Low Dose Dextromethorphan As An Alternative To SSRI's?

passivity

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Dextromethorphan as a potential rapid-acting antidepressant.

Dextromethorphan shares pharmacological properties in common with antidepressants and, in particular, ketamine, a drug with demonstrated rapid-acting antidepressant activity. Pharmacodynamic similarities include actions on NMDA, μ opiate, sigma-1, calcium channel, serotonin transporter, and muscarinic sites. Additional unique properties potentially contributory to an antidepressant effect include actions at ß, alpha-2, and serotonin 1b/d receptors. It is therefore, hypothesized that dextromethorphan may have antidepressant efficacy in bipolar, unipolar, major depression, psychotic, and treatment-resistant depressive disorders, and may display rapid-onset of antidepressant response. An antidepressant response may be associated with a positive family history of alcoholism, prediction of ketamine response, increased AMPA-to-NMDA receptor activity ratio, antidepressant properties in animal models of depression, reward system activation, enhanced erythrocyte magnesium concentration, and correlation with frontal μ receptor binding potential. Clinical trials of dextromethorphan in depressive disorders, especially treatment-resistant depression, now seem warranted.

Dextromethorphan as a potential rapid-acting antidepressant. - PubMed - NCBI


Involvement of Sigma-1 Receptors in the Antidepressant-like Effects of Dextromethorphan

The antidepressant-like effects of dextromethorphan appear to involve σ1 receptors. In the current study, two well-established σ1 receptor antagonists (BD1063 and BD1047) reduced the antidepressant-like actions of dextromethorphan in vivo. They are thought to act in a competitive manner since in the presence of BD1063, the dose response curve for dextromethorphan was shifted to the right. An involvement of σ1 receptors in the antidepressant-like effects of dextromethorphan is consistent with earlier reports that selective σ1 receptor agonists can on their own reduce immobility time in the forced swim test [17], [20], [21], [32] and produce antidepressant-like effects in other animal models such as the tail suspension test and olfactory bulbectomy [18], [33]. Thus, additional studies involving these and other animal models used in depression research (e.g., sucrose preference test, novelty suppression) [3], [29], [30] will be needed in the future to further evaluate the antidepressant potential of dextromethorphan and the involvement of σ1 receptors.

The ability of dextromethorphan to elicit antidepressant-like actions through σ1 receptors suggests future studies to evaluate potential fast-acting therapeutic effects are also warranted. σ1 Receptor agonists can enhance serotonergic neuronal firing in the dorsal raphe nucleus after only two days vs. two weeks of treatment that is typically required of conventional antidepressant drugs [24], [25]. In addition, the fast-acting antidepressant drug ketamine has recently been shown to potentiate nerve growth factor (NGF)-induced neurite outgrowth through a σ1-dependent mechanism [26], supporting the emerging importance of σ1 receptors in modulating neuronal plasticity, which itself is a critical element for conveying both rapid and delayed antidepressant activity.

Earlier competition binding studies showed that dextromethorphan has significant affinity for σ1 receptors (138–652 nM) [13], [27], [28], [34], and thus further characterization of the interaction of dextromethorphan with σ1 receptors was undertaken in the current study. The saturation binding studies indicate that the interaction of dextromethorphan with σ1 receptors is complex, with both a change in Bmax and Kd in the binding of [3H](+)-pentazocine in the presence of dextromethorphan. The reduction in the number of σ1 receptors (Bmax) with which [3H](+)-pentazocine binds suggests non-competitive interactions of dextromethorphan with σ1 receptors. However, there is also a decrease in Kd for [3H](+)-pentazocine binding in the presence of dextromethorphan, suggesting additional competitive interactions. Together, the data support the presence of at least two distinct sites or modes of interaction with which dextromethorphan binds to the σ1 receptor, one with which it has competitive interactions, and another with which it has non-competitive interactions. This interpretation would be consistent with other reports of multiple regions for ligand interactions on the σ1 receptor, some of which have functional ramifications for agonist vs. antagonist activity [35], [36], [37]. The affinity differences of dextromethorphan for its two putative binding sites appear to be similar (<100-fold difference) since competition binding assays of dextromethorphan at σ1 receptors are consistent with a one-site fit [27]. The antidepressant-like effects of dextromethorphan are thought to be mediated through the competitive binding site since i) there appears to be a rightward shift in its dose response curve in the forced swim test with no apparent change in maximal effect, and ii) (+)-pentazocine, the σ1 agonist used to label the receptor, has previously also been reported to produce similar antidepressant-like effects [10], [17].

In addition to interacting with σ1 receptors, dextromethorphan has been reported to alter monoamine reuptake, particularly serotonin and norepinephrine at Ki values of 23 and 240 nM, respectively [38], which have implications for antidepressant effects in humans. The significant affinity of dextromethorphan for SERT (40 nM) [9] would be expected to contribute to antidepressant efficacy in humans, although it would not account for potential fast-acting effects, nor reductions in immobility time herein. Under the experimental parameters used in the current study, the classical SSRI fluoxetine did not produce significant reductions in immobility time in the forced swim test. This is consistent with the reports of others that the forced swim test does not reliably detect the antidepressant potential of SSRIs [39]. Thus, this mechanism, which is a known contributor to antidepressant efficacy in humans, is unlikely to account for the pattern of antidepressant-like effects observed with dextromethorphan herein. In contrast to its high affinity for SERT, dextromethorphan binds much more weakly with NET (>1 µM) [9], but its reported ability to modulate norepinephrine reuptake [38] would be expected to contribute conventional antidepressant effects under clinical conditions.

Compared to the ability of BD1063 pretreatment to significantly block the antidepressant-like effects of dextromethorphan, it failed to attenuate that of imipramine, which has an overlapping binding profile with dextromethorphan: SERT (1.3–20 nM) [40], [41], [42], [43], and σ1 receptors (343 nM) [44]. This indicates that the σ1 interaction may have a larger role in producing the antidepressant-like effects of dextromethorphan than that of imipramine. This is consistent with the wider range of protein targets through which imipramine, but not dextromethorphan, interacts, which include: serotonin 5-HT2, muscarinic, and histamine H1 receptors [9], [45], [46], [47], [48], [49].

In conclusion, the data presented here show for the first time that dextromethorphan has antidepressant-like effects in an in vivo model and provide evidence that this effect occurs at least in part through a σ1 receptor dependent mechanism. This is also the first report of the manner in which dextromethorphan interacts at the σ1 receptor. Together with earlier studies and the potential of increasing dextromethorphan bioavailiabity by using the FDA- and EMA-approved dextromethorphan/quinidine formulation, these data suggest dextromethorphan should be further explored for translational potential as an antidepressant drug in clinical trials, as it may offer rapid-acting relief of depressive symptoms and the ability to resolve cases of treatment-resistant depression. In addition, further studies to understand the molecular and cellular mechanisms by which these effects occur are necessary and may yield important information about how various receptors, transporters and processes are involved in the ability of dextromethorphan to convey its antidepressant effects.

Involvement of Sigma-1 Receptors in the Antidepressant-like Effects of Dextromethorphan

Sigma-1 receptor
An endogenous ligand for the σ1 receptor has yet to be conclusively identified, but tryptaminergic trace amines, as well as neuroactive steroids such as dehydroepiandrosterone (DHEA) and pregnenolone all activate the receptor.
 

DaveFoster

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This is well-known, but thanks for posting the study. Memantine has similar effects on the NMDA receptor and treats OCD effectively, which often coincides with anxiety and depression.
 

passivity

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This is well-known, but thanks for posting the study. Memantine has similar effects on the NMDA receptor and treats OCD effectively, which often coincides with anxiety and depression.

I read somewhere that memantine reverses tolerance for opiates, benzos, coffee, etc.. just for a couple of times but after that you can't actually lower your tolerance anymore, so, that's a bummer. But I'll try it later on,:thumbup it's safe and kinda cheap, have you tried it?

Here is another sigma receptor agonist, opipramol:

Opipramol acts as a high affinity sigma receptor agonist, primarily at the σ1 subtype, but also at the σ2 subtype with somewhat lower affinity.[2] It is this property which is responsible for its therapeutic benefits against anxiety and depression.[3] Opipramol also acts as a low to moderate affinity antagonist for the D2, 5-HT2, H1, H2, and muscarinic acetylcholine receptors. H1 and H2 receptor antagonism account for its antihistamine effects, and muscarinic acetylcholine receptor antagonism is responsible for its anticholinergic properties.[2] Sigma receptors are a set of proteins located in the endoplasmic reticulum. σ1 receptors play key role in potentiating intracellular calcium mobilization thereby acting as sensor or modulator of calcium signalling. Occupancy of σ1 receptors by agonists causes translocation of the receptor from endoplasmic reticulum to peripheral areas (membranes) where the σ1 receptors cause neurotransmitter release. The biphasic action initially makes prompt improvement of tension, anxiety and insomnia. Opipramol is a tranquilizer with a thymoleptic component. After sub-chronic treatment with opipramol σ2 receptors are significantly down-regulated- but not σ1 receptors.[1]

One possible side effect: Paralytic Ileus :shock:

That sounds scary! would you rather use low dose DXM or opipramol?
 

DaveFoster

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@passivity I have not tried memantine. Magnesium seems to have similar effects, and is much safer.
 
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I have tried memantine. Me and my friend ordered some online and started using it early in December.

We both started with 10mg and dosed throughout the night, I made it to 40mg that night. That first night we both felt amazing an alive, we both experienced profound epiphanies about life. My ability to feel pleasure stayed the same but I just felt different and better.

We expected it to be pretty weak but it was surprisingly strong.

I wasn't able to get good sleep for a couple of days afterwards, and I kept redosing like a fool.

At about the 4th day, after not getting any good sleep since starting, I was hanging out with the same friend, and took another dose of 10mg mixed with a small amount of diclazepam, and just felt off. I ended up leaving my friends house to try and get good sleep.

I went home and basically had a panic attack. That never happens to me, and I've never been so scared from a drug. I felt like I was gonna have a heart attack. I was in a dark room and my vision was weird af. I would fall asleep for 10 minutes and wake up because I heard a loud bang (there was no bang, auditory hallucination), and with this bang I would grab my chest in fear of heart attack.

At some point that night I took a shower and literally couldn't feel the temperature of the water. My face felt like it does when you're really drunk. I couldn't feel anything on my skin.

I ended up sleeping and only redosing a couple times more after giving it a break, in hopes of getting the same good effects.

I took around 100mg+ over the course of 5 days.

My other friend did around the same dosing, but he weighs way more than me, and I am very skinny already.

Ray has talked about memantine, and apparently the adamantane group of molecules (which memantine belongs to) structure water.

Memantine is an NMDA antagonist, but at low doses it blocks abnormal NMDA activity and thus calcium influx, which can kill neurons. It's also a D2 agonist, Nach7 antagonist, and 5HT-3 antagonist.

Me and my friend both noticed that ourselves and eachother looked waaayyy more healthy. Our teeth and skin and hair looked way better. We also noticed improvements in bowel health.

Memantine, as a D2 agonist with a long as **** half-life (60-80 hours), will destroy your sleep.
 

DaveFoster

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I have tried memantine. Me and my friend ordered some online and started using it early in December.

We both started with 10mg and dosed throughout the night, I made it to 40mg that night. That first night we both felt amazing an alive, we both experienced profound epiphanies about life. My ability to feel pleasure stayed the same but I just felt different and better.

We expected it to be pretty weak but it was surprisingly strong.

I wasn't able to get good sleep for a couple of days afterwards, and I kept redosing like a fool.

At about the 4th day, after not getting any good sleep since starting, I was hanging out with the same friend, and took another dose of 10mg mixed with a small amount of diclazepam, and just felt off. I ended up leaving my friends house to try and get good sleep.

I went home and basically had a panic attack. That never happens to me, and I've never been so scared from a drug. I felt like I was gonna have a heart attack. I was in a dark room and my vision was weird af. I would fall asleep for 10 minutes and wake up because I heard a loud bang (there was no bang, auditory hallucination), and with this bang I would grab my chest in fear of heart attack.

At some point that night I took a shower and literally couldn't feel the temperature of the water. My face felt like it does when you're really drunk. I couldn't feel anything on my skin.

I ended up sleeping and only redosing a couple times more after giving it a break, in hopes of getting the same good effects.

I took around 100mg+ over the course of 5 days.

My other friend did around the same dosing, but he weighs way more than me, and I am very skinny already.

Ray has talked about memantine, and apparently the adamantane group of molecules (which memantine belongs to) structure water.

Memantine is an NMDA antagonist, but at low doses it blocks abnormal NMDA activity and thus calcium influx, which can kill neurons. It's also a D2 agonist, Nach7 antagonist, and 5HT-3 antagonist.

Me and my friend both noticed that ourselves and eachother looked waaayyy more healthy. Our teeth and skin and hair looked way better. We also noticed improvements in bowel health.

Memantine, as a D2 agonist with a long as **** half-life (60-80 hours), will destroy your sleep.
Thanks for sharing. That's foolish dosing, but I've done the same. That dedication to some regimen always bites me in the butt. Also, rounding off to 5's and other even numbers never goes well.
 
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Thanks for sharing. That's foolish dosing, but I've done the same. That dedication to some regimen always bites me in the butt. Also, rounding off to 5's and other even numbers never goes well.

Yeah for sure. I knew it was a physically safe drug and I never guessed it could ever have pyschological effects like that so it totally blindsided me and kicked my ass :lol:

I felt "great" in the beginning so the motivation for redosing was to keep that feeling going.

And I know what you mean, we used volumetric dosing in glycering and have little needless-syringes, 1ml = 1mg, so 10ml was 10mg and I either did 3ml, 5ml, or 10ml, but at some point stopped caring and just starting dosing whatever :dancingsmileyman

We told ourselves we were doing it for "therapuetic" effect, but in reality we were just high. My friend still doses 5mg every now and then, he used benzos and quit semi-recently so it's completely justified IMO for him to be using memantine, otherwise his glutamtergic tone would be way too high. He says it helped his depression a lot, and I have to agree. It's not life chaning, but it's definitely increased both of ours ability to feel pleasure.:feelsgoodman
 

DaveFoster

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Yeah for sure. I knew it was a physically safe drug and I never guessed it could ever have pyschological effects like that so it totally blindsided me and kicked my ass :lol:

I felt "great" in the beginning so the motivation for redosing was to keep that feeling going.

And I know what you mean, we used volumetric dosing in glycering and have little needless-syringes, 1ml = 1mg, so 10ml was 10mg and I either did 3ml, 5ml, or 10ml, but at some point stopped caring and just starting dosing whatever :dancingsmileyman

We told ourselves we were doing it for "therapuetic" effect, but in reality we were just high. My friend still doses 5mg every now and then, he used benzos and quit semi-recently so it's completely justified IMO for him to be using memantine, otherwise his glutamtergic tone would be way too high. He says it helped his depression a lot, and I have to agree. It's not life chaning, but it's definitely increased both of ours ability to feel pleasure.:feelsgoodman
You mention glutamergic tone, and I think that's an appropriate term for my recent experience with magnesium hydroxide + seltzer water (400 mg before bed.) It's really helped me feel more relaxed today, and I hope the effects last. I've mentioned that magnesium has similar effects to memantine (besides being a universal deficiency.) I urge you to recommend this recipe for your friend to try: Magnesium bicarbonate supplementation - Toxinless
 
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You mention glutamergic tone, and I think that's an appropriate term for my recent experience with magnesium hydroxide + seltzer water (400 mg before bed.) It's really helped me feel more relaxed today, and I hope the effects last. I've mentioned that magnesium has similar effects to memantine (besides being a universal deficiency.) I urge you to recommend this recipe for your friend to try: Magnesium bicarbonate supplementation - Toxinless

Yes, me and my friend are familiar with magnesium's effect on the NMDA receptor, which is why we both use magnesium glycinate - well at least I used to, until I ran out. He still takes like more than a gram a day and will always give me some when I visit.

Is magnesium glycinate better or worse in your opinion than magnesium bicarbonate/magnesium hydroxide? In theory magnesium glycinate should be better for anxiety, as glycine is a GABA agonist and glycine agonist. In fact glycine should also help activate NMDA in a good way too.

From wiki: "100 mg of magnesium is contained in 709 mg of magnesium glycinate" So that's a decent amount of glycine if you want the RDA 100% of magnesium, which is around 500mg, so you'll be getting 3.5g of glycine.

Does magnesium bicarbonate have good bioavalibility? Does it make you ***t? And is it better than other forms of magnesium, in your experience?

Have you tried magnesium glycinate? It'll have additional anxiolytic/metabolism boosting properties, not to mention no laxative effect (in reasonable doses) because of it's good biovailability. If you like the feeling of glycine or gelatin you should try it.

I wonder if the bicarbonate salt indirectly increases Co2... If so that would be pretty cool. I use baking soda sometimes because I notice it makes me calmer. Baking soda might increase Co2 as well.

I have some mag glycinate being shipped to my house as we speak...
 
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Oh yeah, and we've given memantine to a few friends of ours and they all love it.

We have a friend who has a severe disorder in his arms, his nerves in his arms are degenerating and as a result they are extremely weak. It's an autoimmune condition but I forget the name.

He loves memantine too, which makes sense. It's very neuroprotective.
 

feather310

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Memantine was a life saver for me. I've had binge eating disorder as long as I can remember. I also have ADHD symptoms. I've been on 10mg for about 8 months which is the lowest dose recommended. It took a good 3 months for me to really feel a difference and I can't imagine myself without it. I am calm, less OCD, more organized and don't stress eat as much. With the addition of progesterone cream I also felt much happier. I smile and laugh now where before I felt trapped in an endless cycle of exercise and eating. The first few weeks of titration really suck but it is totally worth it. Before starting memantine and continued to today, I also supplement magnesium and inositol for depression. Both of those helped but memantine is exactly what I needed.
 

passivity

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Memantine was a life saver for me. I've had binge eating disorder as long as I can remember. I also have ADHD symptoms. I've been on 10mg for about 8 months which is the lowest dose recommended. It took a good 3 months for me to really feel a difference and I can't imagine myself without it. I am calm, less OCD, more organized and don't stress eat as much. With the addition of progesterone cream I also felt much happier. I smile and laugh now where before I felt trapped in an endless cycle of exercise and eating. The first few weeks of titration really suck but it is totally worth it. Before starting memantine and continued to today, I also supplement magnesium and inositol for depression. Both of those helped but memantine is exactly what I needed.

wow, I also have ADHD and OCD, just a question, do you drink coffee?
 

passivity

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I have tried memantine. Me and my friend ordered some online and started using it early in December.

We both started with 10mg and dosed throughout the night, I made it to 40mg that night. That first night we both felt amazing an alive, we both experienced profound epiphanies about life. My ability to feel pleasure stayed the same but I just felt different and better.

We expected it to be pretty weak but it was surprisingly strong.

I wasn't able to get good sleep for a couple of days afterwards, and I kept redosing like a fool.

At about the 4th day, after not getting any good sleep since starting, I was hanging out with the same friend, and took another dose of 10mg mixed with a small amount of diclazepam, and just felt off. I ended up leaving my friends house to try and get good sleep.

I went home and basically had a panic attack. That never happens to me, and I've never been so scared from a drug. I felt like I was gonna have a heart attack. I was in a dark room and my vision was weird af. I would fall asleep for 10 minutes and wake up because I heard a loud bang (there was no bang, auditory hallucination), and with this bang I would grab my chest in fear of heart attack.

At some point that night I took a shower and literally couldn't feel the temperature of the water. My face felt like it does when you're really drunk. I couldn't feel anything on my skin.

I ended up sleeping and only redosing a couple times more after giving it a break, in hopes of getting the same good effects.

I took around 100mg+ over the course of 5 days.

My other friend did around the same dosing, but he weighs way more than me, and I am very skinny already.

Ray has talked about memantine, and apparently the adamantane group of molecules (which memantine belongs to) structure water.

Memantine is an NMDA antagonist, but at low doses it blocks abnormal NMDA activity and thus calcium influx, which can kill neurons. It's also a D2 agonist, Nach7 antagonist, and 5HT-3 antagonist.

Me and my friend both noticed that ourselves and eachother looked waaayyy more healthy. Our teeth and skin and hair looked way better. We also noticed improvements in bowel health.

Memantine, as a D2 agonist with a long as **** half-life (60-80 hours), will destroy your sleep.
thanks,

do you think clonidine might help?
 

feather310

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wow, I also have ADHD and OCD, just a question, do you drink coffee?

I drink coffee occasionally but not daily. Coffee tends to make me jittery then crash with hypoglycemia. However, I do consume caffeine daily 100-200mg/day when I workout in the form of a pre-workout.
 

passivity

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I drink coffee occasionally but not daily. Coffee tends to make me jittery then crash with hypoglycemia. However, I do consume caffeine daily 100-200mg/day when I workout in the form of a pre-workout.

alright, have you tried theanine or tianeptine with coffee?

No, I don't think it will help.

Ok, but how did you function on memantine then?
 
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@passivity

Well it feels exactly a lot like being piss drunk. Your face and lips and body are numb.

I would constantly get epiphanies and insights into my life and actually made a few changes that helped.

However, for like a week straight I was constantly slurring my words and would stumble around as I walked.

I would laugh this disgusting laugh when I thought something was funny, it was a drunk laugh.

Surprisingly my cognition was pretty much unaffected. A good measure for my cognition is how good I am at video games, and I was ******* amazing, better than I usually am. I would play FPS's and though I usually get MVP in most rounds, I did even better than when I was sober.

I was also able to make coherent and logical ideas and people who know me IRL thought I was still intelligent.

I had a complete cessation of social anxiety, because I was basically drunk.

The only problem was lack of sleep. I tried hanging out with a friend of mine but couldn't, I felt sick and my chest hurt and I had to go home. Getting good sleep fixed my problems but in order to get good sleep I had to stop dosing memantine.

Also memantine completely changes how your brain weigh's pleasure. Pleasure is calculated using an insane amount of variables, and memantine changes the equation slightly, which changes how you perceive pleasure.

For the first 2 days memantine literally felt like it changed my life. I might actually try dosing again at some point but keep the dose low and make sure my sleep is good. Because those first two days were amazing. Complete detachment from ***t that doesn't matter, I felt superhuman. Probably mania.

Oh yeah, at the fifth day mark I was in so much psychic pain that I wanted to die. I felt like I was going bonkers, I just wanted it to end.

So yeah...
 

passivity

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@passivity

Well it feels exactly a lot like being piss drunk. Your face and lips and body are numb.

I would constantly get epiphanies and insights into my life and actually made a few changes that helped.

However, for like a week straight I was constantly slurring my words and would stumble around as I walked.

I would laugh this disgusting laugh when I thought something was funny, it was a drunk laugh.

Surprisingly my cognition was pretty much unaffected. A good measure for my cognition is how good I am at video games, and I was ******* amazing, better than I usually am. I would play FPS's and though I usually get MVP in most rounds, I did even better than when I was sober.

I was also able to make coherent and logical ideas and people who know me IRL thought I was still intelligent.

I had a complete cessation of social anxiety, because I was basically drunk.

The only problem was lack of sleep. I tried hanging out with a friend of mine but couldn't, I felt sick and my chest hurt and I had to go home. Getting good sleep fixed my problems but in order to get good sleep I had to stop dosing memantine.

Also memantine completely changes how your brain weigh's pleasure. Pleasure is calculated using an insane amount of variables, and memantine changes the equation slightly, which changes how you perceive pleasure.

For the first 2 days memantine literally felt like it changed my life. I might actually try dosing again at some point but keep the dose low and make sure my sleep is good. Because those first two days were amazing. Complete detachment from ***t that doesn't matter, I felt superhuman. Probably mania.

Oh yeah, at the fifth day mark I was in so much psychic pain that I wanted to die. I felt like I was going bonkers, I just wanted it to end.

So yeah...

well... at least it was a pretty good time!
 

feather310

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alright, have you tried theanine or tianeptine with coffee?

I tried tianeptine but didn't feel anything from it. However, this was at the same time as memantine and then I read about the possible interaction between the two so I stopped. I didn't give tianeptine enough time and after I read about the withdrawal symptoms I gave up trying it again. I use theanine at night to help calm my brain.

I think you need to figure out what you want to solve. Tieaneptine, Theanine and mematine are completely difference substances and act differently. What neurotransmitter are you trying to target? What symptoms are you trying to account for? Have you ever used amino acids to increase serotonin or dopamine?
 

passivity

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I tried tianeptine but didn't feel anything from it. However, this was at the same time as memantine and then I read about the possible interaction between the two so I stopped. I didn't give tianeptine enough time and after I read about the withdrawal symptoms I gave up trying it again. I use theanine at night to help calm my brain.

I think you need to figure out what you want to solve. Tieaneptine, Theanine and mematine are completely difference substances and act differently. What neurotransmitter are you trying to target? What symptoms are you trying to account for? Have you ever used amino acids to increase serotonin or dopamine?

Well, I'm using baclofen for agoraphobia, it's a really effective anxiolytic.

I still use tianeptine from time to time but I need 50mgs to feel the effect.
 
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