RxISK

Making Medicines Safer for All of Us

Tracking Down the Cause of Withdrawal and PSSD

29 Comments

TRP Channels

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.

The experiment

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.

References

  1. 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
  1. 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
  1. 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.
  1. 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.
  1. Lodish, H. (2000), Molecular Cell Biology 4th edition, WH Freeman, New York
  1. 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

Reader Interactions

Comments

  2. I agree that some adverse SSRI events are peripheral. During my 17 years on SSRI and, latterly, SNRI therapy I experienced what some doctors felt was a form of cauda equina. To be blunt, I experienced such numbness that my inner thighs could be pinched with fingernails and not feel pain.

    Cauda equina was investigated to no avail. Sensation began to return some 15 months after the medication was withdrawn.

    I have also had nerve conduction studies as part of investigations into what turned out to be tardive dystonia. They showed that the condition did not, to quote the neurologist, arise in my head.

    I shall watch this with interest.

    Reply

  3. I’d like to add that I still suffer, five years post withdrawal, from cognitive and memory issues. In one test, I was asked to rattle off as many words as I could beginning with A. I was a journalist. Language is my forte, yet I stumbled my way through just 12 words. Any time I am placed under pressure, my brain scrambles, the persistent nod of my head becomes more marked and it’s difficult to put together a cohesive sentence. Had I been able to write them down, I am convinced that I would have performed better.

    It was this aspect of being on SSRIs which took me off air as a broadcaster. I simply could no longer speak a coherent sentence while trying to cue up music, time into the news etc. My multitasking capacity just disappeared into confusion.

    Reply

  5. Oh, if you had only been here to witness yesterday’s events. I set about making a dress for my six month old granddaughter. I had to relearn long discarded skills – how to read a pattern, how to work a sewing machine, spent two and a half hours painstakingly cutting paper and fabric with scissor -defiant dystonic hands. Three hours in, my sister dropped by and was utterly distressed to see how much worse my nodding had become. The brain seems to flood, causing confusion and exaggerated movements when multi-tasking or relearning things that once came easily. It seems agitated, almost a form of akathisia. I’ve been trying, for many years now, to employ neuroplastic techniques in the hope of restoring normality. In the early months after withdrawal, I was reasonably positive, but feel today that the brain, despite its capacity to reroute so many functions and my continuing to challenge it, is continuing to decline in some important areas. I miss the person I used to be. Mind you, that person was hypomanic (fabulous worker) for all those years while on SSRIs and SNRIs. Makes me wonder if a few circuits just burned out after all the years of heightened activity and minimal sleep.

    Reply

  7. I just found some more info about ion channels and some (natural) substances,I don’t know if these are of any use:
    http://www.sciencedaily.com/releases/1999/01/990113075613.htm
    http://www.sciencedaily.com/releases/2007/04/070420143324.htm
    http://www.sciencedaily.com/releases/2002/08/020826071458.htm
    http://www.sciencedaily.com/releases/2013/07/130728134055.htm
    http://www.sciencedaily.com/releases/2015/09/150908132812.htm
    http://www.sciencedaily.com/releases/2013/03/130305154531.htm

    Reply

  8. The new site is very encouraging and states all the things that we, Di, Ruth and Me, had and are going through.

    In 2010 my potassium was 5.4 and I was told to cut out potassium foods which are high, which I did and its now down to 4.4

    Early in w/d I ate a banana and it made me so dizzy I had to lay down for hours til the effect passed.

    A couple of months ago Di ate banana and she was really ill after so it seems that your bit on bananas and potassium is very relevant to us.

    Many thanks for your continued help

    Reply

  9. All this makes me wonder, yet again, what role Diltiazem may be playing in my continued tardive dystonia. Unfortunately, there would seem to be no safe way to put it to the test. Although not prescribed for heart failure, only high blood pressure, according to medical advice it is apparently not safe to stop taking it. Thoughts anyone?

    Reply

  10. This approach seems valid. There is a rare disease where people can feel no pain called congenital analgesia which also stems from genetic defective neurons and their inability to transmit impulses because of the inactive sodium channels (thats what i understood).

    http://www.independent.co.uk/life-style/health-and-families/health-news/the-people-who-cant-feel-pain-scientists-discover-cause-of-rare-inherited-condition-that-turns-off-10274604.html

    So if SSRI/SNRI cause epigenetic changes, causing Post-SSRI-Syndromes we need some agents to switch things back.

    Reply

  11. I find all of this so disheartening and exhausting. I’m not a stupid person but I find having to wade through reams of content of this kind is impossible for someone with cognitive difficulties.
    The format of the site and the information on what helps with withdrawal needs to be simplified and laid out in a way that’s accessible and straight forward. I have no interest in wading through the chemistry of certain drugs as a little knowledge is a dangerous thing and each person is different, ergo, there are no simply solutions.
    It’s also vitally important that hope is given to those of us who are caught in the catch 22 of being unable to discontinue these drugs without debilitaitng withdrawal and the knowledge that they have reduced the quality of our emotional, intellectual and physical lives.

    Reply

  12. “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.”
    What does this mean? What does one do with this information? How does this help us?

    Reply

  13. Psychiatric drugs have completely demolished my brain. I now have abnormal EEG with severe sleep problems. Years taking psych drugs have literally erased my memory and since withdrawing ‘cold turkey’ from them all I have so many cognitive problems that now who needs sex? Please help those who are still able to enjoy it somewhat, at least. I love this website, and all who are striving to help the rest of us poor patients whose only demise was trusting, and believing our psychiatrists in the first place. Thank God I’m old now and don’t have that much longer to live.

    Reply

  15. I stumbled across this website searching for information regarding withdrawal (from Xanax) pain.
    Although I am a nurse (and so used to reading medical and scientific word speak) I was not able to determine where you were going with reference to foods, in particular garlic, chili peppers.
    The reason this peaked my interest is because it seems that foods that make my pain worse are chili peppers (even bell peppers actually…nightshades??), and garlic salt. I seem to be able to handle dried garlic seasoning but not the salt. It is my understanding that this may be due the fact that the salt absorbs the oils from the garlic and therefore, it stays…active…for lack of a better description.

    SO…my question to you is…where were you going with listing these foods or compounds? Were they meant to indicate they would HELP or HURT recovery?

    Thanks!
    J

    Reply

      • See below. I am likely going through either side effects, tolerance, or interdose withdrawl (or regular withdrawal) from XANAX. I DO have symptoms that started after starting to take a benzodiazapine in January of 2012 and have been searching and searching for an answer since. I used to be able to eat hot/spicy/chili peppers, take a calcium supplement, etc (as described in my second post) with no problems before starting being prescribed a benzodiazapine.
        So, IMO I guess…the right side of your scale just may produce similar bodily reactions/symptoms as some of these drugs (I am on a small dose of Lexapro too) OR these drugs make the body too sensitive to the actions of some of these foods.

        Reply

  16. I’d left another post, not sure where it went. (question as to reasoning for the plants …chili peppers, garlic) and relation to withdrawal or other problems…as my hand and foot pain get worse when I eat them. Wondering if the graph is supposed to mean they might be helpful or harmful. If helpful, I may be on the wrong track. If harmful…this may be of help to you.

    I wanted to add (problems since starting to take a benzo again in 2012. Possibly? related to interdose withdrawal: Other things that make my hand pain, foot pain (all in the interossii muscles), headaches in sub occiptals, sometimes also temples, pain around the eyes, photo-sensitivity (also affects my ability to use computer or TV) worse (besides stress or anxiety). ANYTHING with Calcium added to it, especially Calcium Carbonate. eg: many cereals, breakfast bars, some canned foods. Foods with high calcium content (except dairy…seem to handle dairy okay but that is from an animal so maybe there’s a difference…or I’ve heard that we don’t absorb calcium from dairy…I don’t know). Other: Brocolli, kale (made a smoothie…trying to be healthier…bam! Pain!. Spinach. Most vegetables seem off limits actually.
    Chili pepper, jalepeno, cauliflower (one serving once in a great great while I MIGHT be able to get away with). Bell peppers. I have suspicions about tumeric (an anti-inflammatory…but not with me probably…go figure). I also suspect tomatoes (I’ve been avoiding them for the most part, so difficult to specify on that at the moment). After using Nizoral shampoo. Most antibiotics make me depressed or give me anxiety. Flagyl, which I was prescribed a couple months ago, was really bad for anxiety and obsession. I cannot recall if any made the pain flair, sorry. Exercise (like jogging…even a little … or weight lifting).
    Now, to add another wrench in the works. In the opposite direction…where anxiety/stress can make these symptoms worse … the opposite has happened when I was extremely happy and newly ‘in-love’. The symptoms decreased significantly…to where I could eat almost anything…including hot/spicy foods. I could eat them nearly every day if I wanted. Where-as, I either have to limit them to once in a while or eliminate them completely. I do not know if I handled Calcium supplements in foods or the dark green vegetables during that time (not a big fan of them in normal life anyway) so cannot comment on that. FYI…the relationship was quite a roller coaster and when we’d fight or break up, I would go back to having the pain/anxiety/and not being able to eat those foods and back to pain-free eating what I wanted when we’d get back together.
    If it sounds like I have so many details about this weird stuff, it is because I’ve spent 3 of the last 4 years keeping notes, going to doctors, getting this test, that test,fearing the worst…. blah blah blah…to try and figure out what the heck is wrong…because no one seems to know except there is empathy for the multitude of symptoms on benzo withdrawal support forums. (I do have some other symptoms, but the ones I’ve listed are the ones that stand out that seem to have a connection to foods/substances as well as the emotional ones.

    Reply

  17. Well here we are, five years on – time for an update. Current meds are Diltiazem and Clonazepam. Nothing on that front has changed in almost 9 years. In 2020, my upper legs are in most constant spasm across groin (presumably tendons) quads, inner and outer upper leg muscle groups. My sleep patterns are shattered, such is the severity of the pain. Walking distance and cycling are now a memory.
    The medical profession has seen fit (twice) to provide an inadvertent serotonergic challenge via the use of Fentanyl (with Propofol, if it makes a difference) during surgical procedures. Both times I woke in acute pain, with severe spasms. On the second occasion, I apparently lost any coherent speech for roughly an hour and a half.
    The question is – did these challenges make things worse? Does tardive dystonia worsen with time in some people?

    Reply

Leave a Reply

Your email address will not be published. Required fields are marked *