Abstract

Post orgasmic illness syndrome is a rare, mysterious condition with an unknown pathomechanism and uncertain treatment. The symptoms of post orgasmic illness syndrome last about 2–7 days after an ejaculation. The current hypothesis proposes that the primary injury in post orgasmic illness syndrome is an acute compression proprioceptive axonopathy in the muscle spindle, as is suspected in delayed onset muscle soreness. The terminal arbor degeneration-like lesion of delayed onset muscle soreness is theorized to be an acute stress response energy-depleted dysfunctional mitochondria-induced impairment of Piezo2 channels and glutamate vesicular release. The recurring symptoms of post orgasmic illness syndrome after each ejaculation are suggested to be analogous to the repeated bout effect of delayed onset muscle soreness. However, there are differences in the pathomechanism, mostly attributed to the extent of secondary tissue damage and to the extent of spermidine depletion. The spermidine depletion-induced differences are as follows: modulation of the acute stress response, flu-like symptoms, opioid-like withdrawal and enhanced deregulation of the autonomic nervous system. The longitudinal dimension of delayed onset muscle soreness, in the form of post orgasmic illness syndrome and the repeated bout effect, have cognitive and memory consequences, since the primary injury is learning and memory-related.

Highlights

  • Published: 23 July 2021Post orgasmic illness syndrome (POIS) is a rare, mysterious, but most likely underreported, debilitating chronic condition with unknown pathomechanism and uncertain treatment

  • A current theory suggests that spermidine release enhances olfactory memory and learning [53] during the preprogrammed ejaculation phase of copulation or masturbation, and flu-like symptom are proposed to arise due to ASRinduced spermidine depletion

  • Noteworthy is that late consolidation of memory starts six hours after training [57], which is when the blood-spinal cord barrier (BSCB) and blood-brain barrier (BBB) permeability start to increase in a peripheral nerve injury (PNI) [50] and when the delayed onset of pain evolves in delayed onset muscle soreness (DOMS) [14,15,23]

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Summary

Introduction

Post orgasmic illness syndrome (POIS) is a rare, mysterious, but most likely underreported, debilitating chronic condition with unknown pathomechanism and uncertain treatment. Several pathophysiological hypotheses have been proposed to explain the condition, such as immunological phenomenon [5,7,8,9], opioid-like withdrawal [3], neuroendocrine response [10], transient deregulation of the autonomic nervous system [11], hypersensitivity and disordered cytokines [4,6]. This manuscript proposes to the scientific and medical community to consider an analogous primary injury mechanism in POIS, suggested by the new acute compression. Another interesting correlation is that many clinicians observed a lifelong premature ejaculation condition among their POIS patients [3,5,6,11] and foresee Piezo channels being implicated in the pathomechanism of premature ejaculation [18]

Repetitive Eccentric Contractions and Acute Compression
Activated NMDARs and Low Grade Neuroinflammation
The Repeated Bout Effect
Ontogenetic Relevance
Testing This Hypothesis and Possible Interventions
Cellular Mechanism of the Critical Primary Injury
Findings
Conclusions
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