• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
- - - - -

Supplements to reverse SSRI-induced sexual dysfunction?

libido ssri low libido

  • Please log in to reply
14 replies to this topic

#1 NilsOlav

  • Guest
  • 82 posts
  • -4
  • Location:United States

Posted 17 November 2014 - 07:53 PM


I took an SSRI a few years ago (2011-2012) and definitely noticed a lower libido while on it and upon discontinuing it. I know there are a lot of supplements out there to enhance libido, but are there any that are especially helpful for a case of SSRI-induced sexual function? I know its been years since I stopped taking it, but I still think the SSRI is playing a role in my low libido.



#2 AlexxxB

  • Guest
  • 49 posts
  • 9
  • Location:Japan

Posted 18 November 2014 - 12:21 PM

How old are you?



sponsored ad

  • Advert
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).

#3 NilsOlav

  • Topic Starter
  • Guest
  • 82 posts
  • -4
  • Location:United States

Posted 18 November 2014 - 04:09 PM

How old are you?

 

23. I was on Lexapro for about 6 months in from fall 2011 a bit into winter 2012.



#4 crazepharmacist

  • Guest
  • 94 posts
  • 1
  • Location:USA

Posted 21 November 2014 - 01:48 PM

Have you had blood work? You can get this done privately through mdlabs-it is very cheap(10% off coupon if you Google). I recommend testing testosterone(total+free), estradiol, prolactin, fsh, and lh. It's unlikely in my opinion your sexual dysfunction is caused by your ssri usage as it has been years since you've been off. To answer your quesions though, some notably drugs that increase libido/erections are cabergoline and Toremifene. The former reduces prolactin and the latter increase lh+fsh production and thereby testosterone levels.

#5 forexworld12

  • Guest
  • 150 posts
  • 6
  • Location:India
  • NO

Posted 22 November 2014 - 08:44 PM

I guess what you have is called PSSD ( post - ssri sexual dysfunction)

Here are few discussions and some ways to reverse it -  

http://www.longecity...ncrease-libido/



#6 NilsOlav

  • Topic Starter
  • Guest
  • 82 posts
  • -4
  • Location:United States

Posted 25 November 2014 - 10:28 PM

I guess what you have is called PSSD ( post - ssri sexual dysfunction)

Here are few discussions and some ways to reverse it -  

http://www.longecity...ncrease-libido/

 

Yeah, that sounds more like what I have. Lets say my libido and sexual function was lowered by 50% when I was on the SSRI. Since stopping it, I can tell for sure that I haven't returned to 100%, but maybe 80%-90% or so. I will check out that thread you linked, thanks!



#7 deeptrance

  • Guest
  • 267 posts
  • 82
  • Location:Austin, TX

Posted 30 November 2014 - 09:48 PM

I just posted a long response on this topic here: http://www.longecity...fects/?p=700498, and I'd copy-paste it into this thread but somehow that feels wrong. While my response was long, it only touches on a small number of possibilities out of many. 

 

I could summarize it by saying that dopaminergic substances are dope for sexual function, as long as you don't overdo them. What I didn't go into much was the area of hormones. It really depends on what's driving your lack of drive, and it might have nothing to do with hormone levels. Exercise is great for improving libido and enjoyment of everything including sex. Yoga has some amazing effects on sexuality. If you have any nutritional deficiencies then these could be a factor. 

 

Here are 3 case studies of individuals with post-SSRI sexual dysfunction, and discussion of treatments: http://psychrights.o...aetal(2007).pdf

 

More discussion of PSSD: http://davidhealy.or...-halts-s-death/

 

My comment in the other thread has several suggestions which fall outside the medical profession's approach, thus to be taken with caution and a grain of salt. But I report what works for me, and the mainstream approaches to many issues have reliably failed me throughout the years.

 

 


Edited by deeptrance, 30 November 2014 - 09:49 PM.


#8 forexworld12

  • Guest
  • 150 posts
  • 6
  • Location:India
  • NO

Posted 01 December 2014 - 09:34 AM

I just posted a long response on this topic here: http://www.longecity...fects/?p=700498, and I'd copy-paste it into this thread but somehow that feels wrong. While my response was long, it only touches on a small number of possibilities out of many. 

 

I could summarize it by saying that dopaminergic substances are dope for sexual function, as long as you don't overdo them. What I didn't go into much was the area of hormones. It really depends on what's driving your lack of drive, and it might have nothing to do with hormone levels. Exercise is great for improving libido and enjoyment of everything including sex. Yoga has some amazing effects on sexuality. If you have any nutritional deficiencies then these could be a factor. 

 

Here are 3 case studies of individuals with post-SSRI sexual dysfunction, and discussion of treatments: http://psychrights.o...aetal(2007).pdf

 

More discussion of PSSD: http://davidhealy.or...-halts-s-death/

 

My comment in the other thread has several suggestions which fall outside the medical profession's approach, thus to be taken with caution and a grain of salt. But I report what works for me, and the mainstream approaches to many issues have reliably failed me throughout the years.

YUP excersize is a sure way to rewire and up-regulate dopamine long term this is very important ..

 

PSSD is a condition caused by persistent de-sentisization of serotonin receptors and dopamine down-regulation 

SSRI's also downregulate 5-ht2a and 5-ht2c, as well as type 1 desensitization. The big issue is now all of the other type 1 subtypes, and their corresponding inhibition of dopamine,NMDA, glutamate, acetylcholine etc....also oxytocin decreases are a big one. 5-HT1A downregulation is NOT going to cause libido issues directly, but indirectly because the PreSynaptic heteroreceptors inhibit serotonin release and function. (!)  However, POSTSYNAPTIC 5-HT1A activation may cause sexual dysfunction. (!) (!)

Thus more serotonin is now floating around at 1B,1D,1F,2A,2C,3,4,5 as a result of presynaptic 5-HT1A downregulation, yet the postsynaptic 5-HT1A's induce prolactin, endorphin, cortisol, ACTH and oxytocin release. (!) (!) (!) (!) (!)

Practically every serotonin receptor dampens the libido and sexual function. (!) -- ( http://www.longecity...crease-libido/)

 

More information - http://area1255.blog...on-of-data.html

 

From my understanding (correct me if'm wrong)

 

I am not so sure about using dopamine agonist for people who have down-regulated receptors - Down-regulated receptors of dopamine are major cause for Ahnedonia and lack of emotion and low libido ... 

For people who have up-regulated receptor and do not have ahnedonia -I would say blocking serotonin is the way to resolve the PSSD as persistent ssri use as mentioned above can desensitize serotonin - so now more serotonin is flowing everywhere inhibiting dopamine and various other  sexual neurotransmitter like oxytocin. etc etc -  That is why wellbutrin is prescribed as the most common treatment - it increases the level of dopamine  to much the serotonin level so sexual function becomes normal .. but wellbutrin doesn't work when the dopamine receptor is desentisized nor will catuaba - it doesn't matter how much neurons are left the Receptor won't respond to stimuli because its already downregulated.... in this case A dopamine agonist would work because it  activates dopamine receptors in the absence of that receptor's physiological ligand  and enhances - signaling pathways through the dopamine receptor.. Dopamine agonist reverse Ahnedonia and might reverse 70% low libido ssri induced symptoms  through this mechanism but tolerance is an issue and the effects starts to fade away Because dopamine agonist DOES Downregulate their own dopamine receptors  .....It's like you are Sick and in the hospital bed but you are forced to work under that condition = getting more worse  so ideally  you would want to keep the receptors up-regulated(healthy) while agonizing them for Life-time benefit ..the receptors should be in a healthy condition to respond to the agonists long term .. 

 

SO ideally one would want the receptors up-regulated while Agonizing them or using wellbutrin ( to match up serotonin) !  (Lots of substance on this forum on how to keep them upregulated ) 

 

Even if one is able to up-regulate dopamine and reverse ahnedonia - a complete reversal of PSSD is unlikely due to the fact the serotonin is still desensitized and lets not forget the hormonal imbalance coming from them so The best cure would be to antagonize the serotonin receptor and up-regulate/agonize the dopamine !  Serotonin - up-regulation is a little more complicated as there are some receptors that down-regulate in both response to agonism and antagonism ... If one could up-regulate the 5HTIA, 2A and 2C that would reverse PSSD !(If anyone feel's i'm wrong feel free to correct) 


Edited by forexworld12, 01 December 2014 - 09:55 AM.

  • WellResearched x 1

#9 deeptrance

  • Guest
  • 267 posts
  • 82
  • Location:Austin, TX

Posted 01 December 2014 - 04:42 PM

YUP excersize is a sure way to rewire and up-regulate dopamine long term this is very important ..


Exercise affects everything, far more than is yet known. Every new study seems to find new benefits to the mere act of moving around and not spending too much time sitting. So I wouldn't say it's just about dopamine, but a lot of other things as well. Circulation, mood, hormone balance, cortisol regulation, etc.

From my understanding (correct me if'm wrong)


I don't know if anything needs correcting or if you're spot on about all of it, but I do see that you plainly are better informed about these matters than I am. I really appreciate your contributions and all the references you provide to research literature. Are you a scholar, or is this just your normal way of discussing technical information?
  • like x 1

#10 forexworld12

  • Guest
  • 150 posts
  • 6
  • Location:India
  • NO

Posted 01 December 2014 - 05:14 PM

 

YUP excersize is a sure way to rewire and up-regulate dopamine long term this is very important ..


Exercise affects everything, far more than is yet known. Every new study seems to find new benefits to the mere act of moving around and not spending too much time sitting. So I wouldn't say it's just about dopamine, but a lot of other things as well. Circulation, mood, hormone balance, cortisol regulation, etc.

From my understanding (correct me if'm wrong)


I don't know if anything needs correcting or if you're spot on about all of it, but I do see that you plainly are better informed about these matters than I am. I really appreciate your contributions and all the references you provide to research literature. Are you a scholar, or is this just your normal way of discussing technical information?

 

LOL , No ... I have re-searched a few stuff here and there .. this was my inital thread - http://www.longecity...ncrease-libido/

 

If it is required  I will add a dopamine agonist later in very very low dosage in combination with other compounds 



#11 Voku_Hila

  • Guest
  • 8 posts
  • 2
  • Location:Austria

Posted 19 November 2015 - 06:38 PM

 

If one could up-regulate the 5HTIA, 2A and 2C that would reverse PSSD !(If anyone feel's i'm wrong feel free to correct) 

 

 

Does anyone know a substance, which could do this?

 



#12 forexworld12

  • Guest
  • 150 posts
  • 6
  • Location:India
  • NO

Posted 19 November 2015 - 06:48 PM

If one could up-regulate the 5HTIA, 2A and 2C that would reverse PSSD !(If anyone feel's i'm wrong feel free to correct)


Does anyone know a substance, which could do this?


Amongst the known substance Sjw is known to upregulate 5ht1a post synaptic receptor But in the pfc.

Cant say about the latter two because both agonism and antagonism downregulates them. Usually downregulating 2c will increase Da release so not sure if u would want to upregulate those

#13 a355584

  • Guest
  • 13 posts
  • 6
  • Location:italy
  • NO

Posted 14 February 2016 - 03:01 PM

Looking for a cure for pssd: are why focusing on the right way?
 

Everyone knows the main theory about the pathogenesis of PSSD: the excessive release of serotonin (which has a mixed but essentially inhibitory role on sexual functions) by the serotonergic neurons (concentrated in the raphe nuclei of the midbrain) caused the "desensitization" of 5-HT1A autoreceptors (that act as sentinels that regulate the release of a substance according on how much there is already in circulation, this mechanism is also called negative feedback)[1].
The "down regulation" of the 5-HT1A autoreceptors is instead caused by chronic and excessive activation by its natural "agonist" (serotonin) that is made available in abnormal quantities by the use of SSRIs. It is therefore natural to think to the autoreceptors as something that is "damaged" by excessive competition and that can be cured using an antagonist that lead him to be again "sensitive."

At this point that we have to do a reflection: the autoreceptor is a sentinel, a switch that if "on" sends a chemical signal. What the cell (neuron) have to do when it receives this chemical signal is written in the genes, that is in the sequence of the DNA; how much it should do (that is, how much to increase or decrease the release of serotonin) it depends on the genes expression.
Essentially two mechanism regulate gene expression:

• Binding of chemical groups directly to DNA (covalently) that function as silencers or activators. The main inhibitor is the methyl group that, binding at particular points of the promoter sequences, silences gene expression. The protein that bind methyl groups to DNA is the DNMT.

• The other is the tangling of the DNA around proteins (called histones): if the DNA is wrapped on itself, the molecular machines that should read the instruction contained in the DNA, cannot bind the DNA because there isn’t sufficient space. The ability of a histone to compact a DNA molecules (and thus repress gene expression) depends on the presence of particular molecules bound to the histone. The main one is the acetate group: if it binds to histone, forces him to expand and so molecular machines can come in and gene expression is activated.

The acetyl groups are linked to histone by HAT and detached from it by HDAC. Also histones can be methylated in some particular positions, and this has mixed effects on gene expression.
 

SSRIs activate gene silencing    
                           

It’s well known that SSRIs activate the gene-silencing mechanisms. During the assumption has been seen[2][3][4][5][6][7][8][9][10]:

• Increase in the expression of certain proteins that carry methyl groups (called MeCP2 and MBD1)

• Increase the mRNA synthesis of HDAC2 gene (the HDAC of a particular subtype of histone)

• There’s a decreased acetylation in the histone "H3" in three areas of serotonin projection: the caudate-putamen (striatum), the frontal cortex and the dentate gyrus (5-HT neurons are extensively arborized, and their axons reach all brain areas).

All this suggests the induction of gene silencing.
Now we can rethink to the neuron such a stubborn person who does something of wrong: we told him to correct his behavior (the autoreceptor send his message to the cell) but he will not change his behavior (excessive release of serotonin) because he is a person who does not listen what we told to him (reduced gene expression).

So we cannot think to reactivate the negative feedback mechanism only binding them an antagonist because who is stuck in a situation of "off" is not the autoreceptor, but the DNA is to be.

The right strategy therefore have to be the reactivation of gene plasticity which can then be guided in the right direction by the use of an antagonist of the 5-HT1A autoreceptors.
 

A possible partial theoretical confirmation of this hypothesis is the results of a study in which rats whit an animal model of tardive dyskinesia (a disorder in some ways similar to the PSSD) had a partial remission of the disease using a HDAC inhibitor[11].
 

How to induce gene expression plasticity
 

Firstly, we recall the main objectives:

• To promote the demethylation of DNA by inhibiting DNMT: the new synthesized DNA is less methylated and then whit an increased gene expression.

• Inhibit the deacetylation of histones, in particular inhibiting HDAC

• Encourage the acetylation of histones, in particular by increasing the activity of HAT

It has also been seen that the increase of histone acetylation is accompanied by a demethylation of DNA, that is, the two events have a synergistic effect[12]. It 'important to note first of all that these effects are time and dose dependent, ie the effects are proportional to the dose taken and manifests itself after some time.

Several compounds can do this. Most of them are natural occuring compounds and found in green tea but this does not mean that they are little effective: some are very promising for the treatment of other diseases in which the gene expression change is crucial. Other are drugs are already used for other purposes[13][14][15][16][17][18][19][20][21][22].
Unlucky, often they have a low biodisponibility and a short half-life, than high and multiple doses should be necessary.
Most promising are listed for first.

 

EPIGALLOCATECHINE GALLATE (EPCG)

One of most studied, well caracterized and most effective natural compound that influence gene expression. Is one of major component of green tea extract. It can easily cross blood-brain barrier and is demonstrated that directly bind DNA19[23][24][25]. It is DNMT1, DNMT3, HDAC1 inhibitor and a MeCP2 inhibitor using Mg2+ as cofactor. Increase amount of glutathione and indirectly the acetilation of histone H3 and H4. Unlucky it is also a weak inhibitor of HAT, has a very low biodisponibility and may be hepatotoxic. Has been demonstrated that minimum effective dose in order to induce genetic effect is 800 mg 2 times a day. The ingestion of high grade, dried green extract, which contains a lot of different catechine, gallate and flavonoid, is more effective then the ingestion of pure EPGC: all the “gallate” and “chatechin” compounds are generally HDAC and DNMT inhibitor and they have a synergistic effect. They’re generally recognized as safe.
 

QUERCITINE

A flavonoid, is a strong enhancer of H3 and H4 histone acetylation, thus activates SIRT1 and SIRT6 mediated deacetylation; Inhibit DNMT and LSD1 (histone demethylating protein). It is also a weak MAOI. Was found to be active at a concentration of 75-100 um.
 

GENISTEINA (and less DAIDZEINE and BIOCIANINE A)

They are phytoestrogens and belongs to the category of isoflavones. They are strong inhibitor of HDAC (mostly HDAC1) and DNMT (mostly DNMT1 and DNMT3); less strong inhibitor of MeCP2. Was proved to demethylate ipermethylated genomes without lead to ipomethylation. It has a strong and synergic effect whit other DNMT and HDAC inhibitor.
It is an estrogen receptor agonist and then may produce non-hormonal effects.

 

SODIUM BUTIRRATE

It is a strong and natural occurring HDAC inhibitor and one of most studied. It has a lot of other positive effects and has been demonstred to be neuroprotective.
 

VALPROATE and SULPIRIDE

Valproate is an anticonvulsive and a mood stabilizer drug that act as a strong HDAC inhibitor and this may account of its anticonvulsive and mood stabilizing effects. Sulpiride is a very effective antidepressant (I want to recommend to everyone because is a fantastic drug whit a rapid onset and persisting effect specially on ruminative though, anxiety and bad feeling). It was found that a combination of the two drugs in clinically relevant doses activate brain demethylation. This effect was studied on GABA neurons but may occur also in other type of neurons[26][27][28].
 

CURCUMINE

Strong inhibitor of HDAC, HAT, DNMT, MeCP2. Has been shown to be able to induce demetilation of hypermethylated zone of DNA, in a stronger way than genisteine. Because its potent HAT inhibitor activity it may be a second line treatment or can be used to prevent ssri’s induced modification of genetic expression.

LUTEOLINE

Luteolin is a flavone, a type of flavonoid. Increase histone acetylation, particularly H3 e H4, inhibiting their HDAC and activating SIRT6-mediated deacetylation; Inhibit DNMT and LSD1 (histone demetylating protein). Thus, weak diminish phosporylation on H3 and H4 and is a weak indirect antagonist of DNMT.
 

APIGENINE

A flavone, is a HDAT inhibitor (soprattuto H1 and H3) and weak activator of SIRT6 mediated deacetylation. Apigenin may also stimulate adult neurogenesis. Concentration over 5-10 um are not recommended because gaba agonism and other central effects. It is a weak MAOI.
 

DIALLIL SULFIDE, ANACARDIC ACID and GARLIC

A lot of compounds in garlic and broccoli are HDAC and DNMT inhibitor, then high grade dried garlic extract and to eat broccoli may be strongly recommended.
 

SAM, vitamins B and ZINC

S-Adenosil-Methionine is the natural transporter of methyl groups and work in a synergic way whit DNMT, than induce methylation. Its natural counterpart is S-Adenosil-Omocisteine, a strong demethylating agent which expression increase during the use of HDAC inhibitor: this mean that there’s a synergistic effect between increase of acetylation and the activation of demethylation. For this reason, the supplement of SAMe is not recommended.

The vitamins of group B are used to carrier and bind methyl group, then supplementation of high amount of B vitamins is not recommended if the increase of demethylation is wanted.

The Zn2+ ion is he natural cofactor of HDAC, then the uses of Zn2+ supplements may increase their activities.

I hope that a combination of the induction of gene’s plasticity and the antagonism to serotonin receptors may help to recover from the disease. 


[1] Mechanisms of control of 5-HT neurons are:

·         self-inhibition through 5-HT1A autoreceptors (activation of these receptors by 5-HT diminish neuronal firing and produce a negative feedback regulation of transmitter release)

·         5-HT1B/1D receptors, located on nerve terminals, respond to 5-HT released locally in the terminal fields inhibiting further transmitter release.

 These 2 mechanisms ensure tight feedback control of the activity of serotonergic neurons and of terminal 5-HT release.
Thus, a prolonged treatment whit ssri may lead to a reduction of binding site for serotonin on SERT, then its ability to reuptake serotonin is chronically diminished.
Chronic administration of selective serotonin reuptake inhibitors (but not amitriptyline) results in the desensitization of 5-HT1A somatodendritic autoreceptor function in the dorsal raphe but not in hippocampus, and also results in the desensitization of physiological responses mediated by postsynaptic 5-HT1A receptors.
In general, changes in 5-HT1A receptor number have not been observed following chronic administration of antidepressants.
A study (Julie G Hensler, 2002) ipotizes that the desensitization of somatodendritic 5-HT1A autoreceptors in the dorsal and median raphe following chronic SSRI treatment do not appear to be mediated by changes in 5-HT1A receptor binding but may be due to a reduced capacity of the 5-HT1A receptor to activate G protein. By contrast, no significant change in postsynaptic 5-HT1A binding following chronic antidepressant treatment.

 

[2] Newton SS, Duman RS (August 2006). “Chromatin remodeling: a novel mechanism of psychotropic drug action”. Mol. Pharmacol. 70 (2)
 

[4] The genetics of selective serotonin reuptake inhibitors, Kroeze
 

[5] Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology, Csoka
 

[6] Faure C, Mnie-Filali O, Haddjeri N (February 2006). “Long-term adaptive changes induced by serotonergic antidepressant drugs”. Expert Rev Neurother
 

[7] Palotás M, Palotás A, Puskás LG, et al. (December 2004). “Gene expression profile analysis of the rat cortex following treatment with imipramine and citalopram”. Int. J. Neuropsychopharmacol
 

[8] Kálmán J, Palotás A, Juhász A, et al. (November 2005). “Impact of venlafaxine on gene expression profile in lymphocytes of the elderly with major depression–evolution of antidepressants and the role of the “neuro-immune” system”.
 

[9] Yamada M, Yamada M, Higuchi T (July 2005). “Antidepressant-elicited changes in gene expression: remodeling of neuronal circuits as a new hypothesis for drug efficacy”. Prog. Neuropsychopharmacol. Biol. Psychiatry
 

[10] Boehm C, Newrzella D, Herberger S, Schramm N, Eisenhardt G, Schenk V, Sonntag-Buck V, Sorgenfrei O (2006). “Effects of antidepressant treatment on gene expression profile in mouse brain: cell type-specific transcription profiling using laser microdissection and microarray analysis”.

[11] RGFP109, a histone deacetylase inhibitor attenuates L-DOPA-induced dyskinesia in the MPTP-lesioned marmoset: a proof-of-concept study, Johnston TH
[12] Histone deacetylase inhibitors reverse CpG methylation by regulating DNMT1 through ERK signaling, Sarkar S
[13] Green tea polyphenols for prostate cancer chemoprevention: A translational perspective J.J. Johnson

[14] Flavonoids Influence Epigenetic-Modifying Enzyme Activity: Structure-Function Relationships and the Therapeutic Potential for Cancer Gilbert, E.R.; Liu, D.

[15] Epigenetic activities of flavonoids in the prevention and treatment of cancer, Christian Busch
[17] Epigenome, Cancer Prevention and Flavonoids and Curcumin, Višnja Stepanić

[18] Dietary Polyphenols May Affect DNA Methylation, Mingzhu Fang

[19] Bioactive Nutraceuticals and Dietary Supplements in Neurological and Brain disease, Ronald Ross Watson,Victor R. Preedy

[20] Mechanisms for the Inhibition of DNA Methyltransferases by Tea Catechins and Bioflavonoids, Won Jun Lee

[21] The interaction of histone deacetylase inhibitors and DNA methyltransferase inhibitors in the treatment of human cancer cells, Zhu WG
[22] Epigenetic changes induced by curcumin and other natural compounds, Simone Reuter
[23] Green Tea Polyphenols in drug discovery - a success or failure?, Thomas J. Smith
[24] Phase I pharmacokinetic study of tea polyphenols following single-dose administration of epigallocatechin gallate and polyphenon E, Chow HH
[25] Molecular targets of (-)-epigallocatechin-3-gallate (EGCG): specificity and interaction with membrane lipid rafts, Patra SK
[26] Clozapine and sulpiride but not haloperidol or olanzapine activate brain DNA demethylation, Dong E
[27] Selective DNA Methylation of BDNF Promoter in Bipolar Disorder: Differences Among Patients with BDI and BDII, D'Addario C.

 

[28] Valproate induces DNA demethylation in nuclear extracts from adult mouse brain, Erbo Don

 


  • Informative x 3
  • WellResearched x 2

#14 Darryl

  • Guest
  • 650 posts
  • 657
  • Location:New Orleans
  • NO

Posted 15 February 2016 - 03:38 PM

The side effects of SSRIs on both sexual function and motivation appear due to opponent interactions with dopamine/reward systems.

 

Lorrain DS et al. 1999. Lateral hypothalamic serotonin inhibits nucleus accumbens dopamine: implications for sexual satietyThe Journal of neuroscience19(17), pp.7648-7652.

Daw ND et al. 2002. Opponent interactions between serotonin and dopamineNeural Networks15(4), pp.603-616.

Alex KD and Pehek EA. 2007. Pharmacologic mechanisms of serotonergic regulation of dopamine neurotransmissionPharmacology & therapeutics113(2), pp.296-320.

Abler B et al. 2012. Modulation of frontostriatal interaction aligns with reduced primary reward processing under serotonergic drugsThe Journal of Neuroscience,32(4), pp.1329-1335.

Bijlsma EY et al. 2014. Sexual side effects of serotonergic antidepressants: Mediated by inhibition of serotonin on central dopamine release?Pharmacology Biochemistry and Behavior121, pp.88-101.

 

More research collected here on suppression of dopamine/reward systems by elevated serotonin, and here on diverse issues with antidepressants, categorized.

 

In my personal experience with long-term, chronic SSRI use, tapering fluoxetine (Prozac) down to a minimal dosage that prevented depressive episodes/withdrawal symptoms, and adding buproprion (Wellbutrin), a dopamine reuptake inhibitor, resolved my anorgasmia with SSRIs. Its possible that dopamine precursors like L-dopa (found naturally at therapeutic doses in fava beans) would also help.

 

 


Edited by Darryl, 15 February 2016 - 03:44 PM.

  • Informative x 2
  • Cheerful x 1

sponsored ad

  • Advert
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).

#15 a355584

  • Guest
  • 13 posts
  • 6
  • Location:italy
  • NO

Posted 17 February 2016 - 09:58 PM

So interesting. I think that the effects of bupropion is due to the dopamine reuptake inhibitor properties, and the very high dosage needed to achieve the effects in PSSD (300 mg/day at least) is due to the low affinity of bupropion for the dopamine trasnporter (14% of occupancy). Than a dopamine agonist (like pramipexole, ropinorole or piribedil)  may be more effective than bupropion. Personally I had some benefit from the use of low dosage of sulpiride, a presynaptic D2 antagonist that disinhibit dopamine, and this is an other confirmation of the positive role of dopamine.







Also tagged with one or more of these keywords: libido, ssri, low libido

0 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users