Author Topic: Muon's Case  (Read 101724 times)


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Muon's Case
« on: October 15, 2017, 03:06:21 PM »
I will first start showing privately funded test results regarding POIS(?) and will update this post along the way. Click here for time stamps.

My data:

My brother's data (who has POIS as well):

(I did use free PDF eraser software to delete private info so there is a watermark in the upperleft corner, please respect my privacy)
The only parameters my brother has tested before and after an orgasm were IL-8 and IgE, but these show no change.

Summary of Muon's abnormal parameters (under construction)

Date of testing might be relevant, since the state of the body changes over the years and seasons (Netherlands) affect me as well. RR = Reference range. u (lower case) = micro.

11-beta-Prostaglandin F2 Alpha (24h urine)/Creatinine ratio (H, 2018) 117 ng/mmol, RR: 0 - 105
Alanine-aminotransferase (H)
Alpha-2-Globulin (L, 2008) 7.5%, RR: 7.6 - 13.4
Candida Albicans LTT (H, 2015) 1 ug/mL SI = 26.5, 0.5 ug/mL SI = 19.9, (RR: SI < antigen control SI)
Cholesterol (L, 2004) (2.6, 3.2 ) RR: ?
Cytomegalovirus IgG (H, 2015) 108 U/ml, RR: < 12.0
Cytomegalovirus LTT (Latent, 2015) SI = 7.7, RR: SI < 3
Epstein-Barr virus recombinant early antigen p138 IgG and p138 IgM (H) 1.0 COI and 1.7 COI respectively
Glucose (L, 2004) 2.8, RR: ?
Hematocrit (L, 2008) 0.41), RR: 0.42 - 0.52. (L, 2015) 38.3%, 39.5 - 50.5
Immunoglobulin G4 (H, 2015)(>144, >144) RR: 5.0 - 130 mg/dL (They don't measure higher because it's a deficiency test)
Interferon-gamma (H, 2015) See table below for context
Interleukin-2 (L, 2015) See table below for context
Interleukin-4 (L, 2015) See table below for context
Interleukin-8 (H, 2015) See table below for context
Interleukin-17 (L, 2015) See table below for context
Leukocytes (L, 2008) 4.6 Tsd./uL, RR: 4.8 - 10.8
Lymphocytes (absolute) (L, 2015) 0.98*1000/uL, RR: 1.10 - 4.50
Natural killer cells total pool (L) 113 /uL, RR: 210 - 740
Natural killer cells CD57+ subset (L) 35.0 /uL, RR: 60 - 360
Progesterone (H, 12-4-2021, fasting 12pm) 2.6 nmol/L, RR: 0.16 - 0.48
TH1/TH2 cytokine balance (H) (1, 2, 3, 4, 5)
Varicella zoster virus IgG (H) >2000 U/ml, RR: < 50
Varicella zoster virus LTT (Latent) SI = 6.3, RR: SI < 3

Muon 6-1 Medlon: A collection of tests that were done at one lab. Vitamin D3 (L), B6 (H), B9 (H), Active B12 (H), Phosphate (L), ALAT (H).

Other reports/measurements

Heart rate and blood pressure data (2013)
Body fat percentage (L) (1, 2, 3) (This is not done at a medical clinic but at a local gym)


Summary of my brother's abnormal parameters (diagnosed with POIS, under construction)

Brain-derived neurotrophic factor (L) 14.9 ng/ml RR: 18.3 - 31.4 ng/ml
Eosinophil Cationic Protein (H) 34.5 ug/l RR: < 13.3 ug/l
Glucocorticoid receptor activity (L) 1.3 RR: 1.4 - 2.4
Interleukin-8 (H) (23.7, 24.0) RR: < 15 pg/ml
Interleukin 17 (L) 43.9 pg/ml RR: 49 - 446 pg/ml
Immunoglobulin E (H) (129.0, 125.0) RR: < 87.0 kU/l
Lipoprotein-associated phospholipase A2 (Lp-PLA2) (H) 214 nmol/mi/ml RR: < 151 nmol/mi/ml
Serotonin (L) 64.2 ug/ml RR: 80 - 400 ug/ml
Tryptophan (L) 1.10 mg/dl RR: 1.21 - 2.30 mg/dl
Type IV cellular sensitivity response against Rye, hazelnut and peanut 

My brother's genetic related results:

COMT-V158M-Genotyp M/M
MAOA-Gen (30bp-VNTR) Low
BDNF Val66Met-Polymorphismus V/V
Serotonin-Transp.-Promoter PCR Genotyp K/L

Reminder: He had other genetic tests done. Platelet Serotonin in serum has been checked multiple times at other hospitals and always turned up low. Ask him about it.


Data overview Muon (Work in progress)

9th and 10th of July 2015

Muon 1-1:
TH1/TH2 Ratio: 43.5 Ref: 3.5 - 11 page1: 10:00 AM
TH1/TH2 Ratio: 39.6 Ref: 3.5 - 11 page3: 10:15 AM
TH1/TH2 Ratio: 35.3 Ref: 3.5 - 11 page4: 10:42 AM
TH1/TH2 Ratio: 42.0 Ref: 3.5 - 11 page5: 10:05 AM (24 hours later)

An ejaculation took place between the first and second measurement.
The last ejaculation before that took place at 23-06-2015.
They took blood samples while I was in the supine position.

August 13 and 14 2015 

TH1/TH2 Ratio: 28.9 Ref: 3.5 - 11 Muon 2-1: 10:15 AM
TH1/TH2 Ratio: 32.1 Ref: 3.5 - 11 Muon 2-2: Went in the blood collection room at 10:38 AM and left at 10:43 AM
TH1/TH2 Ratio: 31.5 Ref: 3.5 - 11 Muon 2-3: Went in at 11:10 AM and left at 11:16 AM
TH1/TH2 Ratio: 70.8 Ref: 3.5 - 11 Muon 3-6: 10:25 AM (next day)

An ejaculation took place between Muon 2-1 and 2-2 around 10:25 AM.
The ejaculation prior to this was 4 or 5 days back.
Blood samples were being taken in the supine position.

July 9 and 10 2015 data.

IP-10 July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IP-10~10 min pre O211< 900
IP-10~5 min post O234< 900+23
IP-10~32 min post O232< 900-2
IP-10~24 hour post O286< 900+54

TGF-beta July 9 and 10 2015

ParameterTimeValue (ng/ml)Reference (ng/ml)Delta
TGF-beta~10 min pre O53.418.3 - 63.4
TGF-beta~5 min post O62.218.3 - 63.4+8.8
TGF-beta~32 min post O54.418.3 - 63.4-7.8
TGF-beta~24 hour post O50.118.3 - 63.4-4.3

Interferon-gamma (Th1) July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IFN-g (Th1)~10 min pre O1806374-1660
IFN-g (Th1)~5 min post O1664374-1660-142
IFN-g (Th1)~32 min post O1226374-1660-438
IFN-g (Th1)~24 hour post O1965374-1660+739

IL-4 (Th2) July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IL-4 (Th2)~10 min pre O41.540-198
IL-4 (Th2)~5 min post O42.040-198+0.5
IL-4 (Th2)~32 min post O34.740-198-7.3
IL-4 (Th2)~24 hour post O46.840-198+12.1

IL-2 (Th0) July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IL-2 (Th0)~10 min pre O351384-960
IL-2 (Th0)~5 min post O356384-960+5
IL-2 (Th0)~32 min post O347384-960-9
IL-2 (Th0)~24 hour post O416384-960+69

IL-17 (Th17) July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IL-17 (Th17)~10 min pre O52.549-446
IL-17 (Th17)~5 min post O45.549-446-7
IL-17 (Th17)~32 min post O49.549-446+4
IL-17 (Th17)~24 hour post O43.749-446-5.8

IL-10 (T-reg) July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IL-10 (T-reg)~10 min pre O989760-1900
IL-10 (T-reg)~5 min post O902760-1900-87
IL-10 (T-reg)~32 min post O801760-1900-101
IL-10 (T-reg)~24 hour post O1052760-1900+251

IL-8 July 9 and 10 2015

ParameterTimeValue (pg/ml)Reference (pg/ml)Delta
IL-8~10 min pre O18.4< 15
IL-8~5 min post O38.9< 15+20.5
IL-8~32 min post O18.2< 15-20.7
IL-8~24 hour post O34.3< 15+16.1

Interferon gamma (Th1), august 13 & 14, 2015:

ParameterTimeValue in pg/mlReference range in pg/ml
IFN-g (TH1)~10 min before orgasm1315374-1660
IFN-g (TH1)~15 min after orgasm1147374-1660
IFN-g (TH1)~45 min after orgasm978374-1660
IFN-g (TH1)~24 hour after orgasm3053374-1660

IL-10 (T-reg) august 13 and 14, 2015:

ParameterTimeValue in pg/mlReference range in pg/ml
IL-10 (T-reg)~10 min before orgasm774 760-1900
IL-10 (T-reg)~15 min after orgasm638760-1900
IL-10 (T-reg)~45 min after orgasm542760-1900
IL-10 (T-reg)~24 hour after orgasm1045 760-1900

IL-2 (Th0) august 13 and 14, 2015:

ParameterTimeValue in pg/mlReference range in pg/ml
IL-2 (TH0))~10 min before orgasm433 384-960
IL-2 (TH0)~15 min after orgasm415384-960
IL-2 (TH0)~45 min after orgasm335384-960
IL-2 (TH0)~24 hour after orgasm281 384-960

IL-4 (Th2), August 13 & 14, 2015:

ParameterTimeValue in pg/mlReference range in pg/ml
IL-4 (TH2))~10 min before orgasm45.540-198
IL-4 (TH2)~15 min after orgasm35.740-198
IL-4 (TH2)~45 min after orgasm31.140-198
IL-4 (TH2)~24 hour after orgasm43.140-198

IL-17 (Th17), August 13 & 14, 2015:

ParameterTimeValue in pg/mlReference range in pg/ml
IL-17 (TH17))~10 min before orgasm51.649-446
IL-17 (TH17)~15 min after orgasm40.849-446
IL-17 (TH17)~45 min after orgasm31.349-446
IL-17 (TH17)~24 hour after orgasm57.149-446

IL-8, August 13 & 14, 2015:

ParameterTimeValue in pg/mlReference range in pg/ml
IL-8~10 min before orgasm89.8<15
IL-8~15 min after orgasm59.0<15
IL-8~45 min after orgasm41.9<15
IL-8~24 hour after orgasm36.6<15
« Last Edit: June 01, 2021, 01:45:22 AM by Muon »


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Re: Muon's Case
« Reply #1 on: December 16, 2019, 04:11:26 PM »
  • Chronic Fatigue Syndrome (Questionnaire+symptoms)
  • Bell's Palsy (left side, EMG)
  • Post Orgasmic Illness Syndrome (Subcutane skin prick+symptoms)
  • Postural Orthostatic Tachycardia Syndrome (>30BPM between supine and standing)
  • A possible Intestinal Bacterial Overgrowth and Lactose intolerance (positive lactose hydrogen breath test)
  • Structural Kyphosis (Cobb Angle = 70 degrees by scans)
  • Blepharitis (2019)
The only diagnose that isn't based on physical data is CFS.

  • Enlarged/swollen left testicle, at age ~19/20 I believe , prior to POIS diagnosis (scan revealed benign thickening)
  • Vitamin D deficiency (range:10-20)
  • Iron deficiency (once, when I was 7 years old, don't have the value)
  • Decreased urinary Sodium levels (Once, happened with onset of heavy POTS symptoms)
  • Elevated ALAT (multiple times)
  • Hypercobalaminemia
  • Lifelong Premature Ejaculation (<10s)
  • 3 Positive subcutane skin pricks with semen of 3 different men (same reaction as my own samples)
  • Calcium hydrogen phosphate stones in stool (analyzed it at local hospital)
  • White bumps/acne on shoulders and back
  • White/yellowish uneveness/spots inside cheek which closely resembles oral fordyce granules
  • Pearly penile papulas
  • (past)Fungal infection inside of mouth (2 times), Local fungal skin infections at chest, penis, navel and continuous (present day) toenail infections
  • Gastroscopy: Food from 9 hours ago was still in the stomach and Hyperaemia at the Z-axis. Conclusion was decreased corpus motility
  • Mouches Volentes/floaters (Left eye, black points)
  • Physiotherapist told me I was the only one who he could easily fold up in a certain way. Like pressing knees towards the face in a flat position. Hypermobile in certain positions.
  • March 2008: MRI of the skull and MR-angiography of the carotid arteries: Slight mucosal swelling in the area of ??the nasal sinuses
  • The fiber free diet I had to eat for a few days prior to the hydrogen lactose breath test gave me better stool
  • Steroid injection into the groin area resolved local symptoms completely for at least 4 hours. Reminder: look up in archives what they used for injection, steroid might have inhibited IL-33 mediated MC activation, compare steroid with paper.
  • I could not hold my left eye steady during measurements at the optometrist. I wasn't able to focus my eye to one point, it kept circling away and around that point. Something I noticed when reading but this time a professional noticed it as well.
  • During recovery of Bell's palsy: I could not close my left eye without smiling (contracting a muscle(s) around corner of mouth). Neurologist told me that something might have went wrong during recovery, in that, nerves could touch eachother. He injected Botulinum toxin to destroy end plates again to let it recover properly. It helped somewhat.
  • Reminder: Finding picture of anomaly in stool.

POIS Symptoms
  • Extreem fatigue
  • A tingling/burning sensation, it leans more towards tingling than burning. It's difficult to describe this symptom. I have the idea that most tissue being affected by this symptom is located in a layer close to the skin
  • Dark circles around eyes
  • Muscle ache
  • Stiff muscles
  • Muscle cramp
  • Joint pain
  • Exercise/motion intolerance
  • Heavy body
  • Feeling cold/warm, feeling cold happens far more often than warm
  • Decreased endurance, especially with the duration of standing and sitting straight
  • Sensitive teeth
  • Stinging pain at liver area
  • Yellowing of facial skin (only when POIS puts emphasis on liver area)
  • Pale skin and facial skin becomes like a babyskin
  • Decreased vocabulary
  • Articulation problems
  • Poor concentration
  • Grammar problems (constructing sentences suddenly becomes a puzzle)
  • Short term memory loss (temporary)
  • Motivation in general is being lowered and often completely wiped out
  • I become someone without personality
  • Indecision
  • Accelerated Bowel movement, loose stools and sometimes diarrhea
  • It amplifies my food intolerance/sensitivity
  • Decreased digestion
  • A sense of being full (digestion)
  • Fasciculations
  • Itching
  • Soar Throat
  • Mood swings
  • Bad body odor
  • Decreased accuracy of handwriting ,also problems with controlling videogames like aiming in FPS
  • Faster spreading of local fungal skin infection at feet in POIS
  • It can influence the heart, I suspect it's a change of heart rithm.
  • Lung problems (bronchoconstriction or dilation?)
  • Dry or greasy skin
  • Decreased sense of smell
  • Increased pressure in and/or behind the eyes, most frequent in left eye
  • Dry mouth and activity on surface layer inside mouth (inflammation of mucosal membranes?)
  • Stomach pain and/or makes stomach sensitive to foods, especially acidic food
(the above list is not complete, can also add frequency and relative intensity)

POIS Dynamics

Before desensitization:
Phase1 (Build up phase): POIS sets in immediately and builds up gradually. Sometimes the starting intensity is so low and speed of intensity build up (slope) slow that you only will notice it after some time (in some instances this could mean 30 min for example or in rare cases a few hours).

Phase2 (constant intensity phase): After approximately 24 hours symptom intensity reaches its maximum. It stays a bit lower by a small margin than the max and constant from the ~24 hour mark up to day 4.

Phase3 (Recovery phase): After day 4 symptom intensity will decrease. It feels like flipping a switch at the end of day 4. This recovery phase can take up 1-3 days. After that I still have POIS symptoms, this is like a constant offset.

There is a peak/maximum of fatigue intensity during the recovery phase.
!Perhaps I need to draw a graph to make it more clear

Strength of ejaculation/orgasm

Weak ejaculation: Faster onset of symptoms (immediately) with higher intensity at onset.
Stronger orgasm + stronger ejaculation: Delayed onset and intensity of symptoms rise slower compared to scenario with weak ejaculation.
Larger volume of ejaculate (only noticed it after desensitization): Higher intensity peak of fatigue

Multiple orgasms

Symptoms get worse but the second orgasm reverses the symptoms of the first one for a major part. You can use this effect to reset symptoms of POIS if orgasm is sufficiently high in strength but it will come back in full force as time goes by. If you could make a mathematical function of the peak intensity of multiple orgasms then it would probably behave like a logarithmic function (I’m not talking about the symptom intensity vs time curve but peak intensity vs # of sequential orgasms). Reset behaviour could be linked to values of parameters depicted in table dropping post O. POISers should be questioned about reset behaviour.

Scenario with sticky ejaculate:

If the ejaculate is sticky some of it will stay behind post ejaculation, which leads to:
Burning sensation in urethra.
While it burns: The continues urge to urinate while having an empty bladder.
My anus starts to burn.

Urinating quickly after ejaculation helps prevent the above symptoms.

Lower part of spine/leg jolt:
Lung/POIS dynamics:
Event of cold attack by POIS during hot day:
Cold/Warm dynamics:
Social isolation dynamics:
Add reminder: Dynamics of Pre-ejaculate release without ejaculation and combination of pre-ejaculate phase with orgasm.

Chronological order of events

2 days/1985: Cardiac arrest while my mother was breastfeeding me. I turned blue, strenght of pulse weakened up to point of cardiac arrest. Heart massage brought me back to life.
Age 7/1992: Iron deficiency. I looked very pale, had dark rings around my eyes and was thin.
Age 12/1997(age 10 or 12): My body failed regulating my breathing pattern, I had to do this manually which led to hyperventilaton. This happened on a very hot day.
Age 14/1999: Started to masturbate in my late 14's
Age 15/2000: Started to get really tired and I could not be in school on time early in the morning. There were also strange events like an erection that was not getting soft again and had no control over it. One time I was getting a burning sensation in my glans penis while I had a semi erection and was peeing.
Age 16/2001: I was questioning myself if there was something wrong immediately after a particular orgasm at one situation. I didn't take it that serious and shrugged it off. I was stupid not observing my general well-being the days after that orgasm.
Age 17/2002: I was playing a soccer match under hot weather conditions and felt like I didn't receive enough oxygen resulting in very deep and slow inhalations (blood pooling, typical POTS symptom). The same thing happened a few times during summer time on hot days in school where maintaining posture was more difficult than usual and displayed the same behaviour as the situation when I had that soccer match namely very deep and slow inhalations (not to be confused with hyperventilation). People sitting next to me were quite irritated by this breathing pattern.
Age 18/2004 Facial paralysis left side when I woke up in the morning after I visited someone who was celebrating her birthday. I drank 3 bottles of beer that night (I rarely drank alcohol at all, was never a drinker) which was a lot for me and also ate a lot of peanuts and remembered I was tired. This was a point where more symptoms starting to appear, it felt like an acceleration. Around this time I also did not get enough energy by meals even when I ate more because I was more physically active with sports. I could not get enough energy by eating.
Age 19 and up: Don't know the exact age and order, have to look it up. Oral fungal infection, tennis/golf elbow, heavy nerve pain at the inside of arms for one year, after that I got capal tunnel-like symptoms for a year, food intolerances went gradually worse in particular fruits.
Age 24/2009 POIS symptoms were so extreme that it became clear to me that ejaculation was the culprit. Searched the internet for sickness after orgasm, made an appointment with Prof. Dr. Waldinger, did get diagnosed with POIS and started hyposensitization treatment in early 2010.
Age 28/2013 Crisis year. Complete escalation during summer when I sat in a train and the sun shone on me, POTS symptoms exploded. Cardiovascular problems, autonomic instability, extreme temperature sensitive, tons of weird events. Around December food sensitivities suddenly became extreme out of nowhere, mucosal membranes were highly reactive to food.
Needs editing, to be continued Reminder: I can remember clearly I had food sensitivities around  8/9 years of age. Have to look it up if I had them before the age of 7. Liesproblemen vergeten. I have always been intolerant to hot baths as a kid. Slijmproductie in keel door Yoki. Doorslikken voedsel ging niet makkelijk als kind zijnde, moest appelmoes erbij eten. Lot of IBS-like symptoms early 20's (GP gave me Psyllium which made symptoms worse, took it a few times). Drank a lot of cow milk as a kid and had a mild intolerance to it, fatigue and nausea.

General Symptoms

List of triggers

Release of pre-ejaculate
High temperatures
Temperature change (Like going from >20 C inside and putting a garbage bag outside during winter <0 C without winter jacket (this can lead to sudden tension build up slightly above adam's apple at left and right side), however when dressed properly it has a positive effect)
Drinking tapwater
Airborne particles: Dust, Diesel exhaust, sigaret smoke, parfums, Food scent
Sleep deprivation
Large meals
Prolonged standing or sitting (sitting on a chair without back support wrecks me)
Prolonged discussions leads to fatigue which leads to more cognitive symptoms
Medicine/supplements: Citalopram 10 mg/day (headache), Daktarin oral gel (additional problem when addressing fungal oral infection)
Thunderstorm: breathing difficulties which can lead to hyperventilation at the moment before the storm hits.
Duration and frequency of triggers can make symptoms worse
Each trigger has its own dynamics and set of symptoms with overlap, I could add this later.

Synergy of triggers

Food (split up in food and diet?)

I react to everything at a certain degree. Below are some examples. On top of my head:
  • Apples. Wave of fatigue sets in approx ~1 mins after ingestion. Fatigue lasts about 10 or so mins. Different brands giving different intensity but same type of symptom.
  • Banana. Lightly Nauseous once it enters the stomach, oral and throat mucosa can react to it as well. Unripe green banana's are far better tolerable.
  • Fruit juices. Nauseous, fatigue, throat/stomach irritation, feeling it won't digest, horrible stuff.
  • Tomato's. Nasal drip, runny nose, within 30 sec.
  • Whole grains. Loose stools, heavy on my digestion system, other GI complaints which I have to look up, don't eat them anymore. Wheat can give me red pencil sized dots on my hand
  • Nuts. Loose stools or Diarrhea, nasal drip or runny nose. Walnuts can give me a painful tongue. Pistache nuts give me relatively the least symptoms.
  • Chocolate. Just not feeling well especially in my head, sometimes my brain react to it, brain fog. Sets in 60 min after ingestion but depends on the amount, you can clearly feel the difference from 50 g pure chocolate. Some chocolate brands give me sticky stool instead.
  • Spinach. Activity in oral mucosa upon contact. Sets in immediately.
  • Watermelon. Variable and depends on the amount. Fatigue. Sets in within a few mins I think. I can react to the scent of it as well. Watermelon is the best tolerable one out of all melons I have tried.
  • Spices. Nasal drip or runny nose.
  • Passion Fruit. Upper wall of mouth cavity hurts and nasal drip or runny nose.
  • Oak leaf lettuce. Dry mouth and slightly painful mouth cavity, looser stools than usual.
  • Citrus fruits. Just out of the question, sore mouth, sore throat, irritated lips with oranges. Green lemon Stool problems.
  • Mix of frozen grilled vegetables: Bell Peppers, Eggplant(Aubergine), zucchini. Painful tongue. Did test this mix multiple times, symptom consistent.
  • Chicken thights. (They used some spices, need to test them natural) Diarrhea.
  • Leeks. Can't remember exactly but I believe it gave me gum problems, haven't eaten this for a long time
  • Whey protein powders. Red Pencil like dots on hand, probably more symptoms but can't remember at this moment.
  • Shrimp. Diarrhea. Dutch shrimps are the best tolerable.
  • Potato skin. Fast and short lived flare of dryness at a spot within throat upon contact. Felt like center of spot being triggered and dryness spread out.

Food that are relatively better tolerable:
Fresh big black ripe cherries (red ones or the smaller ones are giving symptoms)
Dragon Fruit (White Pitaya), maybe the best tolerable fruit for me.
Iceberg lettuce
Chicken filet and legs.
Potato's well-baked depends on brand.
Egg yolk (don't feel well on egg white)


  • Heavy body
  • Weakness
  • Fatigue
  • Pressure in lower spine
  • Feeling of low grade systemic inflammation as a function of temperature
  • Cardiac problems, blood pooling
  • Decreased digestion and GI motility.
  • Focal headache in centre of brain
  • Fasciculations
  • Stiff muscles
Tons of other symptoms to add here.

POTS Symtoms

Symptom dynamics/situations

Factors contributing to symptom reduction

  • 5 year long desensitization treatment 2010-2015 (permanent improvement, the amount varies with type of symptom. Fatigue is by far the most improved symptom, perhaps 80% reduction. For other symptoms it's harder to estimate how much they have been reduced, for most of them I think maybe around 50% but this is a very rough estimate). My POIS was quite extreme. Questions about desenz
  • A long and good night of sleep
  • Cold, especially Sub-zero environmental temperatures (perhaps have to put details about this one somewhere else)
  • Gradually feeling better after midnight and best at 3:00 am
  • Taurine (minor effect, 45 min before Orgasm ~1g)
  • Antihistamines (minor effect, only clemastine if I'm not mistaken)
  • Protein rich diet (minor). Quicker recovery. Best source for me is meat especially chicken.
  • CBD oil (minor effect, need at least 2 drops of 10% to feel something)
Desensitization peculiarities: A few occasions where I felt normal (never felt so good), the onset (rapid within minutes to max) is somewhere between 30-60 min after subcutaneous injection. Happened more than once. Mucous layer in mouth felt fully developed as in thick, no dry throat, muscle strength increased, no food reactions, better resistance to weather conditions/temperature. The effect diminished from the point of onset over the course of tens of minutes (after that maybe some minor effect still present over the course of a couple of hours, hard to say, I could have some notes about it somewhere). If this effect was permanently then my health issues would basically have been fixed in my opinion. And I wonder whether that was a window of opportunity to apply rush therapy as in getting another injection.

  • Intens (heavy weights) body building exercises (most of them in flat or inclined position). Short powerful movements, almost explosive with Reps between 3-5. The trick is you need to induce a pump. Need to add more details
  • Breathing slow and deeply (this is done instinctively when symptomatic)
  • Strong beta blocker (need to look it up what type and dose)
  • Low Carbohydrate diet
  • Cold (heat exacerbates it)
  • Laying flat (even the slightest head tilt can worsen symptoms)
  • Salt (water without salt can exacerbate symptoms)
Food reactions
  • Heating food by high temperatures. Cooking food in boiling water doesn't do much. Cooking in pans, ovens or fryers leads to significantly less food reactions. The thickness of food is relevant as well. For example I'm more tolerant to thin sliced potatoes than thicker ones, some semi raw regions inside the centre of ticker potatoes can still trigger reactions
General Symptoms
  • Eating less in general
  • Eating less sugar
  • Skipping grains, nuts & seeds, diary for improvement of stool density
  • Cold temperatures
  • Low dose oral intake of food grade Liquid Hydrogen Peroxide solution (best thing I ever took needs details)
  • Avoiding triggers
  • Gradually feeling better after midnight and best at 3:00 am

Fungal skin infection feet
Vicks vaporub ointment a few times a week, add a thin layer that dries quickly.

Fungal infection oral cavity
Dakterin gel, flushing mouth (adverse reaction when swallowing)

More to add and need to go more into dynamics
« Last Edit: September 08, 2021, 04:47:50 PM by Muon »


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Re: Muon's Case
« Reply #2 on: December 16, 2019, 04:13:06 PM »
    Family members

    Family members on my mother's side show similar symptoms as I do. All the females who got health problems felt better during their pregnancies and felt worse during their menstrual cycle. My grandma actually looked forward to her pregnancy. My mother has 3 children, my aunt got one and my grandma has 4. They all felt physically better for every single pregnancy.

    My younger brother:
    • Diagnosed with Post-orgasmic illness syndrome (started in his 20's)
    • Pectus excavatum
    • Emphasis on neuropsychiatric symptoms
    • Burning feeling in brain
    • Very sensitive to food (had years of food sensitivities prior to the development of POIS)
    • Insomnia
    • High libido
    • Sleepwalking
    • Developed heat intolerance
    • Cyst in his knee which impaired walking and was removed surgically
    • He told me that benzodiazepines were the best type of meds he tried but stopped due to increasing tolerance and tendency to addiction. Nootropics had some effect on cognitive symptoms
    • Feeling at his best at 3:00 am.
    • High insulin, normal insulin sensitivity, reactive hypoglycemia (I have seen the measurements of low glucose vs time, data is lost)
    • They did do a non-specific allergen degranulation test. My brother told me they observed degranulation before allergens were even applied. The source of degranulation is unknown
    • Did measurements of HR changes between flat and standing position on brother during summer, this gave changes within the range of 20-30 bps but all <30. Measurements of mother and father did not exceed 5 bps.
    Tons of symptoms and he had other diagnosis, I have to ask him about it. Will add later.
    2020 summer: He had an acute attack of blood pooling (he underestimated how heavy this symptom is).
    2020 Dec: Episode of schizophrenia/depersonalization, psychosis, whole body weakness, breathing difficulties. All together and went on for days. He told me he had the impression that there was a lack of oxygen in the brain and thought he passed out a few times.
    2021 Jan: Hospitalized indefinitely mainly due to psychosis (Accompanied by OCD-like behaviour when I first met him in this state, repeating words/sentences to reach a certain number).
    2021 feb: Catatonia: response to IV Lorazepam. Immune system?
    Note: When he was in a state of psychosis with additional OCD he was clearly a different person. I asked him why he kept repeating words and sentences, he answered that his brain felt better when he did so.
    The Neurosteroidogenic Enzyme 5a-Reductase Mediates Psychotic-Like Complications of Sleep Deprivation

    • Osteoporosis (5 years on Bisphosphonate had no effect on her osteoporosis, 2020: Using prolia injections)
    • Carpal tunnel syndrome and delivering squeezing power with hand is difficult
    • Pollen induced hayfever (elevated IgE)
    • Low vitamin D
    • Intravaginal sensitivities: Burning sensation upon contact with semen and latex sensitivity.
    • A cold sore every now and then
    • Easy bruising
    • Unexplained areas of the skin that can turn red
    • High cholesterol levels
    • Blood pressure problems
    • Calves feel heavy
    • Varicose veins in legs (painful lower legs)
    • Red eyes (Blood eyes, no visible eye white)
    • Alternating constipation
    • She had an accute attack of intestinal inflammation (Blood in stool, pain, elevated CRP)
    • Getting attacks of cold
    • Sense of feeling cold much of the time
    • Stiff muscles
    • She can touch her toes from a standing position while legs are straight
    • Fluctuating pattern of symptoms
    • Sometimes she feels and hears a big 'tick' inside her head, it's only one when it happens. Her most scary symptom.
    • Brain MRI shows a small black dot (need to ask her about the position)
    • My mother laying often on bed during the day when I were a young kid. She was stressed. She was probably in her early 40's.
    • Often forgetting things
    • Speaking mistakes (meaning one thing but saying something different)
    • Difficulty coming up with the right word, searching for that one word that completes her sentence.
    • Sometimes her tongue hurts by eating food, walnuts for example.
    • Problems with citrus fruits.
    • She can't sit still for a long time and has to be in motion.
    • Difficult to sit in 90 degree angles.
    • A flare of a nasty feeling around the heart area. (I got this as well, I think it's an inflammatory flare at the surface of the heart or heart muscle.)
    • Bladder infection (peeing blood, used antibiotic)
    • Eye Lid tremor
    • Early satiety
    • Idiopathic miscarriage
    • Physical exertion can induce symptoms the next day
    • She feels significantly better overal after menopause
    • TIAs
    • Neuroprotek, Quercetine phytosome and ibuprofen helps her
    July 2020: She had to push against a mobile caravan for a short time window with alot of force and felt immediately better afterwards.
    Jan 2021: Involuntary Defecation, stressful period, Butterfly rash on her face (what you see in lupus) appears more frequently.

    Aunt (my mother's sister):

    She had some sort of reddish/blueish rash over her body when she was a few years old. She was placed in quarantine and doctors couldn't figure out what is was, they were thinking of Rubella. Her skin became like sandpaper, when that happened dermatologists literally peeled the upper layer off. When they got rid of this sandpaper like layer she recovered. Dental decay despite good hygiene and dental care. She had food sensitivities.

    I have asked her about her symptoms a while ago because Waldinger was curious about it. I will translate it literally what she has sent me.
    • Persistent fatigue which is not restored with adequate rest and sleep.
    • Always feeling sick, broke, general malaise.
    • Temperature fluctuations (increase, hour later sub-temperature again, etc.)
    • Vegetative reactions (sweaty hands, dizziness, disorientation, unstable feeling on the legs (rubber legs)).
    • Orthostatic hypotension (seeing stars after squatting, getting up from a sitting position, etc.)
    • Immune problems (pick up every virus that prevails and then spend 2 or 3 weeks with it under the pans that others have or do not suffer from or get rid of within a day or three) (non-specific and specific defense)
    • Cognitive problems: difficulty concentrating, unable to focus, being woolly in the head, being unable to hold or complete thoughts, problems formulating sentences or coming to words. (one day better than the other, unpredictable).
    • Short attention span (unsure with translation: korte spanningsboog), cannot maintain concentration or perform work for long periods. Must have limits in it.
    • Light shyness (dutch = lichtschuwheid)
    • Difficulty reading, double vision, night blindness (for my feeling from one day to another, according to optician at the time nothing wrong with my eyes).
    • Sounds sound loud and penetrating (whiplash-like complaints).
    • Headaches, sore throat.
    • Regularly swollen glands in the neck and groin.
    • Urticaria (urtica's, allergic skin reactions but no idea what I'm triggering from, often after picking up a virus or the like and often at the time of menstruation but sometimes also without any apparent cause).
    • In the past: pituitary dysfunction resulting in no menstruation (approx. 3 to 4 years), sleep disorders, no melatonin production, disturbed biological clock (examined and determined by specialist), maternity mask (also called melasma) without being pregnant. Determined by dermatologist. Advice dermatologist at the time: have your thyroid function checked regularly. That done: TSH thyroid at 0.42 (on the lower limit). Just fell within the reference value so GP saw no reason for treatment. I gained 15 kilos in two weeks without changing my diet (blew up like a puffer fish), dry skin, night sweats, etc. I had all the symptoms of the transition while I was 32 or 33 years old. After taking blood samples I turned out not to be in transition, but my pituitary gland turned out to be working a little below standard but according to the doctor not to the extent that treatment was needed.
    • Leucocyte values ??always increased! Whenever I have blood sampled, always increased! Hemoglobin just on the border.
    • Adrenal dysfunction (cortisol, adrenaline) (mesologist diagnosis).
    • Calcium household problems (mesologist diagnosis)
    • Calf cramps (every day, night and morning to such an extent that it wakes me up).
    • Must always dose my activities, including fun activities. After a birthday o.i.d. overtired.
    • Avoid crowds regularly for that reason or have to plan that and reserve rest after that time to be able to refuel. And often that's not enough.
    • Battery is empty quickly and takes a long time to get some spare. Limited taxability in many respects.
    • Fungal infections are a common thread through my complaints. From about my 17th almost continuously suffer from vaginal fungal infections until around my 35th. Also regularly bladder infections where I got antibiotics from the doctor. But that naturally encouraged fungal formation. From around the age of 32 I was diagnosed with intestinal dysbiosis with opportunistic candida (by a nature doctor). Candida diet, anti-candidate drugs etc. These improved my health, mesological treatment has also contributed to this. To date, sensitive to yeast/fungi. Noticeable by stubborn athlete's foot and lime nails (sign that it is still not right). For years no longer suffer from vaginal fungus. Immune problems and others remain.

    Grandma (My mother's side):
    • Brain aneurysm (Age>70 years, according to her doctor she was walking around with a time bomb in her head)
    • Vascular dementia (Age>70 years)
    • Periods where weakness in legs led to bedriddeness and couldn't walk stairs (this improved by oral injection of unknown substance).
    • She went swimming during summer, accute locked up feeling in lower back once her hip got submerged when she entered the water, she couldn't get out of the water and had to be dragged out. She had weakness in her legs since this event.
    • Multiple Transient ischemic attacks (TIA); One-sided facial droop etc
    • Colorectal polyp
    • She felt better when she did not eat
    • Was intolerant to chocolate
    • Even in her late 70s she could pick up her foot and plant it against her face
    • Fainting (had this since childhood). She felt it coming. She didn't feel well and was getting hot prior to fainting. She had to lay down for better circulation when these signs showed up and had to cool down her forehead and wrists.
    • Heavy pain around her feet and ankles. Did not happen a lot but it ramped up fast and she screamed. People had to put her feet into a tile of water. My mother can't remember what the temperature of the water needed to be, cold or warm.
    • They did do a muscle biopsy on her but found nothing. It's unknown what they were looking for.
    • Couldn't sit still for long periods of time. Need to be in motion.
    • Bladder infection
    • She felt better on Enterosalicyl.
    • Constipation
    • Bloating in the abdomen
    • Episodes of low blood pressure
    • They injected her something in her throat via the oral way and she did get better in general (substance unkown).
    • Tight feeling behind her ear
    • Went a little crazy at the end of her life and died just like her grandmother.
    • She used blood thinners because she had thick blood.
    There was something with the hands, Raynaud?

    Healthy Family members

    These folks are, from what I know, basically healthy but there are some oddities.

    My older brother
    • Stuttering as a kid
    • Insomnia
    • Sleep apnea (mouth piece works)
    2020 Dec (ask for exact month): Diagnosed ADHD and developed insomnia after periods of increased stress in his life (25 mg Quetiapine before bed time works for his insomnia).
    2021 Oktober: Developed loss of memory and fatigue.

    My mother's younger brother
    • At 3 weeks of age, 3 months hospitalized in critical condition due to upset intestines. Possible trigger: He drank porridge just before symptoms appeared, which were, continuously throwing up and upset intestines. My mother saw that the porridge was too thin, there was too much water in it in her opinion. She thought the brand of the porridge was called Nutrix. Symptoms disappeared spontaneous.
    • He did get rashes over his body as a kid when entering chlorinated swimming pools. He outgrow this symptom when he got older.
    • Chronic Depression
    • Can have angry outbursts over nothing
    • ADHD
    • Slow eater
    I heard he had more problems during the past years like gut pain (details unknown) after he stopped smoking weed (was a daily weed smoker from what I know).

    My mother's older brother
    • Cardiac issues (details unknown to me)
    • He told me once that he finishes his showers with cold water and made him feel better.
    • Isolated lifestyle
    My older brother's daughter
    • She reacted to dust and milk when she was a few years old. I asked if this was a true allergy but nobody knows.
    • Spontaneous bursts of saliva production
    • Sometimes she looks pale with dark coloration under her eyes.
    • Sugar cravings
    • Acne
    • She forgets to hydrate because she isn't thirsty. (I have this symptom, need to remind myself to drink)
    • She has light asthmatic-like symptoms at this moment in time (15 years of age, Dec 2019). Her lungs make sound when exhaling quick which makes her breath heavy afterwards.
    • Jan 2020, Runny nose when transitioning from warm to cold environment.

    Deceased relatives

    My mother's father
    Cause of death was unknown. Autopsy revealed holes in intestines. Officially diagnosed with leaky gut after he died.

    The son of my grandma's sister (mother's side)
    Organ failure due to persistent benign tumor growth

    My dad's father

    My dad's mother

    Other family members, health status unknown

    The daughter of the brother of my grandmother (mother's side)
    • She walks around with a body temperature of 35.0 Degrees Celsius since birth and is always cold, sometimes it drops to 34.5.
    • Arthritis
    • Her daughter faints when her daughter's core temperature rises

    Commentary and thoughts on symptoms

    Symptom triggers are similar as seen in MCAS patients but are also a form of stress. Stress signaling/response could (be abnormal) affect the ANS which on its own could be in a state of sympathetic dominance outside of stress.

    Looking at the factors which reduce symptoms I noticed that they increase parasympathetic activity by stimulating the vagus nerve.[/list]
    « Last Edit: February 19, 2022, 02:16:41 PM by Muon »


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    Re: Muon's Case
    « Reply #3 on: December 16, 2019, 04:16:32 PM »
    Comments on table

    Reset behaviour regarding multiple orgasms could be linked to values of parameters depicted in table dropping post O. POISers should be questioned about reset behaviour.

    Interferon gamma vs time: It seems bimodal (IL-12 is a major driver of IFN-g) with domains < X hour and > X hour (X=24?) for inhibition and enhancement respectively, similar what Theoharides is talking about:

    Mast Cells to Dendritic Cells: Let IL-13 Shut Your IL-12 Down
    "The effect of IL-13 on the expression of the p40 gene of IL-12 is bimodal with inhibition at early times (< 24 h) and strong enhancement at later times; in fact, IL-13 is often used to generate DCs in vitro from monocytes and these cultured cells produce more IL-12 than ex vivo-purified DCs."

    Direction of slope July

    - - +: IFN-g, IL-10
    + - +: IL-2, IL-4, IL-8, IP-10
    - + -: IL-17
    + - -: TGF-beta

    Direction of slope August

    - - +: IFN-g, IL-4, IL-10, IL-17
    - - -: IL-2, IL-8

    Comparing slopes July and August

    IFN-g and IL-10 show similar dynamics for both dates relative to eachother. Dynamics for both dates are the same.
    IL-2 and IL-8 show similar dynamics for both dates relative to eachother. Dynamics for each date is different.

    But they may not be comparable because the time difference between Orgasm and the second data point is different for each date. 5 min vs 15 min post O for second data point. A graph would show a better picture...or not...because data points are scarce.

    Comment august data
    Release of cytokines need intracellular calcium, they all go down post O. Is there a decrease of intracellular calcium inside leukocytes? IFN-g may still be climbing days later as in a type IV reaction.

    Muscle stiffness, spasms post-orgasm could indicate changes in intracellular calcium concentration. Another trigger is heat/high ambient temperatures especially during rest after movement (just taking a walk) through hot environments.

    Immunophenotypical Characterization of a Brazilian POIS (Post-Orgasmic Illness Syndrome) Patient: Adding More Pieces to Puzzle
    "The majority of these cells are expressing CD38+, which suggests that the activation in this patient is more likely to happen via the CD38 molecule and there is no clinical explanation to that finding"

    Roles and mechanisms of the CD38/cyclic adenosine diphosphate ribose/Ca2+ signaling pathway

    IL-4 and IL-17 return to their former values. IL-10 is slightly higher 24h. IL-2 and IL-8 don't seem to return to their values post O while IFN-g is higher. IFN-g may be suppressing IL-2 and IL-8. Everything is in normal range for the first measurment except IL-8, the latter may come from a different source. Low IL-2 can be a problem since "IL-2 plays a critical role in the maintenance of CD4+CD25+ FOXP3+ regulatory T cells (Tregs) in vivo." Ref

    Something else, I had painfully stiff muscles due to POIS a week ago. The higher part of the back, shoulders and part of the upper arms were affected, the weird thing was it kept getting stiffer and stiffer up to the point I could barely move my right arm, it was that painful (there was only pain present during movement, not in rest). Moving my arm/shoulder, was like the feeling of almost tearing some muscles. I slept one night with clothes on because undressing was too painful. Quite a weird event, I have never experienced this intensity of stiffness before.

    Throwing some ideas around:

    Calcium signaling in immune cells

    Calcium, Channels, Intracellular Signaling and Autoimmunity

    Regulating T helper cell immunity through antigen responsiveness and calcium entry

    Decreased intracellular calcium stimulates renin release via calcium-inhibitable adenylyl cyclase

    Voltage gated calcium channel autoantibodies? Or mast cell mediators interfering with calcium homeostasis?

    Reminder: Could take a look at AMPAR's/Calcium/L-Theanine?

    Values dipping post O seen in other members.


    No-POIS state:
    TNF-alpha: 32.6 pg/ml above reference range (<12.0)

    4 hours after ejaculation:
    TNF-alpha < 12.0 pg/ml

    Iron dipping during POIS?:
    I've had blood tests done multiple times during my worst fever episodes, and everything comes back normal except for very low levels of iron (I usually have normal or even high iron and hemoglobin levels), and through-the-roof amounts of C-reactive protein. This led doctors to think I could have mononucleosis or some kind of bacterial infection, but all specific tests came back negative. They put me on antibiotics anyway, and that solved most symptoms almost immediately and made me able to get out of bed and finally get better during the worst episode I've ever had.

    Hello,i wanna tell sth,but first in private,maybe i'll post it
    Considering that it is said that is possible for some Allergy,i tried to swallow my cum and guess what.After a few hours i couldn't swallow shit for about 3 weeks,i was anxious as fuck when trying to swallow anything solid. My Family MD told me that my throat is "red".Went to an Otorhinolaryngologist and he told me that it is allergy without me telling you what i did.Do you think i should that again and what could he check for in the blood if that repeats?
    3) well, i don't know that,it was in my neck,my family doctor told me that my neck is "red" that's everything i know and i know that i couldn't swallow  cause i didn't feel the food going down and was always anxious that i was gonna   choke,cause the food is gonna go down the wrong pipe,i  couldn't contract my muscles,lots of thing,was like i wasn't also feeling the lower part of my  throat that you "consciously " contract when you swallow.It was weird cause everyone thought i was crazy,at least untill family md told me that  my throat is "red"

    People also complain about their muscles being locked up during POIS.

    Spine MRI calcium related?:

    Additional studies further showed that opioid signaling may play a key role in mast cell activation and the downstream inflammatory responses associated with HO.
    The Immunological Contribution to Heterotopic Ossification Disorders

    Opioid signaling in mast cells regulates injury responses associated with heterotopic ossification

    Metabolic and Epigenomic Regulation of Th17/Treg Balance by the Polyamine Pathway

    "there was a trend towards a decrease in IFN-g, IL-17 and TNF production with an increase in IL-9 production in response to antigen"

    Seminal exosomes
    SE have already been implicated as immunosuppressive, inhibiting lymphoproliferative responses (2), the activity of phagocytic cells (11) and natural killer cell function (12). Thus, the immunosuppressive properties of seminal plasma appear to reside at least in large part within its exosome fraction.


    Other tests and meds I tried

    Hepatitis B, C, E: negative
    Intestinal permeability test: Mannitol and lactulose in urine after ingestion-->negative
    HIV negative
    Lyme negative
    Lung capacity test: Slightly lower than normal
    Did a bicycle test because of tissue around groin that gave problems with exercise. Oxygen gas and lactacte couldn't be measured at the end of the test because I got sick and had to throw up.
    Hormone tests: Cortisol measured once, normal. Thyroid hormones normal (which ones?)

    Tried oral NSAID and steroid for symptoms before POIS diagnosis, like joint pain: No effect
    Acyclovir+(prednisone or diclofenac, can't remember which one) 14 days for Bell's palsy: No effect, not even side effects (dose unknown).
    Norethisterone: No effect
    Pyridostigmine: No effect
    Niacin flush gives symptoms
    Used some sort of gel for my acne on back, didn't do anything (name?)
    Metronidazole 11-day trial for positive lactose H2 test: No effect, last day of intake some gut pain.
    Vitamine E: No effect
    Vitamine B complex: Adverse effects
    Vitamine C complex including zinc and a herb (link somewhere in comments): Adverse effects
    Vitamine D: Felt slightly better overal when transitioning from deficient state to normal value.
    DAO enzymes (DAOsin): Nothing
    Glucosamine (can't recall what form): Nothing
    Digestive enzymes for stomach: Nothing
    Caprylic acid (dose unknown) = no effect


    Results from people with similar syndromes:

    Input: my Immune profile from IMD Berlin

    Results of the German Cell Trend laboratory for POTS

    She (Learner1) got elevated IFN-g, IL-12, IL-18 and elevated antibodies @ celltrend: Alpha-1 adrenergic receptor and Muscarinic cholinergic (M4) receptor.
    « Last Edit: May 30, 2021, 11:07:16 AM by Muon »


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    Re: Muon's Case
    « Reply #4 on: December 16, 2019, 04:18:31 PM »
    Past Events



    Recent Events

    Summer 2019

    Intense flares of pressure at heart area accompanied by weakness in left arm.
    All the time pressure at lower part of spine when standing plus weakness in legs.

    Somehwere around November 2019

    Walked in supermarket, felt some activity in brain (not at the middle of brain) at them same time my left side of my face was hanging for a moment, as in decreased muscle tension.

    Also had a moment where I had to help someone with their homework. Got a bit stressed by prolonged talking, felt activity in brain and couldn't talk properly for a minute. Could not create any word with my lips.

    There were a lot of days where I couldn't get warm and was cold all the time.

    Late December 2019/early januari 2020

    Activity at lower part of spine plus pressure at that area. Weakness in legs when standing.
    Bladder control problems, Frequent urination, this was getting worse when there was more activity at lower spine.

    Januari 2020

    A few times tingling sensation at the glans penis and became very sensitive to any friction (not sexual related just limp penis).

    Februari 2020

    I ate some liver and suddenly became feverish and nauseous for less than 30 sec of duration immediately after ingestion. Perhaps 5-10 mins after there were migratory colds traveling over my body and turned into systemic cold (shivering) after the migratory cold ended.

    Problems with stress as a trigger, most of the time physical stress by static body positions. Starts with tension -->stress---> inflammation.

    Weak spot in lower part of spine ---> local tension ---> standing/sitting/bad posture ---> focal tension turns into focal inflammation ---> as time goes by other parts in body one by one, most often the weaker parts have a higher chance, getting smoldering focal inflammation ---> when it stays this way it turns into systemic symptoms, like fibromyalgic-like weakness around the hip area and fatigue.

    This behaviour can be prevented if local/focal stress is reversed in time. There is a certain intensity threshold that when you cross it you are unable to reverse the above process.

    Symptoms of stress can be very subtle, it can gradually increase without notice. Local/focal stress, even by immobilization is able to induce the following symptoms lately:

    1) Very light burning on top of forearms and/or shoulders. Goes away immediately when stress stops.
    2) Worsening of Blepharitis
    3) Activating oral mucosa (sense of activity, surface fizzing) ---> bad taste ---> increased reactivity of food/mucosal contact
    4) Runny nose (also when taking a walk in POIS and certain muscles can't handle standing posture thus again, focal stress turns into focal inflammation at the same weak spot--->runny nose)
    5) Weakness in legs
    6) Inflammation (especially at spine lately)
    7) Some activity in the lower abdomen sexual organ related (only after multiple parts of the body are affected)
    8 ) Some activity in lower part of abdomen GI related, same spot as triggered by temperature in summer 2014 (again only when after multiple parts of body are affected).
    9) Joint pain, not sure if this is triggered by stress. Joint pain seem to be a late reaction, can't put my finger on it with certainty what triggered it.
    10) Fatigue, only when inflammation by stress has affected mutliple spots.
    11) Fibromyalgic weakness/pain around tendons of hip. Again, only when inflammation by stress has affected multiple parts of the body and is ongoing.

    Eating apples again and symptoms induced by apples have changed from fatigue to a runny nose. Reactivty with oral mucosa is worse when oral mucosa is being activated by stress/inflammation in other parts of the body.

    New symptom, happened only once: Intense sharp pain for maybe 2-3 seconds at right kidney location. Never felt anything like it before.

    June 2020

    Developing symptom: Sharp localized pin point stings in urethra mostly by low grade stress.

    Developing symptom: Neck tension/pain

    Improved Brain fog (large improvement. It took at least 6 months, slow trending motion) and mood swings much better. Improvement in facial appearance.

    October 2020

    Had pinpoint activity next to my eye in my skin. This lead to a brown coloration of that part of the skin. Happened again at a later date close to the same spot, same behaviour, led to another dot of brown coloration.

    Washing the glans penis during shower led to activation in lower back at the spinal area (which is already sensitive), no pain, just activation of something and it isn't muscle, no feeling of contraction. Activation stops when friction stops. Applying friction again flares up activity in my lower spine again.

    Encountered multiple episodes where I'm suddenly out of breath during rest. The behaviour you see after taking a sprint, but I haven't done anything like that.

    5 red dots with diameter 2-3 mm appeared on the upper palm of my right hand a few cm equally distant apart. Went away after one week. Same thing?

    November 2020

    Startled by one loud bang from a firecracker that someone threw. I felt physically better immediately.
    Hair getting thin and slightly less hair growth at area, front of my head.

    December 2020

    Starting pyridostigmine

    januari 2021

    Stressful period-->intestines are upset, same spot as pineapple trigger. Gut pain-->led to muscle weakness and nausea.
    Jan31: Drank 0.5 L water with salt and a few drops of citric acid in the morning. 1 hour later water was coming out on toilet, no absorption.  21:00 hour, temperature below freezing point--->muscles working better, good typr of muscle pain in quadriceps was present after picking something up from ground.

    Februari 2021

    Smell outside of POIS is ~5-10% ~24h/day (happened only during POIS in the past) sometimes a flare of increased smell and other times no smell at all. Lower libido, Orgasm is absent during ejaculation. Wax and waning fluctuations of activity at a spot close to the brainstem. Lower back problems still present. Still reactive to stress. Starting intake of Cromolyn Sodium.

    March 2021

    Very cold for the time of the year:

    Went outside. The cold induced some kind of cardiovascular event where segments of the main artery started to constrict and relax back and forth per segment. It affected my heart rate which became irregular and induced irregular breathing. This went on for at least a min.

    Went outside. Felt cold and couldn’t get warm. Hands turned blue. Impaired circulation everywhere especially limbs. Pumping power of heart decreased.

    Measured blood pressure. One pulse of blood got stuck on my bicep with pain for a moment while aircuff was wrapped around it and eventually got through. It left a bump on my bicep. No discoloration, hard painfull bump.

    Sensitivity to low temperatures has increased this year. It has become a serious cardiovascular trigger. POIS makes me more susceptible (vascular inflammation—->local vascular dysfunction?)

    June 2021: Blood pressure 100/60 sitting

    Make summary of temperature vs parameters.


    2020/2021 Age 35: I never felt so many (frequency) fluctuations throughout my entire brain as at this age.


    Developing insights

    Release of pre-ejaculate induces local symptoms in the genitourinary tract which spreads outward and becomes systemic (only noticed this dynamic after desensitization). Certain hotspots react more intense like the border of groin area and upper leg (injury age 18) once it reaches that area. I now come to think of it that the spot may be related to injury to local blood vessels, in fact, I start to suspect that many old and current injuries are related to blood vessel injuries/lesions.
    Immune reaction--->damage to blood vessels--->cardiovascular dysfunction. I get the impression that the (local) dysfunctional vascular system due to the history of inflammation is not able respond properly to orgasm as in over excitation aside from contact reaction to (pre)-ejaculate. The 'injury' discussed above is one of the first symptoms that arose before hell broke loose.

    The upper leg/groin hotspot can react at the same time in a similar way as the area in mid lower spine. The latter could be blood vessel related as well. If POIS is auto-immune then it's probably targeting blood vessels/connective tissue. Hotspots in the body seem to be more sensitive to other triggers as well. Even out of POIS the cardiovascular system is rarely calm; local spams, feel of friction blood flow, local pressure fluctuations, these hop around they don't stay in one spot. Mast cells are present in the lining of blood vessels as well.

    Increased orthostatic intolerance induced by stress or POIS could be due to low levels of norepinephrine.
    « Last Edit: June 09, 2021, 02:21:35 PM by Muon »


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    Re: Muon's Case
    « Reply #5 on: December 16, 2019, 04:26:29 PM »


      Sympathetic overactivity or parasympathetic underactivity (Dysautonomia)
      Mast cell activation disorder/cascade/hyperresponsive mast cells
      Hyperpermeability/barrier dysfunction in genitourinary system (connective tissue problems)
      Th2 response
      Regulatory T cell dysfunction or abnormal numbers
      Type IV Hypersensitivity
      Denervation supersensitivity
      Edit 18-8-23: Involvement of area in the middle of the head (guess: brainstem/pons)
      Edit 18-8-23: Involvement of neural networks (autonomic & sensory pathways)


      Mast cell activation disorder:
      Evidence of Mast Cell Activation Disorder in Postural Tachycardia Syndrome (P1.277)

      ''Triggering events include long-term standing, exercise, premenstrual cycle, meals, and sexual intercourse''
      Hyperadrenergic Postural Tachycardia Syndrome in Mast Cell Activation Disorders

      A New Disease Cluster: Mast Cell Activation Syndrome, Postural Orthostatic Tachycardia Syndrome, and Ehlers-Danlos Syndrome

      Autoimmunity/Viral illness
      Autoimmune Basis for Postural Tachycardia Syndrome

      HPV vaccines:
      Human Papillomavirus Vaccine and Postural Orthostatic Tachycardia Syndrome: A Review of Current Literature.

      SIBO and POTS?
      Successful treatment of postural orthostatic tachycardia and mast cell activation syndromes using naltrexone, immunoglobulin and antibiotic treatment

      Transport-mediated choline deficiency:
      Mechanism of choline deficiency and membrane alteration in postural orthostatic tachycardia syndrome primary skin fibroblasts

      Vascular Endothelial Dysfunction (abnormal sheer stress/NO response to acetylcholine & heat)
      Cutaneous neuronal nitric oxide is specifically decreased in postural tachycardia syndrome

      Decreased Microvascular Nitric Oxide?Dependent Vasodilation in Postural Tachycardia Syndrome

      Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome

      Relation between Endothelial dysfunction and autonomic nervous system dysfunction
      The Relationship between Vascular Function and the Autonomic Nervous System

      C-fiber involvement:
      Small-fiber neuropathy with cardiac denervation in postural tachycardia syndrome.

      POTS + CFS

      Autonomic Nervous System Dysfunction in Adolescents with Postural Orthostatic Tachycardia Syndrome and Chronic Fatigue Syndrome Is Characterized by Attenuated Vagal Baroreflex and Potentiated Sympathetic Vasomotion

      Bell's Palsy

      Immunological concept/mast cell activation/hypersensitivity:
      Immunological Concept for Bell's Palsy

      An immunological concept for bell's palsy ? Experimental study**

      Infection theory:
      Frequent detection of Mycoplasma pneumoniae in Bell's palsy.

      Hormonal metabolic changes?:
      Familial juvenile onset of Bell?s palsy

      Impairment of microcirculation of the facial nerves:

      Blood viscosity:
      Bell?s Palsy and Viral Infections

      Elevated Serum Interferon Levels in Patients With Bell's Palsy

      Recurrent Bell’s Palsy During Takeoff on a Commercial Flight: A Case Report


      Disturbance to cholinergic pathways/vascular endothelial dysfunction
      Prolonged acetylcholine?induced vasodilatation in the peripheral microcirculation of patients with chronic fatigue syndrome

      Premature Ejaculation

      Autonomic nervous system dysfunction in lifelong premature ejaculation: analysis of heart rate variability.

      The Role of Brain Derived Neurotrophic Factor in Etiology of Premature Ejaculation

      ''Our study indicates that premature ejaculation is significantly related with a higher level of seminal NO.''
      Relevance of seminal plasma nitric oxide levels and the efficacy of SSRI treatment on lifelong premature ejaculation

      ''From these results it can be concluded that PE occurs because decreased levels of serotonin. Decreased levels of serotonin are associated with increased levels of IFN-g.'':
      Flouxetine improved intravaginal ejaculatory latency time through decreased levels of interferon-gamma and increased levels of serotonin in patient with premature ejaculation

      Elevated IFN-g/Th1 polarization

      "It is consistently observed that mast cells [8] and mast cell-derived exosomes preferentially induce Th1-type responses as evidenced by the production of IL-2, IFN-g and IL-12 by activated lymphocytes."
      Nonspecific B and T Cell-Stimulatory Activity Mediated by Mast Cells Is Associated with Exosomes

      Latent Viral Infection:

      Polarization switch from Th2 to Th1 due to desensitization?

      Temporary IFN-g decrease after orgasm

      Mast Cells to Dendritic Cells: Let IL-13 Shut Your IL-12 Down

      1)Mast cell activation -> PGD2 -> activation of CRTH2 on Th2 cells -> Th2 response -> decreased IFN-g
      2)Th2 response -> induction of IgG4 -> dampening of Th2 response -> Stops IFN-g decrease
      (T-regs might play a role in this)

      Th1 polarization + IL-8

      The delayed-type hypersensitivity reaction is dependent on IL-8. Inhibition of a tuberculin skin reaction by an anti-IL-8 monoclonal antibody.

      Human Cathelicidin Peptide LL-37 (need ref)

      Interferon-g enhances both the anti-bacterial and the pro-inflammatory response of human mast cells to Staphylococcus aureus


      "Importantly, Treg exert a direct effect on B cells, suppressing the production of allergen-specific IgE and inducing IgG4"
      Role of Treg in immune regulation of allergic diseases

      Growth hormone and insulin-like growth factor I induce immunoglobulin (Ig)E and IgG4 production by human B cells.

      Nerve growth factor specifically induces human IgG4 production

      Potential drivers: IL-4, IL-5, IL-10, IL-13 (MC), IL-21, Follicular helper T cells, TGF-beta, expanded Tregs, IL-33?.

      Mast cells have been suggested as an altenative source of TH2 cytokines, based on their colocalization with IL-4 and IL-13 in IgG4-RD lesions from salivary glands. Page 62: Ref

      "Thus, our results do not support the hypothesis that T cells express the cytokines associated with IgG4-related disease; rather, our data indicate that mast cells are the source of these upregulated cytokines."
      T helper 2 and regulatory T-cell cytokine production by mast cells: a key factor in the pathogenesis of IgG4-related disease

      Hyper-IgG4 disease: report and characterisation of a new disease

      What's your diet like anyway?

      I don't eat any refined grains or sugars, though I do eat fruit and plenty of whole grains. My last IGG4 test showed a pretty strong candida response, which my physician said means I had an overgrowth at some point.

      IL-8 (CXCL8)

      Central sensitization

      CRH-->mast cell activation
      Substance P (SP) Induces Expression of Functional Corticotropin-Releasing Hormone Receptor-1 (CRHR-1) in Human Mast Cells

      Mast Cell–Mediated Stimulation of Angiogenesis

      Drop in IL-8: Combine
      Specificity of the neuroendocrine response to orgasm during sexual arousal in men
      Neuroendocrinology of mast cells: Challenges and controversies.

      Increased gut MCs:
      Comparative evaluation of Inflammatory cells and Interleukins in Irritable Bowel Syndrome subtypes

      Essential involvement of interleukin?8 in acute inflammation

      IL-33 (table 4)
      Recent advances in our understanding of mast cell activation - or should it be mast cell mediator disorders?

      LPA ---> LPA2 receptor, table 1:
      Non-IgE mediated mast cell activation

      "Stromal cell-derived factor-1 alpha (SF-1?) selectively produced IL-8 from human mast cells without degranulation as well. Activation of human cultured mast cells by CD30 ligands led to release of the chemokines IL-8 and MCP-1 without histamine and without degranulation. IL-33 induced IL-13 release independent of IgE stimulation" Ref

      IL-13 can induce IgE and IgG4. IL-33 can induce IL-13 and IL-8.
      Brother: Elevated IgE and IL-8. Me: Elevated IgG4 and IL-8. Thus IL-33 is a potential candidate.

      "Stimulated T cells were found to generate microparticles that induce degranulation and cytokine (IL-8 and oncostatin M) release from human mast cells. Mast cell activation by T cell microparticles involved the MAPK signaling pathway." Ref

      "We recently reported that extracellular vesicles are increased in the serum of children with ASD, contained mtDNA and stimulated cultured human microglia to secrete the pro-inflammatory molecules IL-1? and CXCL8 " Ref

      Candida Albicans and mast cells (?-Hexosaminidase?):

      OxLDL and mast cells:

      Weakness in upper legs (+spasms) worsen with high temperature, standing, POIS and stress. Relief with exercise, laying down, bending forward.

      P/Q-type VGCC antibodies? As in
      Spinal stenosis? (pressure in lower back as well)

      Female family members and decrease/increase of symptoms in pregnancies/menstrual cycle period

      Neuroimmunoendrocrine disorder:
      ''These results suggest that mast cell secretion may be regulated by progesterone and may explain the reduced symptoms of certain inflammatory conditions during pregnancy.''
      Progesterone Inhibits Mast Cell Secretion

      Progesterone triggers selective mast cell secretion of 5-hydroxytryptamine

      Role of female sex hormones, estradiol and progesterone, in mast cell behavior

      Shift in Th1/Th2/Th17 balance:
      Inflammation and Pregnancy

      REVIEW ARTICLE: Th1/Th2/Th17 and Regulatory T?Cell Paradigm in Pregnancy

      Microbial changes during pregnancy:
      Microbial Changes during Pregnancy, Birth, and Infancy

      Diabetogenically beneficial gut microbiota alterations in third trimester of pregnancy


      Normal human pregnancy is associated with an elevation in the immune suppressive CD25+ CD4+ regulatory T-cell subset

      Progesterone Increases Systemic and Local Uterine Proportions of CD4+CD25+ Treg Cells during Midterm Pregnancy in Mice

      Membrane progesterone receptors in human regulatory T cells: a reality in pregnancy

      "Hepatic synthesis of corticosteroid-binding globulin more than doubles in pregnancy; that is, bound plasma cortisol in term pregnancy is approximately 2 to 3 times that of nonpregnant women"

      hCG goes up as well during pregnancy.

      Vagal tone during pregnancy???

      Plasma Levels of the Endocannabinoid Anandamide in Women—A Potential Role in Pregnancy Maintenance and Labor?

      Progesterone--->cardiovascular protective effects
      Progesterone--->Tight junction proteins?

      Idiopatic miscarriage

      Treg cells in pre-eclampsia, miscarriage and infertility

      "In spite of MC heparin content, MCAD-induced coagulopathy (67) may spur placental microthrombi, preventing nidation or disrupting embryonic blood supply and threatening miscarriage" Ref

      Burning sensation in vagina upon contact with semen in mother

      Manifestations of immune tolerance in the human female reproductive tract

      Low NK cell count

      Decreased Expression of the CD57 Molecule in T Lymphocytes of Patients with Chronic Fatigue Syndrome

      Stress, beta-AR activation:
      Adrenergic regulation of innate immunity: a review

      Decreased Alpha-2-globulin

      High MMP 2 or 9 --> joint pain, which can bind to alpha-2-macroglobulin which is a subset of Alpha-2-globulin.

      Accelaration of frequency and intensity of symptoms during period of exercise/sports on daily basis

      The open window of susceptibility to infection after acute exercise in healthy young male elite athletes[/list]


      The correlation between the Th17/Treg cell balance and bone health (IFN-g inhibits osteoclast formation)

      Carpal Tunnel Syndrome

      Vasomotor dysfunction in carpal tunnel syndrome

      Pathophysiology of Carpal Tunnel Syndrome
      « Last Edit: October 16, 2023, 07:45:42 AM by Muon »


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        • MCAD Thread
      Re: Muon's Case
      « Reply #6 on: December 16, 2019, 04:28:14 PM »

      Spinal MRI and reminder to look for spinal findings in more patients (including MCAS):

      5.- Magnetic Resonance Imaging of the entire spine(June 2018):
           multiple focal lesions were observed in the dorsal and lumbar spine, hyperintense in T2 and most of them isointense in T1, although the larger lesions have a trabecular structure suggesting that they are hemangiomas. However, given that the signal characteristics in the T1 sequence are not typical of hemangioma, it is recommended to do image control to assess evolution.

      Translated with Google Translate from Maxwell of Russian POISCenter

      If you read my conclusion after the MRI of the "lumbosacral spine", you can find words like "the anterior and posterior longitudinal ligaments are compacted", which means the so-called "Ossification" written here -svyazki-grudnogo-otdela-pozvonochnika and here
      ... squeezes the spinal vertebral nerve ...

      Ossification of the posterior longitudinal ligament of the thoracic spine is a permanent neurological disorder in which the nerves of the spinal canal are compressed as a result of hardening of the posterior longitudinal ligament, the purpose of which is to preserve the structure of the vertebrae in the spine, maintaining its balance and mobility. Including South Korea, in China, Japan and other Asian countries, this disease more often occurs in men over 40 years of age, which must be treated at an early stage due to the impossibility of restoring the functions of the damaged nerve if it is compressed for a long period.

      Myelopathy is a dysfunction of the spinal cord associated with abnormal pressure on the spinal cord. Unlike conditions that put pressure on individual nerve roots, this type of damage can lead to loss of nerve function anywhere in the spinal cord below the damaged area.

      Chymase and cardiovascular problems:
      Contributions of ACE and mast cell chymase to endogenous angiotensin II generation and leucocyte recruitment in vivo

      In vivo, Ang II is primarily generated by ACE under basal conditions, but in inflammatory conditions, the release of MCP amplifies local Ang II concentrations and the associated inflammatory process. Thus, AT1 receptor antagonists may be more effective than ACE inhibitors for treating ongoing Ang II-mediated vascular inflammation."

      Pressure Overload–Induced Transient Oxidative Stress Mediates Perivascular Inflammation and Cardiac Fibrosis through Angiotensin II

      Targeting Cardiac Mast Cells: Pharmacological Modulation of the Local Renin-Angiotensin System

      Chymase cleaves prescursors of Endothelin and MMPs. Endothelin is mentioned in Bell's palsy.

      Bell's palsy?:

      POIScenter member:
      I feel exhausted after fetching drinks from the shop, carrying up a lot of stuff...
      I can barely stand, want to just lie flat on the couch (yay for home office..)

      Then I eat a salami sausage and drink one of those and I'm completely normal again:

      The stuff is really magical. I really believe that it pushes all the liquid and minerals directly into your body.

      wheat beer also contains Uridine btw.

      Paper dump section

      A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

      Balancing tissue homeostasis and inflammatory responses against Candida albicans infections: is it a matter of mast cells' immunological memory?

      Gut fungi in irritable bowel syndrome : A painful recognition

      Is burning semen syndrome a variant form of seminal plasma hypersensitivity?

      Is skin testing reliable for confirming sensitization to seminal fluid proteins?

      Review of flavonoids: A diverse group of natural compounds with anti-Candida albicans activity in vitro

      Immunodominant Semen Proteins III: IgG1 and IgG4 Linkage in Female Immune Infertility

      Patients with chronic prostatitis/chronic pelvic pain syndrome show T helper type 1 (Th1) and Th17 self?reactive immune responses specific to prostate and seminal antigens and diminished semen quality

      IgG4 breaking the rules

      Immediate hypersensitivity to seminal fluid and atopic dermatitis

      "Serum from the husband and nonrelated men also contained antigen that provoked histamine release from the patient's leukocytes in vitro. The antigen in serum was associated with the globulin fraction and had a temporal relationship to ejaculation, appearing within 12 hours of ejaculation and disappearing within four days."

      It's an antigen for the woman's leukocytes but circulates in the serum of men up to 4 days? Just like the timing seen in POISers.

      A new manifestation of seminal fluid hypersensitivity

      Manifestations of immune tolerance in the human female reproductive tract

      Human seminal plasma allergy: a review of a rare phenomenon

      -mefenamic acid, 500 mg 2 h before intercourse and every 4 h thereafter as needed.
      -tranexamic acid abolished the symptoms

      The seminal fluid of the partner of one of these three patients also contained IgE reactive with Candida albicans.

      A comprehensive characterization of the peptide and protein constituents of human seminal fluid

      Selective desensitization to seminal plasma protein fractions after immunotherapy for postcoital anaphylaxis


      Low-Dose IL-2 Induces Regulatory T Cell–Mediated Control of Experimental Food Allergy

      Targeting IL-2: an unexpected effect in treating immunological diseases

      Androgen receptor modulates Foxp3 expression in CD4+CD25+Foxp3+ regulatory T-cells


      Successful treatment of Post-orgasmic illness syndrome with human chorionic gonadotropin

      Case of post-orgasmic illness syndrome associated with hypogonadism.

      Neuroendocrinology of mast cells: Challenges and controversies.

      Low tryptophan brother:
      Low-dose IL-2 therapy compensates for metabolic shifts and reverses anxiety-like behavior in PD-1 deficiency-induced autoimmunity


      Tried ~4 types of antihistamines. Only clemastine/Tavegyl had a minor effect. "Clemastine does also act as FIASMA (functional inhibitor of acid sphingomyelinase)".


      Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – Evidence for an autoimmune disease

      Blood test reference ranges:

      Wrinkled finger test, dysautonomia:

      Brother IL-17, tryptophan:
      Candida albicans Dampens Host Defense by Downregulating IL-17 Production

      Oral candida infection:
      IL-17-mediated antifungal defense in the oral mucosa is independent of neutrophils

      Gastrointestinal Candida colonisation promotes sensitisation against food antigens by affecting the mucosal barrier in mice

      IL-9 and Mast Cells Are Key Players of Candida albicans Commensalism and Pathogenesis in the Gut

      Involvement of Cervical Muscle Lesions and Autonomic Nervous System in Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS


      Potential neuro-immune therapeutic targets in irritable bowel syndrome

      Hormone regulation via vagus nerve, what hormones?

      Metabolic and Epigenomic Regulation of Th17/Treg Balance by the Polyamine Pathway

      "there was a trend towards a decrease in IFN-g, IL-17 and TNF production with an increase in IL-9 production in response to antigen"

      Fungal infection in cerebrospinal fluid from some patients with multiple sclerosis

      Nightingale had a candida infection:
      It was partially my fault, because I was in the midst of treating my candida infection and went overboard with antifungals and probiotics, making me feel terrible and compromising my immune system.  On top of that, I was surrounded by family who probably brought all sorts of germs with them.

      Adenosine receptor mediated stimulation of intracellular calcium in acutely isolated astrocytes

      Potential involvement in exercise intolerance:

      Acute Peripheral Facial Palsy: Recent Guidelines and a Systematic Review of the Literature (2020)

      New Insights on the Role of TRP Channels in Calcium Signalling and Immunomodulation: Review of Pathways and Implications for Clinical Practice


      Papers about opioid receptors and immune system. MOR activation leads to T-cell inhibition.
      respiratory depression: (also depression)
      Mu opioid withdrawal and psychosis link?
      Paper about stress increasing TLR in brain.

      Filter out some stuff later:
      Stabilization of Perivascular Mast Cells by Endothelial CNP (C-Type Natriuretic Peptide)

      Nox inhibition:
      A Role for Nox Inhibition in Coronavirus Infection

      Can't unlock, try later:
      The role of intestinal mast cell infiltration in irritable bowel syndrome (2021)


      Cytokine driven muscle loss:

      Cytokines and cachexia
      Geriatric cachexia: the role of cytokines
      Waste management—Cytokines, growth factors and cachexia



      As a ligand for the orphan G protein-coupled receptor GPR35 (cromolyn acts on GPR35)
      increased levels were associated with confusion and psychotic symptoms


      Free blood gases analysis [Netherlands]

      "Do you know about the correlation of serum phosphate and respiratory alkalosis? The respiratory alkalosis somehow makes a loss of phosphate"
      Emootje1973's results (CFS and POTS):
      Plasma Volume: 40ml/kg (87% of normal)
      ANP: 116.3 pg/ml (9-68 pg/ml)
      Aldosteron: 0.37 nmol/L (0.08-0.44 nmol/L)
      Norepi: 4.4 nmol/L (0.4-3.0 nmol/L)

      The Clinical Efficacy of Pollen Extract and Vitamins on Chronic Prostatitis/Chronic Pelvic Pain Syndrome Is Linked to a Decrease in the Pro-Inflammatory Cytokine Interleukin-8

      Recently, Moriyama et al. have reported that murine ILC2s express high levels of b2-adrenergic receptor (b2AR) (62) and the treatment with b2AR agonist (salmeterol) inhibits IL-33-induced IL-5 and IL-13 production of ILC2s

      Therapeutic Strategies for Targeting IL-33/ST2 Signalling for the Treatment of Inflammatory Diseases

      This enzyme catalyses the following chemical reaction: (R)-lactate + NAD+ <----> pyruvate + NADH
      Page 52/61 from the file you provided:
      "NOTE: The presence of Candida in the GI tract diverts Pyruvate away from its preferred pathway (Kreb's Cycle), and results in less cellular energy."
      I wonder whether blocking pyruvate decarboxylase helps.


      She has a similar exercise intolerance as me. I had an iron deficiency as a kid, her iron levels fell down when symptomatic. She reaches an orgasm fast, I got PE. She started to react to Vit B Complex, same for me.
      Her CRP was high during gut symptoms. Similar situation for my mother, high CRP and gut.
      My uncle did get skin reactions from the water of chlorinated swimming pools.
      However, due to covid, we started using bleach at home for general cleaning, and I developed some kind of reaction to it. It took me months to figure out that bleach was the cause, and it completely short-circuited everything in my body: I've had tachicardia, a continuous horrible feeling of shortness of breath,  dizziness, loss of appetite, fever... somehow, I know this is all related to POIS, because I'm not allergic to bleach.

      Evaluation of immune response after moderate and overtraining exercise in wistar rat



      I've always noticed after drinking milk I suffer a really minor POIS-like affect (brain fog). Looking into milk, it contains an opiod called casomorphin. Casein has been documented to break down in the stomach to produce the peptide casomorphin, an opioid that acts as a histamine releaser.


      My mother told me that her stomach feels better upon contact with raw milk kefir.
      Gastroprotective effect of kefir on ulcer induced in irradiated rats

      Side Note: MMP-2 and 9 are MC mediators.
      "which were accompanied by a significant decrease in the mucus content, the stomach GSH level, the GSH-Px activity and DNA damage. Pre-treatment with kefir milk exert significant improvement in all the tested parameters."

      I'm homozygous for the GST and GPX genes which are the glutathione enzyme genes that detox chemicals, liposomal glutathione would be helpful for you.

      Vit D link:


      "During an immune response, CD4+ T cells are activated and proliferate, and their metabolism adjusts to fulfill increased bioenergetic and biosynthetic demands. For example, activated effector CD4+ T cells are highly glycolytic and use aerobic glycolysis and oxidative phosphorylation (OXPHOS) for proliferation"
      Niacin: NAD+ --> NADH
      ADP + PO4 <--> ATP + H2O
      Immune response --> increased pyruvate, decreased NAD+, decreased Phosphate

      Pathogens Hijack Host Cell Metabolism: Intracellular Infection as a Driver of the Warburg Effect in Cancer and Other Chronic Inflammatory Conditions


      Chronic mild stress induces anhedonic behavior and changes in glutamate release, BDNF trafficking and dendrite morphology only in stress vulnerable rats. The rapid restorative action of ketamine

      Decreases in peripheral-type benzodiazepine receptors in postmortem brains of chronic schizophrenics

      Peripheral?type benzodiazepine receptors in anxiety disorders


      Cellular stress-sensing kinase Target Of Rapamycin Complex 1 (TORC1)


      Long standing low grade (oral) mucosal inflammation/activation.
      Sometimes I can wake up with a well-developed layer of mucus in oral cavity. Thickness will be decreased withing a few minutes. Consuming food while layer is intact will give no contact sensitivity, friction or irritation. Consuming food while layer is diminished will induce symptoms. Not eating will still give a sense of low grade activation (has to do with wake and sleep state, as soon as I wake up subtle activation creeps in). Stress will induce or increase sense of activity in mucosal layer and makes me more reactive to food upon contact.

      Intestinal B cell-activating factor: an indicator of non-IgE-mediated hypersensitivity reactions to food?
      Food Intolerance of Unknown Origin: Caused by Mucosal Inflammation? A Pilot Study
      Intestinal Epithelial Barrier Dysfunction in Food Hypersensitivity
      Food intolerance and mucosal inflammation


      Intestinal B cell?activating factor: an indicator of non?IgE?mediated hypersensitivity reactions to food?

      Hyperexpression of CD40 ligand by B and T cells in human lupus and its role in pathogenic autoantibody production

      Androgen-Mediated Anti-inflammatory Cellular Processes as Therapeutic Targets in Lupus

      Stress-->CRHR on B-cells-->mucosa?

      Immunophenotypical Characterization of a Brazilian POIS (Post-Orgasmic Illness Syndrome) Patient: Adding More Pieces to Puzzle
      "The majority of these cells are expressing CD38+, which suggests that the activation in this patient is more likely to happen via the CD38 molecule and there is no clinical explanation to that finding"

      Seminal CD38 is a pivotal regulator for fetomaternal tolerance


      Neurological and spinal manifestations of the Ehlers–Danlos syndromes

      platelet storage pool deficiency:

      Abnormal circulation head/body, something I dealt with (CSF as well?):
      ME/CFS at the Intersection of the Nervous & Immune Systems (Lecture) - Michael VanElzakker, PhD


      Stress, mTOR, ER proteins-->danger signal
      Cell-Based Blood Biomarkers for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome


      More Igg4 stuff:
      LGALS3 inhibits B-cells differentiating into immunoglobulin secreting plasma cells.
      High Expression of Galectin-3 in Patients with IgG4-Related Disease: A Proteomic Approach
      Autoantibodies to autoantigens:
      The front line of research into immunoglobin G4-related disease - Do autoantibodies cause immunoglobin G4-related disease?

      Biomarkers in IgG4-related disease: A systematic review


      POIS & Connective tissue
      Early march 2021: There is emphasis on tissue that sits close to bone. Release of a drop of seminal fluid activates surrounding tendons/connective tissue rapidly. Mechanical stress does something similar as well as heat. Connective tissue: A body-wide signaling network?
      Interactions between Mast Cells, Fibroblasts and Connective Tissue Components
      Chondroitin sulphate inhibits connective tissue mast cells
      Sympathetic dominance ---> reduced connective tissue blood flow?


      Furthermore, an increase in anti-flagellin antibodies has been observed in PI-IBS patients:
      Microbiome, antibiotics and irritable bowel syndrome
      Some have suggested that this is indicative of an exaggerated immune host-microbial response due to underlying increased epithelial permeability.35 Supporting this concept is the finding of increased pro-inflammatory cytokines, including interleukin (IL)-6, IL-8 and tumour necrosis factoralpha in IBS patients.


      I have been using lidocaine spray already for half year. It helps me a lot. It reduce all my symptoms for 95%. I just  feel sleepy next day a bit. I spray it to penis head 30 minutes before sexual activity. There is just one problem.If you had some night dream, tiny amount of liquid (which seems like cum) may appear. And i think it does not influence me. Anybody tried it?
      When injected near nerves, the nerves cannot conduct signals to or from the brain. Lidocaine alters signal conduction in neurons by prolonging the inactivation of the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for action potential propagation


      Had repeatedly inflammatory flares at a few locations. Especially muscles at left shoulder blade area and in ~2019/2020 focus at lower back right next to spine. Those muscle don't feel smooth when moving and make sound, they feel harder as in some sort of stiffness.

      Tissue at the groin areas never recovered since age 19. They are quickly overloaded when applying force/pressure. They also start to feel hard the more I move, as in walking. You can feel friction-->more friction-->loss of firmness/less functional.  That tissue gets affected quickly by POIS, as well as heat. It leads to fatigue when I keep walking around with these symptoms.


      Is postural orthostatic tachycardia syndrome (POTS) a central nervous system disorder?

      IDO: a double-edged sword for TH1/TH2 regulation

      Brainstem, limbic system:
      The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings

      Poiscenter member Fox improved by gluten free diet. He feels there is sympathetic activation upon standing. The two could be linked.



      Keto POISers skip glycolysis:

      Among the varied consequences of increased CD38 expression, the implications of a substantial decline in NAD+ levels on the inflammatory response and the outcome on the course of infection offer an open area for exploration. Different studies have indeed generated discrepancies in regard to the effects of NAD+ depletion on inflammatory pathways. For example, a decrease in intracellular NAD+ through different mechanisms correlated with activation of the inflammasome in murine macrophages and the administration of exogenous NAD+ counteracted these effects.

      Immunophenotypical Characterization of a Brazilian POIS (Post-Orgasmic Illness Syndrome) Patient: Adding More Pieces to Puzzle
      "The majority of these cells are expressing CD38+, which suggests that the activation in this patient is more likely to happen via the CD38 molecule and there is no clinical explanation to that finding"

      His monocytes could have trouble responding properly to bacterial infection:
      Low Cellular NAD+ Compromises Lipopolysaccharide-Induced Inflammatory Responses via Inhibiting TLR4 Signal Transduction in Human Monocytes

      CD38 and ANS:
      ?-NAD and CD38 provide a novel mechanism of autonomic nervous system control of vascular and visceral smooth muscle

      Novel localization of CD38 in perivascular sympathetic nerve terminals




      Na =nicotinic acid
      NMN = Nicotinamide mononucleotide
      NR = nicotinamide ribose
      NAM = nicotinamide
      NAD = Nicotinamide adenine dinucleotide NAD exists in two forms: an oxidized and reduced form, abbreviated as NAD+ and NADH (H for hydrogen) respectively.
      NADPH is the reduced form of NADP+

      Revisiting B cell tolerance and autoantibodies in seropositive and seronegative autoimmune rheumatic disease (AIRD)



      Endothelial inflammation

      New Markers of Inflammation and Endothelial Cell Activation

      Diagnostic and prognostic blood biomarkers in vascular dementia: From the viewpoint of ischemic stroke

      Cerebral Small Vessel Disease: A Review Focusing on Pathophysiology, Biomarkers, and Machine Learning Strategies

      Small vessel disease

      New Treatment Approaches to Modify the Course of Cerebral Small Vessel Diseases

      Pharmacological Treatment and Prevention of Cerebral Small Vessel Disease: A Review of Potential Interventions

      Response of Norepinephrine and Blood Pressure to Stress Increases With Age


      High progesterone levels are associated with family history of premature coronary artery disease in young healthy adult men

      Progesterone: the forgotten hormone in men?

      Endogenous Progesterone and the Exogenous Progestin Norethisterone Enanthate Are Associated with a Proinflammatory Profile in Healthy Men

      Progesterone Triggers Selective Mast Cell Secretion of 5-Hydroxytryptamine

      Regulation of the immune response to Candida albicans monocytes and progesterone

      Demonstration of progesterone receptor mediated gonadotrophin suppression in men

      Progesterone Reduces Sympathetic Tone without Changing Blood Pressure or Fluid Balance in Men

      Serum ionized magnesium and calcium and sex hormones in healthy young men: importance of serum progesterone level

      NK Cells Expressing a Progesterone Receptor Are Susceptible to Progesterone-Induced Apoptosis

      Progesterone: The neglected hormone in schizophrenia? A focus on progesterone-dopamine interactions

      Estrogen and progesterone receptors in vessel walls: Biochemical and immunochemical assays

      The Influence of Estrogen and Progesterone on Aldosterone Excretion

      Effect of progesterone on aldosterone secretion in rats

      Adiponectin increases insulin-like growth factor I-induced progesterone and estradiol secretion in human granulosa cells

      Progesterone Level Predicts Serotonin-1A Receptor Binding in the Male Human Brain

      Progesterone and estrogens in rat brain: Modulation of GABA (gamma-aminobutyric acid) receptor activity
      « Last Edit: April 17, 2021, 04:31:53 PM by Muon »


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        • MCAD Thread
      Re: Muon's Case
      « Reply #7 on: December 16, 2019, 04:29:15 PM »
      In male patients with cytochrome P450C17 (steroid 17a-hydroxylase/17,20-lyase; EC deficiency, the progesterone levels are clearly elevated.
      It has 3 cofactors: NADH, NADPH, and Heme


      Smoldering Inflammation in Cardio-Immune-Metabolic Disorders

      Osteopontin produced by several immune cells, endothelial cells, and fibroblasts, is involved in cardiovascular diseases (Abdelaziz Mohamed et al., 2019; Vianello et al., 2020). Moschetta et al. reported that osteopontin is linked to pathological dysregulation of the arginine pathway in patients with coronary artery disease.

      Relationship Between Plasma Osteopontin and Arginine Pathway Metabolites in Patients With Overt Coronary Artery Disease


      Discussion one post back about tissue at groin area might just be an artery that gives problems.

      Method for the treatment of CFS using an inhibitory or cytotoxic agent against plasma cells


      fluoroquinolone class and hBD2 (member Bream)

      I'm no longer going to reply on this thread as it's really long but yeah it's possibly some kind of pathogen that gets triggered by the fluoroquinolone class of antibiotics.

      I'm still not recovered 3 years after the Ciprofloxacin, I've learnt to change my diet and that minimises my symptoms. I'm now very intolerant to strange things like sea salt and coffee so I have to be careful what I eat.

      My Cipro issues are located in very specific areas of my body, like only one leg has some burning sensation, one ear has tinnitus, one hand has lost some of the fat padding. My working theory is maybe it's a systemic candida infection, I'm still looking for a cure.
      Vitamin D, Testosterone, Epigenetics and Pain an Evolving Concept of Neurosignaling, Neuroplasticity and Homeostasis

      Vitamin D Deficiency Reduces Vascular Reactivity of Coronary Arterioles in Male Rats

      Neuroendocrine control of male reproductive function. The opioid system as a model of control at multiple sites

      The role of vitamin D in autoimmune diseases: could sex make the difference?

      Mast cells drive pathologic vascular lesions in Takayasu arteritis

      Intestinal epithelial barrier function and tight junction proteins with heat and exercise

      Extracellular Vesicles

      The role of exosome in autoimmune connective tissue disease

      Recent advances in Extracellular Vesicles and their involvements in vasculitis

      The emerging roles of exosomes in autoimmune diseases, with special emphasis on microRNAs in exosomes

      The Role of Extracellular Vesicles in the Pathogenesis and Treatment of Autoimmune Disorders

      Abstract 14723: Autoreactive T Lymphocytes Activate Cardiac Endothelium Independently of Tnf-? and Cause Endothelial Dysfunction Through Exosomes in Experimental Autoimmune Myocarditis

      Exosome-mediated inflammasome signaling after central nervous system injury

      Exosome in intestinal mucosal immunity


      Neurogenic orthostatic hypotension: roles of norepinephrine deficiency in its causes, its treatment, and future research directions

      suggesting ‘denervation supersensitivity.’
      Pharmacologic distinction of different orthostatic hypotension syndromes

      Inherited arrhythmias: The cardiac channelopathies

      Interleukin-6 deficiency modulates testicular function by increasing the expression of suppressor of cytokine signaling 3 (SOCS3) in mice
      Am I the only person who has noticed that ACE (Angiotensin-converting enzyme) is implicated in both Covid and POTS? the coronavirus gains access to human cells by plugging its spike proteins into the ACE receptors. ACE receptors are particularly prevalent in the lungs. Well, POTS patients often have altered levels of ACE in their blood plasma. Do we also have higher or lower numbers of ACE receptors? I don't know, but it would seem like having more ACE receptors would make you more vulnerable to the virus and having less ACE receptors would make you less vulnerable to the virus.  I am surprised no one else has commented on this yet on Dinet.

      Sigma receptors

      Factors that increase Atrial Natriuretic Peptide (ANP) secretion
      « Last Edit: July 27, 2021, 02:50:19 PM by Muon »


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      MEDS/supplements that could be tested

      Quercetin phytosome + bromelain + chondroitin sulfate
      Nicotinamide riboside (Niagen)
      Slow release nicotinamide
      Ivabradine (cardiac, Purkinje cells, funny channels)
      Larazotide acetate
      L-glutamine high dose
      Nimodipine (blood flow brain)
      Oregano oil
      Lactobacillus rhamnosus GG (LGG)
      Tryptophan/serotonin related supplements
      Rifaximin (if + on SIBO)
      CBD (highly purified)
      Pure omega 3


      Synergism between luteolin and sulforaphane in anti-inflammation
      Catechin and Caffeine
      « Last Edit: January 06, 2022, 08:34:40 PM by Muon »


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      « Last Edit: December 16, 2019, 05:18:19 PM by Muon »