers. MMP is also on my mind for connective tissue damage and decreased vascular integrity. Nanna suspects I might have an additional increase in GM-CSF. That combination (IL-8+GM-CSF) is being expressed by a type IVd hypersensitivity, T-cell mediated neutrophil inflammation. I get the impression that low grade mucosal inflammation is present, IL-8 might be involved.

Coffee seems to give very minor relieve.
Curcumin+piperine gives more relieve but still minor.
Resveratrol: no effect. Haven't tried high dose.
EPA/DHA: can't say these fishoil capsules do anything. Bottled fishoil however doesn't give me any negative reaction and It's perhaps the best thing that my body is able to digest. It might suppress local stomach inflammation who knows. 
« Last Edit: June 13, 2022, 07:54:44 PM by Muon »

Muon

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Re: Muon's Case
« Reply #235 on: June 20, 2022, 06:48:20 AM »
My unpleaseant body odour, dating from my teen years but particularly strong after sexual arousal
Same here

Progecitor

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Re: Muon's Case
« Reply #236 on: July 24, 2022, 10:17:06 AM »
Yes I had a list with these things but I lost it. Doctor's don't cooperate with IL-8 suppression. I'm aware of ~75% what you have written. I would measure that cytokine in seminal plasma for other POISers. MMP is also on my mind for connective tissue damage and decreased vascular integrity. Nanna suspects I might have an additional increase in GM-CSF. That combination (IL-8+GM-CSF) is being expressed by a type IVd hypersensitivity, T-cell mediated neutrophil inflammation. I get the impression that low grade mucosal inflammation is present, IL-8 might be involved.

Coffee seems to give very minor relieve.
Curcumin+piperine gives more relieve but still minor.
Resveratrol: no effect. Haven't tried high dose.
EPA/DHA: can't say these fishoil capsules do anything. Bottled fishoil however doesn't give me any negative reaction and It's perhaps the best thing that my body is able to digest. It might suppress local stomach inflammation who knows.

I am sorry to hear that resveratrol was of no use to you. Although I also tested some resveratrol supplements that were not particularly effective and only the one made from Polygonum cuspidatum was really effective presumably by the synergistic activity of resveratrol and emodin.
Well we may just not fall in the same POIS type category, though I found some research data that may suggest otherwise.

For one you may be interested to know that the same factors mentioned in your post are also involved in cellular senescence that I believe to be the primary cause of POIS.

SASP in irradiated BPH-1 cells was associated with activation of STAT5, AKT, and the ERK1/2 Map kinase, and induction of mRNAs for pro-inflammatory cytokines (IL-1alpha, IL-1beta, IL-6, IL-8; TNF-alpha) and other known SASP components such as the chemokines CXCL12, GM-CSF; the IGF-binding protein IGFBP3; and metalloproteases (MMP1, MMP3, MMP10). Abundant p16 expression in the epithelium and stroma of clinical BPH indicated the presence of senescent cells in BPH tissue.
The prevailing view on BPH pathogenesis is that the cumulative effects of low-level chronic stimulation of prostate cells by inflammatory secretions from the reactive stroma and infiltrated inflammatory cells promote excessive cell proliferation in aging prostate.

https://faseb.onlinelibrary.wiley.com/doi/full/10.1096/fba.2018-00084

Another study of considerable interest states that an excess of estrogen at pre-puberty may underlie chronic inflammation later in life and mast cells are highly involved in this process.

As estrogens cause prostatic inflammation, here we characterize the murine prostatic phenotype induced by elevated endogenous estrogens due to aromatase overexpression (AROM+). Early-life development of the AROM+ prostate was normal; however, progressive changes culminated in chronic inflammation and pre-malignancy.
Additional data obtained from further rodent studies show that the prostate gland is particularly sensitive to estrogenic exposure during development in fetal and neonatal life; transient estrogen exposure before puberty results in inflammation later in life, well after the exposure has occurred. Several decades of research from various laboratories, including our own, has demonstrated that this action is mediated by the estrogen receptor (ER) alpha subtype and involves a cascade of events that permanently and irreversibly alter gene expression patterns in the gland. These data indicate that exposure to estrogen causes prostatic inflammation and directly links estrogen and prostatitis.
The elevation in mast cell numbers observed on the AROM+ mouse is a highly significant and novel finding. Mast cell numbers rise immediately following puberty and this is likely a result of the profound changes to the hormone levels that occurs at this time. Mast cells are known to express ERalpha and are estrogen responsive, therefore the increase in estrogen levels that is evident in the AROM+ mice with puberty may be responsible for the increase in mast cell numbers. This putative role for estrogens increasing mast cells numbers is also supported by other previously reported data where mast cell numbers were increased in the inflamed testis of AROM+ mice.
Of particular note is that mast cells have specifically been reported to mediate the recruitment of neutrophils and macrophages, as well as the activation of T-lymphocytes, all of which were significantly increased in the chronic inflammation observed in the AROM+ animals.
The relevance of the AROM+ mouse as a model, not just of prostatitis per se, but of chronic pelvic pain syndrome, is supported by the presence of testicular abnormalities and inflammation, as well as infravesicle obstruction and bladder dysfunction, all of which are potential symptoms that are indicative of chronic pelvic pain syndrome.

https://www.sciencedirect.com/science/article/pii/S0002944010606281

I haven't given much thought to MMPs before, however it is clear that they play a role in prostatitis.

These activities were strongly attenuated by treatment of estradiol (E2)-implanted animals with testosterone, which also reduced inflammation; but they were only weakly affected by DHT given with E2, which did not reduce inflammation.
Prominent MMP activities were detected in the lateral lobes of E2-treated rats, including both the active (55 and 81 kDa) and proenzyme (72 and 92 kDa) forms of MMP-2 and MMP-9, respectively.
Thus, elevated MMP-2, MMP-7, and MMP-9 activities in lateral lobe prostatitis correlate with leukocyte infiltration in the inflammatory response. These proteinases may help mediate the accompanying epithelial atrophy and tissue damage in this organ.

https://www.sciencedirect.com/science/article/abs/pii/S0014480004000206

In the South Korean POIS study the patient had excessive E2 and quite low testosterone levels. Furthermore the researchers found a 55 kDa protein that was in great abundance before the ILIT treatment.
https://www.sciencedirect.com/science/article/pii/S2050116118300199

Given these facts I was wondering if this 55 kDa protein could have been actually the active form of MMP-2. I ran through some earlier supplementation data and several of them which also proved beneficial for me inhibit MMP-2 and MMP-9. Of particular note may be mangosteen which not only inhibits these MMPs, but is also an aromatase inhibitor.
https://link.springer.com/article/10.1186/1741-7015-9-69

The formerly mentioned emodin also behaves similarly.
https://www.sciencedirect.com/science/article/pii/S2211802012000241

Astaxanthin is another example.
https://sci-hub.se/https://www.sciencedirect.com/science/article/abs/pii/S1043661819327367

Needless to say these proved relatively beneficial for me.
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.

Muon

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Re: Muon's Case
« Reply #237 on: July 25, 2022, 12:59:29 PM »
I was also unable to read, because reading triggerd very bad symptomes. I stoped having sex for two years, and my Pois is now so better I have only slight pain after orgasem lasting one day. But I never stoped reading, because I have to read in my job and everywhere else. So this trigger "the reading" is still very painfull and making me big truble. I can loose strenght in arms and legs if I read to much, I can get pain so strong in my groin that I can't do anything. Orgasem is not a big problem for me anymore, its reading! And I can't se the conection between semen and reading... I had checked my semen and everything is OK.

My brother drops things on the floor when he walks, carries objects and uses his brains as in thinking at the same time.

My mother has trouble doing two things at the same time. (cooking+talking)

Since my POIS induced systemic inflammation has gone down in the last years other mechanics are easier to observe. Like meals may affect breathing. Bowel movements from big meals can disregulate breathing. Prolonged low grade stress can disrupt breathing like it's uncoupling the autonomic function from the body if that makes sense. Carrying extra weight will make it harder to hold a conversation, I also may lose tension in facial muscles. Sudden diminished cardiac pumping power. Loss of strength of voice. Suboptimal digestion. General weakness.

I think all of the above is what I called a waterbed effect earlier in my thread. It's some kind of "power" distribution problem that may stem from the brain. It's shunting power away from certain functions when it's needed elsewhere. Like the total pool of "power" is sub optimal.

I've experienced all kinds of orgasms throughout the years. Even something close to anorgasmia. Stress and existing inflammation seemed to interfere with my orgasm response. When the middle of my head is activated by orgasm plus when it doesn't affect the rest of the brain that much plus low stress and low background inflammation is present, it actually is able to recover quickly and doesn't seem to cause intense systemic inflammation as opposed to when the rest of the brain is affected. The brain doesn't seem to recover to its previous state quickly in the latter scenario, it keeps hanging (or something has been released).

I'm now questioning the intensity of orgasm in my younger years, whether it has been abnormal all along. Like there is an additional excitation and/or inhibition problem in orgasmic brain response present.       

It is as if orgasm is draining the pool of power.
« Last Edit: July 30, 2022, 07:01:26 PM by Muon »

Muon

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Re: Muon's Case
« Reply #238 on: August 08, 2022, 03:47:47 PM »
My mucus production (throat, mouth) is suboptimal. I get the impression that this situation makes me more susceptible to food sensitivities.

Muon

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Re: Muon's Case
« Reply #239 on: August 09, 2022, 02:43:53 PM »
I wonder whether there is a neurovascular response involved accompanied with inflammation during sexual arousal and orgasm. I feel changes in systemic circulation, stiffness/tension, systemic inflammation, look more pale. Aside from that, I wonder if low grade stress and high ambient temperature taps into the same pathway as sexual arousal. Had some mild systemic inflammation, the feel of poorer circulation, slightly lack of oxygen upon arousal and were briefly relieved by orgasm. Increased activity of middle of head always seems to play a role.