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POIS Theory Master List

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Post theories/ideas regarding the Pathophysiology of POIS. This thread can function as a central hub. You may dump links to threads from other members in the comment section.

Rudimentary version

* Acute compression proprioceptive axonopathy in the muscle spindles.(1)
* Adenylyl cyclase mediated mechanism: (1), (2) (Note: D1/D2 activates/blocks Adenylyl cyclase)
* Autoimmunity (Extracellular Vesicles, G-protein coupled receptor autoantibodies, adrenergic receptor autoantibodies, dopamine receptor autoantibodies)
* Autoinflammation (activation of NLRP3 inflammasome, Exosome-mediated inflammation)
* Impaired Barrier function: VEGF, tight junction proteins: (zonulin, occludins, claudins, JAMs), leaky gut, IL-33-ST2-ILC2 axis, leukocyte infiltration, collagen defects, protease-activated receptor-mediated epithelial barrier dysfunction
* Brain signal misinterpretation/misfiring
* Brain waves (abnormal response)
* Central and/or peripheral sensitization
* Cerebral blood flow: abnormal orgasm induced cerebral perfusion, altered blood flow to nerves
* Channelopathy: Piezo2, NaV1.5
* Cytokines: Disordered profile, abnormal response, cytokine depression
* Damage-associated molecular pattern (AKA danger signals, alarmin): (IL-33-ST2-ILC2 axis, Stress proteins)
* Dysbiosis (Commensal): Seminal proteome/microbiome, Gut microbiome, gut virome, loss of butyrate producing strains, Gut/Brain axis
* Dopaminergic hypofunction: low level, slow return to baseline, DA/DBH/NE metabolism, loss of dopaminergic neurons, too many dopamine transporters.
* Dysautonomia: Autonomic hyperreflexia, Sympathetic hyperactivity, norepinephrine (transporter) deficiency
* Endocrine: Hypogonadism, Progesterone deficiency
* Endogenous opioid system disorder (Mu-opioid withdrawal, endorphin signaling)
* Endothelial Dysfunction, (Regional) Vasomotor Dysfunction
* Epididymitis
* Excitotoxin Syndrome
* Enzymes: COX, impaired 17-20 lyase activity and 17-a-hydroxylase activity
* Hyperammonia
* Hypersensitivity Type I, II, III, IV (4 subtypes!), V, Type VI. (A48), adrenergic-mediated cellular hypersensitivity
* Intracellular calcium: Decreased post O in lymphocytes
* Limbic deregulation
* Malabsorption
* Mast Cell Activation Syndrome (MCAS), Impaired Glia/Mast cell communication, Genetic disposition, CD117 in GI tract
* (PI3K-Akt-)mTOR activation
* Mechanical: radiculopathy of the sacral spinal nerve roots (SSNR), pinched vagus nerve, (cranio) cervical instability, Atlas Subluxation, nerve root irritation, brainstem compression
* Metabolism: Catecholamines, Histamine (HNMT, DAO), NO/NOS/Arganine, Tryptophan.
* Methylation related problem
* Molecular mimicry
* Mucosal Immunity
* Myofascial Pain Syndrome
* NAD+ or NAD+/NADH ratio: Low--> CD38/NAD+ axis signaling, IDO/TDO induced depletion of Tryptophan.
* Natural killer cell response
* Neuroendocrine response: Abnormal HPA response, Uncoupling between the vagal tone and HPA axis.
* Neuroinflammatory disease (stress mediated + increased stress susceptibility)
* Neurosensory disorder, altered nociception
* Neurotransmitter profile (unique to POIS, Glutamate/GABA etc.)
* Neurotropic Virus Reactivation, Post-Viral Syndrome
* Polyamines: Spermidine and Spermine depletion
* Receptor over/under expression/activation: CD38 (CD4+ freq.), CRH-R1/2 (Mast Cell), alpha1AR/betaAR, H1-4, mu-opioid (PAG neurons), DAR (Immune cells?, D2 autoreceptor), androgen receptor, NMDAR, PAR-2, estrogen receptors, ST2, Sigma receptors, VDR, 5-HT2C/Melanocortin (underweight), 5-HT2A/5-HT2C (Premature ejaculation).
* Ripoptosome activation
* ROS/antioxidant capacity ratio is off--->oxidative state, ROS cascade
* Semen regeneration
* Seminal exosomes: Dysregulated function, Altered content
* Small fiber neuropathy/dysfunction
* Spinal Cord Injury
* Synaptic Fatigue
* Th1/Th2 imbalance
* Transiently Induced Immune Deficiency
* Tregs (self tolerance): Abnormal count, FOXP3+ expression or impaired IL-2/IL-10/TGF-b signaling.
* Tyrosine kinase; abnormal signal transduction
* Low Tryptophan and 5-HT. High IDO1 activity, Kynurenic acid and Quinolinic acid.
* Vagus nerve dysfunction/infection, withdrawal of vagal tone
* Varicocele
* Vitamin D deficiency-associated disorderOr a combination of more than one of the above.

What else?

Reminder: Some ideas might be left inside other threads like POIS paper treatment summary etc.

Reserved 2

Reserved final

POIS Patients are rarely tested for DAMPs:


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