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There are over 2000 members on a Yahoo Group with PSSD for which there is no cure, and likely thousands more with this condition that is not acknowledged in the medical literature. Thousands suffer with no libido as a direct result of formerly using an SSRI.
http://en.wikipedia.org/wiki/Post-SSRI_sexual_dysfunction
http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=1479
SSRIs are also known to reduce free testosterone levels in some patients.
http://priory.com/psych/sexdys.htm
There are young men in their 20s with PSSD whose total testosterone levels are in the 300s after quitting the SSRI but their doctors tell them their testosterone level is fine because it is “within the standard reference range”.
Generally, when a person is prescribed an SSRI, it is for treatment of anxiety, depression, premature ejaculation, irritability, or other condition where serotonin signaling increases may help reduce symptoms of the illness. Generally, in these conditions, norepinephrine signaling is excessive.
These conditions, themselves, are caused by a variety – and often multiple – underlying problems. For example, mental illnesses generally occur only if numerous problems in signaling, structure, or metabolism occur simultaneously in the body.
The underlying problems which lead to the illness for which SSRI treatment was indicated may also predispose the affected person to prolonged sexual dysfunction with SSRI treatment even when the SSRI treatment is withdrawn.
SSRI treatment increase serotonin signaling, which then can directly blunt libido. The increase in serotonin also reduces norepinephrine signaling. Norepinephrine signaling is also involved in libido, maintaining erections, and in triggering ejaculation. The increase in serotonin also reduces dopamine signaling. Dopamine is important to activate libido circuits in the brain. A problem of excessive SSRI dosing is that it can lead to excessive norepinephrine signaling rather than a reduction. This can cause motor restlessness or agitation when coupled with lower dopamine signaling. This can also lead to immune system inflammatory signaling. Inflammatory signaling can shut down libido circuit activity.
Generally, most SSRIs (except for Prozac, which lasts longer) are mostly gone from the body 1 week after stopping them.
If sexual dysfunction persists, often this may mean that problems in signals affected by the SSRI persist. This may indicate that these problems are involved in positive feedback loops, which prolong the signal way after the triggering signal is stopped.
Note, however, that these signals, themselves, are already dysfunctional in the conditions which lead to SSRI treatment in the first place. And they may already be involved in positive feedback loops before SSRI treatment. Thus, the affected persons are already predisposed to prolonged sexual dysfunction even before treatment with the SSRI. The SSRI just tipped the scales so that sexual dysfunction is triggered and maintained. For many, other triggering factors may already have caused sexual dysfunction even before SSRI treatment.
They key to evaluation and treatment is to then identify the problems which lead to the illness for which SSRI treatment was done, which may be further worsened by the addition of the SSRI. The treatment is designed to address these problems, so that function is restored. A systemic evaluation needs to be done – sexual function depends on numerous circuits and signals which influence the libido circuits.
This is the general idea. It is difficult to be more specific since the underlying problem varies with the individually affected person.
Dr Mariano, thanks so much for your reply.
I took the SSRI Paxil/Paroxetine for high anxiety which did not even help. I never had any sexual dysfunction in my life (nor any depression) despite the formerly high anxiety. Unlike many others, I had no sexual dysfunction whilst on the SSRI. I developed PSSD upon the abrupt discontinuation of the SSRI Paxil. At the time, the manufacturer’s leaflet said one could simply stop taking it. No mention of tapering off. So stopping the SSRI suddenly, I experienced a significant reduction in my anxiety level but also developed an abnormally low libido, absense of morning erections some mornings, loss of feelings of love for my girlfriend, loss of dream recall, pleasureless orgasms, constant warm hands (they used to be constantly cold), etc. I now have mild anxiety. I was not given my blood test results but I remember my cortisol and free testosterone numbers were in the middle of the standard reference range.
I had a morning erection every day all my life (I’m in my 30s now). Since PSSD, some mornings I wake up with a morning erection which disappears quickly even before getting out of bed, but some mornings, including several days in a row, I wake up without a morning erection. I have read that morning erections are an indication of a man’s free testosterone levels and if a healthy man wakes up without a morning erection for two days in a row, then it’s generally an indication that his free testosterone level has declined. Is this generally true? Could my free testosterone need to be higher? There are some mornings when I have some libido as soon as I wake up but after I wake up properly and get out of bed the morning libido disappears. Could this be due to free testosterone not high enough causing the morning erection and morning libido to disappear as soon as I wake up properly and get out of bed?
I’ve taken L-Tyrosine to increase dopamine to try and improve my low libido but it only increases anxiety. I assume I have elevated norepinephrine causing the anxiety. I once tried 150mg of Wellbutrin to restore libido but that gave me a horrible panic attack.
Many thanks.
@dancetochaos 3257 wrote:
Is the Low T a permanent thing or does it come back?
It all depends on the individual. For some testosterone returns to normal some time after quitting the SSRI (a person on an SSRI should always taper off slowly over a long period of time when deciding to come off it). For others their testosterone level remains low. Unfortunately some GPs don’t even check estradiol, SHBG, Vitamin D, etc. SSRIs are known to cause an increase in estradiol, prolactin, cortisol, etc. in some users.
I found this article of a link between Vitamin D and testosterone levels.
http://www.telegraph.co.uk/health/healthnews/7127197/Sunbathing-boosts-mens-sex-drive.html
Morning erections are not an indication of free testosterone.
Morning erections are determined by multiple factors including one’s level of hydration, one’s sympathetic nervous system activity, one’s immune system activity, endocrine function, one’s level of emotional stress, structural issues, etc. etc. If one is dehydrated, for example, and is not getting morning erections as a result, then improving hydration would help solve the problem. If one has excessive stress, then addressing that can help restore erectile function. Etc. Etc.
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Norepinephrine is the signal for stress. Increasing norepinephrine produces anxiety and/or irritability.
Tyrosine can be converted to dopamine. Dopamine can then be converted to norepinephrine by norepinephrine releasing cells. When the brain is set to produce norepinephrine, then it will make norepinephrine from tyrosine and dopamine. Dopamine production from dopamine producing cells may even be reduced in order to allow the brain to produce norepinephrine from norepinephrine releasing cells.
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Wellbutrin increases norepinephrine signaling as its primary mechanism of action. Whatever increase in dopamine it can produce quickly wears out as other mechanisms also go into play, negating the increase in dopamine.
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@DrMariano 3273 wrote:
Morning erections are not an indication of free testosterone.
Morning erections are determined by multiple factors including one’s level of hydration, one’s sympathetic nervous system activity, one’s immune system activity, endocrine function, one’s level of emotional stress, structural issues, etc. etc. If one is dehydrated, for example, and is not getting morning erections as a result, then improving hydration would help solve the problem. If one has excessive stress, then addressing that can help restore erectile function. Etc. Etc.
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Norepinephrine is the signal for stress. Increasing norepinephrine produces anxiety and/or irritability.
Tyrosine can be converted to dopamine. Dopamine can then be converted to norepinephrine by norepinephrine releasing cells. When the brain is set to produce norepinephrine, then it will make norepinephrine from tyrosine and dopamine. Dopamine production from dopamine producing cells may even be reduced in order to allow the brain to produce norepinephrine from norepinephrine releasing cells.
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Wellbutrin increases norepinephrine signaling as its primary mechanism of action. Whatever increase in dopamine it can produce quickly wears out as other mechanisms also go into play, negating the increase in dopamine.
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Thank you for your reply, Dr Mariano.
Regarding dehydration, I may be dehydrated as for over 2 years I drink at least 8 glasses of water daily but still have constant mild thirst with mild dry mouth and dry lips all day, every day. I have no idea what could be causing these symptoms. My constant mild thirst is insatiable. I don’t have diabetes.
I was refered to an endocrinologist because of an overactive thyroid but after a couple of months on medication from my GP my thyroxine blood test showed it was just below the highest reference point so was now “fine” but I still have low libido, etc. In fact, the endocrinologist said my GP should not have put me on medication to lower thyroxine as the thyroxine had been a few points above the highest point of the standard reference range and I didn’t have a goiter either. I wonder if my body is still producing too much thyroxine – even though the thyroxine was just inside the standard reference range – causing the anxiety, low libido, absent morning erections, underweight and inability to gain weight, etc.
Since norepinephrine and dopamine are catecholamines, I assumed that if norepinephrine is high then dopamine will be high too but I see from your reply that norepinephrine can be high and dopamine low…so it’s most likely my high norepinephrine is causing low dopamine. Are pleasureless orgasms due to low dopamine?
What is scary for me is that an endocrinologist said my hormones such as thyroid hormones, free testosterone, cortisol, etc. are “within the normal reference range” and therefore my hormones are “fine” so my low libido, absent morning erections, etc. are not due to my hormones. He didn’t test for estrogen/estradiol, SHBG, DHT, etc.
Persistent sexual dysfunction after discontinuation of selective serotonin reuptake inhibitors.
Csoka AB, Bahrick A, Mehtonen OP.
University of Pittsburgh–Medicine, Pittsburgh, PA, USA.
Abstract
INTRODUCTION: Sexual dysfunctions such as low libido, anorgasmia, genital anesthesia, and erectile dysfunction are very common in patients taking selective serotonin reuptake inhibitors (SSRIs). It has been assumed that these side effects always resolve after discontinuing treatment, but recently, four cases were presented in which sexual function did not return to baseline. Here, we describe three more cases. Case #1: A 29-year-old with apparently permanent erectile dysfunction after taking fluoxetine 20 mg once daily for a 4-month period in 1996. Case #2: A 44-year-old male with persistent loss of libido, genital anesthesia, ejaculatory anhedonia, and erectile dysfunction after taking 20-mg once daily citalopram for 18 months. Case #3: A 28-year-old male with persistent loss of libido, genital anesthesia, and ejaculatory anhedonia since taking several different SSRIs over a 2-year period from 2003-2005.
RESULTS: No psychological issues related to sexuality were found in any of the three cases, and all common causes of sexual dysfunction such as decreased testosterone, increased prolactin or diabetes were ruled out. Erectile capacity is temporarily restored for Case #1 with injectable alprostadil, and for Case #2 with oral sildenafil, but their other symptoms remain. Case #3 has had some reversal of symptoms with extended-release methylphenidate, although it is not yet known if these prosexual effects will persist when the drug is discontinued.
CONCLUSION: SSRIs can cause long-term effects on all aspects of the sexual response cycle that may persist after they are discontinued. Mechanistic hypotheses including persistent endocrine and epigenetic gene expression alterations were briefly discussed.
PMID: 18173768 [PubMed – indexed for MEDLINE]
Persistence of Sexual Dysfunction Side Effects after Discontinuation of
Antidepressant Medications: Emerging EvidenceAudrey S. Bahrick
University Counseling Service, 3223 Westlawn S., The University of Iowa, Iowa City, Iowa 52242-1100, USA
Abstract: Post-market prevalence studies have found that Selective Serotonin Reuptake Inhibitor (SSRI) and Serotonin-Norepinephrine Reuptake Inhibitor (SNRI) sexual side effects occur at dramatically higher rates than initially reported in pre-market trials. Prescribing and practice conventions rest on the untested assumption that individuals who develop sexual dysfunction secondary to SSRI and SNRI antidepressant medications return fully to their pre-medication sexual functioning baseline shortly after discontinuing treatment. Most individuals probably do return to their previous level of sexual functioning, however recent case reports, consumer-provided Internet-based information, incidental research findings, and empirical evidence of persistent post SSRI sexual benefits in the premature ejaculation literature suggest that for some individuals, SSRI and SNRI-emergent sexual side effects persist indefinitely after discontinuing the medications. The literature poorly captures the full spectrum of SSRI/SNRI sexual side effects, and a lack of systematic follow-up in the sexual side effects research precludes detection of post SSRI/SNRI sexual dysfunction, leaving the formal knowledge base inadequate and even inaccurate, raising informed consent issues, and leaving clinicians vulnerable to practicing in ways that may be hurtful to patients in spite of their best efforts to inform themselves.
………
EVIDENCE OF PERSISTENT SEXUAL SIDE EFFECTS AFTER DISCONTINUATION OF SSRI/SNRI MEDICATIONS
An Incidental Finding
Montejo et al. [11] appear to have found incidental evidence of SSRI-induced sexual side effects continuing after cessation of the medication. The study’s aim was to assess the impact of changing to another medication in patients whose depressive symptoms had successfully remitted with a variety of SSRIs, but who had developed treatment-emergent sexual dysfunction. Patients were switched either to amineptine (n=47), an atypical tricyclic antidepressant that is no longer available, or to paroxetine (n=38). A third group of depressed patients was treated with amineptine only (n=26) and had no prior SSRI treatment. All three groups were followed with multiple assessments over a six month period.
Montejo et al. [11] report for those patients taking amineptine only, amineptine was not a cause of secondary sexual dysfunction, and also effectively treated depressive symptoms. In the group switched to amineptine, the incidence of sexual dysfunction dropped from 100% to 55% over the six month period, while depressive symptoms remained in remission. In the group switched to paroxetine, sexual dysfunction decreased only slightly from 100% to 89.7% after six months. The authors interpret these findings to support with high confidence (p<.001) the conclusion that amineptine is an effective antidepressant that is able to significantly improve the SSRI-caused sexual dysfunction, yet maintain the efficacy of the antidepressant treatment used before. An alternative interpretation is that for 55% of individuals switched to a medication that successfully treated depressive symptoms and was not a cause of secondary sexual dysfunction, the initial SSRI-induced sexual dysfunction persisted for at least six months after discontinuing the SSRI [10].
http://psychrights.org/Research/Digest/SSRIs/PersistentSSRISexSideEffects.pdf
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