Editorial Note: Between now and the end of the year, RxISK will have a major revamp. Among the first new features will be a Complex Withdrawal and PSSD research section. The philosophy behind this is that no-one knows what Protracted Withdrawal Syndromes and PSSD actually are and it’s more difficult to find an answer if we don’t know. Both are conditions that cannot be found in the textbooks. There is no expert that can shed light on either. Such a situation calls for a few form of research – Crowd-Research. We are hoping you will help find the answers.
Last week’s post by DA, Relief at Last gives some hints of the kind of thing that can help. This week’s by Brooks Witzke shows another angle. There is a lot that points to a role of Sodium channels in both withdrawal and PSSD. Few primary care doctors and almost no mental health professionals know a thing about Sodium, Potassium or Calcium channels or Transient Receptor Potential Channels featured above. But as the image above hints, there are lots of foods and other things that act on some of these channels that might hold a key to recovery.
Starting from a background of knowing little more about physiology than the fact that he has a body, in his efforts to find a cure Brooks opened our eyes to a lot of information about Sodium channels and TRP and other channels. We reproduce an outline of how he went about doing this below. The point is that anyone can hunt these things down. You don’t need to be an expert. Motivation is worth more than expertise – as Anne Marie has shown everyone in tracking down the role of SSRIs in causing alcoholism.
Voltage-gated sodium ion channels & PSSD
This article explores the possible and theoretical role of the voltage-gated sodium ion channels in the rare condition defined as Post SSRI Sexual Dysfunction Syndrome (PSSD), and the possible underlying mechanisms which contribute to its life-changing symptoms. Please be advised that our theories are still in the testing phase of agricultural roosters and have not been tested on humans as of the date of this article.
Post SSRI Sexual Dysfunction Syndrome (PSSD) is a condition in which no one should have to experience, it is a permanent condition which arises from the prior use of Selective Serotonin Reuptake Inhibitors (SSRIs), nobody knows a cure for this condition to date. The symptoms are described by patients as:
- Decreased libido
- Impotence or reduced vaginal lubrication
- Difficulty initiating or maintaining an erection or becoming aroused
- Persistent sexual arousal syndrome despite absence of desire
- Muted, delayed or absent orgasm (anorgasmia)
- Reduced or no experience of pleasure during orgasm (ejaculatory anhedonia)
- Premature ejaculation
- Weakened penile, vaginal or clitoral sensitivity
- Genital anesthesia
- Loss or decreased response to sexual stimuli (Healy, 2014)
In addition to these symptoms, many patients describe that the condition takes away a person’s ability to love, to intimately connect with the person they love, or even feel the warmth of a first kiss. Many patients also complain that the condition causes cognitive/memory dysfunction similar to that seen in Post Finasteride Syndrome (PFS) (Ganzer 2015).
As of 2015, nobody has identified a specific culprit to the condition. Antonei Benjamin Csoka (Phd) a pioneer in PSSD research from Howard University, has expressed opinions that the condition is linked to a downregulation of the serotonin transporter by tryptophan hydrolase (SERT).
An experiment conducted by writer, Brooks Witzke, actually showed that lowering bodily serotonin including inside the synaptic cleft, worsened PSSD in one test subject. A worsening that continued after discontinuation of the substance.
Another study published as of 2015, using Low Powered Laser Irradiation demonstrated some reversal of the genital numbing seen in PSSD. This suggested that at least one of the factors contributing to the condition was as a result of alterations within sodium ion or else TRP channels in the peripheral nervous system (Waldinger, 2015).
Then one must ask the question, is PSSD really peripheral? I mean, how could it be if the patient is suffering from cognitive impairment, low libido, and an inability to love or have those warm fuzzies inside?
That’s a good question, lets start by saying the human body is more complex than anything we know, not even the best doctors in the world (including Dr. Healy), understand the full inner workings. We DO know that the human body works like the timing on a car, if one thing is off so will many other functions. Human function works almost as a chain reaction, so the dysregulation of one of the body’s main functions can cause many other adverse effects.
Research gathered by myself on the US National Library of Medicine National Institutes of Health (Pubmed) has helped to further explain these mechanisms. Research of the role of “sodium ion channels on oxytocin release” a main neurotransmitter contributing to love, cognition, and human sexual function, is affiliated with the activation of sodium channels (Scala-Guenot, 1987). Many patients suffering from PSSD also have hormonal imbalances, mostly lower testosterone and higher prolactin, that does not improve the condition of PSSD upon hormonal replacement. Once again, testosterone is produced in the peripheral nervous system. Research has shown that the role of the voltage-gated sodium ion channel in the production of these hormones (and their activation in the brain) is substantial (Barann, 1995).
Then that leaves viewers with our last question, how does the voltage-gated sodium ion channels effect the cognitive dysfunction seen in PSSD? The voltage gated ion channels in the body actually control the release and the function of acetylcholine in the human brain, a neurotransmitter responsible for cognitive and memory function, even in Alzheimer’s Disease Patients (Molecular Cell Biology 4th edition).
The hypothesis constructed by myself is that the role of voltage gated sodium ion channels in the condition PSSD may be substantial, the effect may not be constrained only to the role of the peripheral (genital) nerves as hypothesized in previous studies.
Every doctor and scientist who specializes in PSSD has told writer me that my hypothesis is WRONG. Perhaps it takes the “outside the box” thinking of an attorney with no real education in medicine to see what everyone else is missing. I refuse to give up on all those effected by PSSD, a condition that results in suicide for some people.
This led me to the IUPHAR Guide to Sodium and other Channels. This I understand will feature on RxISK soon. If I can find material like this – so can you.
What these tables make clear is that there are lots of different compounds acting on sodium and other channels. Many of them are very toxic. This led me on to an idea for an experiment.
I am currently funding an experiment, employing the services of trained professionals, to actually produce a substance that opens the Voltage-Gated Sodium Ion Channel through a method of depolarization. The experiment is extremely dangerous, as it involves using a derivative of a specific type of neurotoxin.
The optimistic hope for this experiment is that re-opening the channel will cause regeneration of previously inactivated pathways, providing a potential cure for PSSD, the substance produced will be used concurrently with a specific frequency of microcurrent to facilitate regeneration and replenishment of bodily functions. The experiment is currently using organic, healthy chickens to test for safety.
Wish me all the best.
- Ganzer, PA, (2014), Persistent sexual, emotional, and cognitive impairment post-finasteride: a survey of men reporting symptoms, Amj Mens Health, retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/24928450
- Waldinger, MD, (2015), Penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) responds to low-power laser irradiation: a case study and hypothesis about the role of transient receptor potential (TRP) ion channels, European Journal of Pharmacology, Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/25483212
- Di Scala-Guenot D, (1987), Electrical stimulations of perifused magnocellular nuclei in vitro elicit Ca2+-dependent, tetrodotoxin-insensitive release of oxytocin and vasopressin. Neurosci Lett. 1987 May 6;76(2):209-14.
- Barann, M. (1999), Inhibition by steroids of [14C]-guanidinium flux through the voltage-gated sodium channel and the cation channel of the 5-HT3 receptor of N1E-115 neuroblastoma cells. Naunyn Schmiedebergs Arch Pharmacol.
- Lodish, H. (2000), Molecular Cell Biology 4th edition, WH Freeman, New York
- Csoka, ABL, (2015), Post-SSRI Sexual Dysfunction: Clinical Characterization and Preliminary Assessment of Contributory Factors and Dose-Response Relationship, J Clin Psychopharmacol. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/25815755