23 replies to this topic

[nowayout]

After trialing several antidepressants without success (Zoloft, Remeron, Agomelatine, Tianeptine), I have for the moment given up on antidepressants and am using Tramadol (which I am prescribed for chronic pain anyway) as a crutch on the days where I feel I'm hanging by a thread. To be honest, at this point I need it less for pain than for depression. Amitriptylene is the only antidepressant that seems to help so far but it also takes away my libido completely.

Tramadol works relatively well for depression. It is sometimes used for treatment resistant depression. So in principle I could just continue with it. However, it completely destroys my libido and motivation to leave the house, which makes me unhappy.

Libido would IMO be important if I am to have any hope of recovery. Having libido would allow me to date. I haven't had a date in 5 years and I feel like life is passing me by, which gives me a huge amount of existential anxiety. In the past when I did date I found that it would completely take away my depressive symptoms. Social and physical interaction with other people are fundamental to mental health.

So I see two options:

(1) I could try to augment the tramadol with something else to try to bring my libido back. Since I (sometimes) need pain control anyway, this wouldn't be so bad. But what? Bupropion, for example, does not agree with me at all. Augmenting tramadol with trazodone, remeron, tianeptine, or agomelatine does not bring back libido. I have tried.

(2) I could try to replace the Tramadol with an antidepressant that I haven't tried yet that doesn't cause loss of libido. The only one left is moclobemide, which I have, but haven't tried. But how do I go about the replacement? I know theoretically I should taper off the Tramadol completely first, but it doesn't work. I feel too unbearably bad. I really need some kind of gradual replacement.

Any ideas?

Edited by nowayout, 01 December 2013 - 05:26 PM.

[Tom_]

You have got hold of Moclobemide! Yes, Yes and Yes!

There is no gradual replacement to use Moclobremide. Its an RIMA. Using both at the same time is contraindicated. Once you have been stabilized on Moclobremide it could be re-started very carefully but its dangerous even then. Either way scrap the Tramadol for codeine/dihydrocodeine or other mild opiate (for the pain). Pethidine (demoral) is also contraindicated other opioids are fine - just those two.

The half life for Tramadol is short and theoretically you could start taking Moclobremide just after a day of being off it. This in my opinion is plain madness. 5 days is enough for it to be out of your system. Then you start Moclobremide at 150mg for two days before increasing to 300. Wait at 300 for 6-8 weeks and then increase the dose if required. Good news is if Moclobremide works, it works quick.

You know my view on using Tramadol as an AD. Eventually its going to poop and the other risks aren't worth it. If required take time off work, stock up on Phenibut and use that for the five days to manage the coming off Tramadol. Take a break for the first two days on Moclobremide and if you still need it lower the dosage and use as a PRN (when required) until Moclobremide kicks in. Don't think you can handle longer on Phenibut and then get yourself addicted...lots of people do it and its not worth it. Maximum dose in a day for the first five shouldn't exceed 5 grams, you will probs sleep through most of it.

When I say contraindicated combined the two could kill you. You're more likely to end up in A&E/ER with a terrible headache and a mild serotonin toxidrome but there is a very realistic risk of a lot worse than that happening. There is no safe cross titration.

[Ark]

Consider this stack -

Memantine

Nuvigil
Noopete
Picamillon
Lions mane
Sunifram
cerebrolysin
Lithum carbohydrate

Edited by Ark, 01 December 2013 - 08:08 PM.

[Tom_]

Lithium carbohydrate doesn't exist. I assume you mean Lithium carbonate - which is an excellent idea ONCE he has been stabilized on an antidepressant and effects can be determined. The rest is just a load of crap.

[Ark]

@Tom yes and yes

Lithium carbohydrate doesn't exist. I assume you mean Lithium carbonate - which is an excellent idea ONCE he has been stabilized on an antidepressant and effects can be determined. The rest is just a load of crap.

The rest is just a bunch of crap.... right .....
auto spell fixed carbonate
Don't call my suggestion crap unless you can back it.


=========================
That being said Lithium levels need to checked via blood test now and again.

[Tom_]

I'll call anything crap that can't be backed. The only thing with a shred of evidence in comparison to standard pharmacological treatments is the Armodafinil and that shows poor results and no improvement in mean depression just certain symptoms. Our friend here however suffers terribly with insomnia. Everything else is poorly studied (apart from memantine) but in the case of depression has either 1 or 2 small studies supporting it. I believe there is also one not separating from placebo. Poorly studied means it could cause all manner of side effects or simply waste money. Not to mention with such a large stack it would take a year to add them all in and test them properly.

Lithium when used in proper dosages (and form - none of that orotate stuff) comes with some heavy side effects and require monitoring on day 1, 3, 5, then weekly for three weeks and then quarterly.

Edited by Tom_, 01 December 2013 - 10:05 PM.

[Ark]

I'm just offering what has worked well for me in the past, and since he has listed a number of conventional treatments I wanted to give him some fringe suggestions for him to consider, if everything else fails. Depression is a funny thing and while often has allot to do with the 5 HT receptors it is not a golden rule. Since I noticed that most of the treatments he has used work mostly on the 5 HT receptor i thought something else could be the culprit or a multi-facade depression meaning one thing keeps another down, something throwing the oscillation off etc.  1381464_718406481520916_1788969565_n.jpg   112.22KB   21 downloads

Edited by Ark, 01 December 2013 - 10:15 PM.

[BlueCloud]

I haven't had a date in 5 years and I feel like life is passing me by, which gives me a huge amount of existential anxiety. In the past when I did date I found that it would completely take away my depressive symptoms.

Well then, if it has such a big impact, the solution is not more antidepressants that kill your libido, but to work on getting back into the dating scene. Are you getting depressive because of the lack of social interaction/dating, or is it the depression that made you get out of social interactions ?

[nowayout]

I haven't had a date in 5 years and I feel like life is passing me by, which gives me a huge amount of existential anxiety. In the past when I did date I found that it would completely take away my depressive symptoms.

Well then, if it has such a big impact, the solution is not more antidepressants that kill your libido, but to work on getting back into the dating scene. Are you getting depressive because of the lack of social interaction/dating, or is it the depression that made you get out of social interactions ?

Both.

I spent a lot of time last year going out and trying to meet people, to no avail. Trying to meet people just dumps me into an extremely dysphoric depressive state when I fail, so I have developed a very strong aversion to going out. I'd rather take pills to calm me down and stay home reading a book. I know there is the internet blah blah blah but it doesn't work. I know this is self-destructive behavior, but at this point I am going to need more than just a pep talk to fix things, if anything can be fixed.

[BlueCloud]

I haven't had a date in 5 years and I feel like life is passing me by, which gives me a huge amount of existential anxiety. In the past when I did date I found that it would completely take away my depressive symptoms.

Well then, if it has such a big impact, the solution is not more antidepressants that kill your libido, but to work on getting back into the dating scene. Are you getting depressive because of the lack of social interaction/dating, or is it the depression that made you get out of social interactions ?

Both.

I spent a lot of time last year going out and trying to meet people, to no avail. Trying to meet people just dumps me into an extremely dysphoric depressive state when I fail, so I have developed a very strong aversion to going out. I'd rather take pills to calm me down and stay home reading a book. I know there is the internet blah blah blah but it doesn't work. I know this is self-destructive behavior, but at this point I am going to need more than just a pep talk to fix things, if anything can be fixed.

I'm quite familiar with this situation, having lived nearly all my life with chronic anxiety and social phobia, to the point where my life and my career have been built around minimising social interactions as much as possible. Things got better with years and with more exposure , but I still have periods where I can barely leave home or even answer the phone for days.

The thing is, it's a vicious circle, a loop that you have to forcefully break at some point. Lack of social interactions makes you depressed, getting depressed makes you even less likely to have social interactions, wich in turn gets you more depressed, etc.. It's a downward spiral.

Some people can live perfectly happy with minimal social interaction and don't feel the need to have a partner, but obviously it's not your case ( mine neither ). Whatever depression I might have, it's been always secondary to my anxiety. Lift the anxiety, and every symptom of my depression vanishes immediately. Wich is why antidepressants ( especially the SSRI sort ) have been absolutely useless in my case, while most anxiolytic or dopaminergic substances helped one way or another. And your depression seems very secondary to your social life, since it completely lifts when you dated.

In my case, I know that I will never be a social animal, I'm pretty introverted and prefer ( and enjoy) to work alone , but I still need a certain amount of social and romantic/sexual life to maintain good mental health. There is simply no way around it, no matter how hard I tried to do without it.

So unless you live in the middle of the desert, in prison or severely handicapped, there's no reason you should give up on dating. Use supplements, social strategies, technology , whatever it takes.
I don't know what part of the world you live in and what's your particular situation , but Internet did work for me, it's been a (social) life saver. I wish I could just talk spontaneously with strangers in real-life, but I can't, so I'll take second best. Maybe dating thru Internet only really works if you live in a big city ( my case ), I don't know, perhaps the pool to choose from is much smaller in your area.. But I wouldn't give up on it.

Apart from using the Internet and dating sites if needed, what I could recommend from experience to help break that downward spiral and get active again in dating as a priority :

- Buspirone : It works for a very small minority of people ( and is therefore considered pretty much a failure, despite whatever statistics the pharma company tries to push on ), but when ( and IF) it works and you're among the lucky ones , it has many advantages over benzos. Lower cognitive impairement, no tolerance/withdrawal issues, and not only it doesn't negatively impact libido, but it actually enhances it ( it did made me a bit hornier and gave me better erections ) probably due to its effects on D2 receptors.
It's dirt cheap, and has a very benign secondary effect profile, the most serious being strong nausea/dizziness. Unfortunately for me , the dizziness was so strong I had to give up on it ( and is one of the main reasons so many people can't tolerate it), but you might be more lucky. Worth a shot if you didn't already.
- Sulbutiamine : among it's effects , it made me more talkative, more social, more motivated but also slightly less sensitive to negative interactions, less fear of rejection. And no negative impact on libido whatsoever. Check this thread if you haven't already : http://www.longecity...-the-long-term/
- L-Tyrosine :for some reason, it only works if I take CDP-Choline for a few days before taking the tyrosine, maybe because of the dopamine receptors upregulating effect of cdp. When of the best combos I found for motivation and getting out of a rut. Although I find Sulbutiamine's social effects more powerful overall.
- Uridine could give similar results, but I don't have any experience with it yet. I have some coming in the mail soon.
- Sam-e : this can be truly powerful in terms of motivation and energy, and for social interactions. Be careful however if you're very prone to anxiety like me, as it can increase it and make you irritable. its'a cofactor of the PNMT enzyme wich increases conversion of norepinephrine to epinephrine. It was too much for me, but it is absolutely worth a shot. And it has a libido boosting effect.
- Magnesium, Kava, Picamilon are decent additional choices to add , mostly because their anxiolytic effect has no negative impact on libido, and no serious cognitive impairment.
- If worse comes to worse, a small dose of a benzo during social interactions will make you less sensitive to rejection/failure. As long as it's used in a very occasional manner, and at the smaller doses possible, there shouldn't be any serious issues. They do have more cognitive impairment than Buspirone/Kava/Magnesium in my experience.

If buspirone works for you, I would stack either Sulbutiamine , Tyrosine or Sam-e with it for the additional push in socialising/motivation and positive libido effect.
Remember , it only takes one person wich you like and get along with, and all the frustration about social interactions is forgotten.It's worth it.

[nowayout]

Thanks. You've given me a lot to think about. Much of my depression is indeed secondary to anxiety also.

As for the dopaminergics you recommend, though, I don't react well to dopaminergics. For example, I recently tried just one Adderall and it just made me feel anxious and jittery, not a good feeling, different from what other people feel from it. I also did try Mucuna for a while, with no effect at all, as well as pramipexole, also to no effect, and a few years ago cabergoline, again with no effect. Also, I am already prone to obsessive-compulsive thinking and behaviors - doesn't that perhaps indicate already "overheated" dopamine circuits, whatever that may mean, and perhaps a need to damp dopamine down, if anything?

Edited by nowayout, 03 December 2013 - 10:11 PM.

[Tom_]

Sulbutramine is a bad choice for you in the long term. It increases glutamate activity in the pre-frontal cortex and D1 receptor sensitivity - the closest receptor there is to an OCD receptor. In the short term it could be very useful, increasing pro-social behavior. In the long term it has the potential to plunge you in to the depths of a severe depressive disorder and worsening obsessive behavior- which is a beast I hope you don't have to face, you already have enough. Buspirone is a possible choice and I disagree that it isn't an effective option, the main problem is side effects. Sedation and othostatic intolerance cause a lot of people to discontinue it or never reach an effective dose (30-60mg/day) - however its sedation may be of benefit. I still believe Moclobremide should be started first and is your best choice. Adjunctive Buspirone or Pregabalin is a great idea, although adjunct Buspirone would have to be carefully instigated. I maintain that Psychotherapy is vital because I do believe you have a personality disorder and its a tried and tested method for OCD, MDD and Social anxiety. Cognitive Behavioral therapy is the gold standard but third gen CBT therapies may be even more effective (mindfulfulness based CBT, ACT etc), CAT (cognitive analytic therapy) would be a good option for you - as it would allow you to develop a better understanding of what is going on but you will be hard pressed to find a practitioner in the US.

Another option medication wise open to you is glutemnergic modulation. Pregabalin, Lamotragine and Carbenzapine are options on this front.

I have mentioned it before but Aripiprazole could also be very useful. With its mood stabilizing qualities, dopamine patial agonist and 5ht1a activity its an excellent choice.

[BlueCloud]

Thanks. You've given me a lot to think about. Much of my depression is indeed secondary to anxiety also.

As for the dopaminergics you recommend, though, I don't react well to dopaminergics. For example, I recently tried just one Adderall and it just made me feel anxious and jittery, not a good feeling, different from what other people feel from it. I also did try Mucuna for a while, with no effect at all, as well as pramipexole, also to no effect, and a few years ago cabergoline, again with no effect. Also, I am already prone to obsessive-compulsive thinking and behaviors - doesn't that perhaps indicate already "overheated" dopamine circuits, whatever that may mean, and perhaps a need to damp dopamine down, if anything?

L-Tyrosine is less hardcore than the options you mentionned, it's simply the amino-acid, and you body will metabolise whatever it consider as needed in the form of dopamine, then l-dopa

On the other hand, perhaps you don't even need any dopaminergics at all. Just work on correcting your anxiety and your depression will take care of itself. The key thing in my opinion, is to identify first WHAT needs to be corrected before bombarding yourself with all sorts of substances with strong undesirable secondary effects that willl just add to your depression and anxiety.
Regarding your obssesive-compulsive behavior, does it really conform to the strict description of OCD ? Or could it be also just another subset to your anxiety ? I thought I was OCD for a long-time, until I realised it was simply a way to discharge my anxiety. Even negatively and through somewhat hurtful behavior, it was a way to get rid of some of the crippling anxiety. Again, everytime my anxiety lifted, all my OCD symptoms magically disappeared... Chronic anxiety brings a lot of behavior that sometimes look like OCD , it shifts behavior from flexible to being dominated by habits :
http://www.sciencema...nt/325/5940/621

Probably a good part of your issues (anxiety/depression) are not entirely endogenous, but rather reactive to your social situation/environment. So the only long-term solution is to correct the source, to ACT and CHANGE your social situation/environment , the issues that put you in this state in the first place. Again, it's a negative self-reinforcing loop : external issues --> internal issues (depression/anxiety) --> agaravates external issues --> aggravates internal issues (depression/anxiety) etc..
The goal is to replace it with postitive self reinforcing loop . More success comes to success. It sucks and it's unfair, but that's life and we might as well make the most of it. Positive environment/situation --> better internal mood --> even better environment/situation --> even stronger positive mood, etc..

So, unless your problem is truly endogenous ( and it doesn't seem to be the case) , whatever supps/meds you decide to use, keep in mind this : " How is it going to assist me in changing and acting on the external issues that are creating the problem in the first place ?" . The supp/med should not be seen as the final destination but as a tool ( and a temporary one if possible) , an assistant to help you change external reality and modify your situation, . Otherwise, reality will come back later to bite you in the ass, and it will hurt tenfold more. It happened to me.

So yeah, psychotherapy and all that is certainly helpful, even if it's just to help you get a more precise image on what the problem is and what is the target you should act on , instead of bombarding everything that looks fishy inside of your head. And you seem to have already identified a good portion of it ( lack of social interactions, lack of romantic/sexual partner ).

Edited by BlueCloud, 04 December 2013 - 10:45 AM.

[Tom_]

If he does go down the amino acid route and I don't think he should DLPA would be better for him - doesn't deplete sulfur (apparently for some reason).

I also think he doesn't have a very good understanding of the situation (not you're fault, I don't have a good one of mine either) but questions such as where did the lac of social interactions come from, why do they persist, how can this be changed need answering.

Otherwise apart from perhaps what drugs to use I think we are in perfect agreement. I think that's pretty good for me, I ususally disagree with everything. Look at how many down votes I have! WOO!

[nowayout]

...stock up on Phenibut and use that for the five days to manage the coming off Tramadol.

Okay, I got phenibut from the forum sponsor and took a gram this morning. It had absolutely no effect on me though. I guess I'm just going to have to do a slow taper off the tramadol.

[Tom_]

Takes about three hours to kick in. If that doesn't have enough effect, increase the dose but I doubt 1 gram won't have effects.

[nowayout]

Takes about three hours to kick in. If that doesn't have enough effect, increase the dose but I doubt 1 gram won't have effects.

It's been about 8 hours since the one gram dose that I took around 8 this morning. Nada. I normally don't have a strong response to GABA drugs and need high doses of benzos (usually roughly 4 times the usual starting dose) for any effect. I guess I'll just increase the dose then.

By the way, could this GABA insensitivity perhaps be part of my problem?

Edited by nowayout, 05 December 2013 - 08:57 PM.

[Tom_]

What are the results of an increased dose. You can't have global GABA insensitivity, you'd die from a constant seizure.

[Deep Thought]

Keep a log of all the negative thinking you do.
http://videnskab.dk/...d-simpel-ovelse

Basically, you can reduce your anxiety by writing down the negative thinking you do, which frees up more "RAM", i.e. your working memory. The article is about anxiety, but from my perspective it's still worth a shot, as you could amongst other things theoretically use your common sense to identify illogical rambling and really, any thought that doesn't seem real and thereby reduce the impact it has on your emotions. Even manly men have emotions.

Recommending a pharmaceutical carries with it some risks. I hope this is a place where I can freely voice my opinion. I think thos is sorely needed, when considering certain pharmaceutical companies have a history of withholding studies showing the dangerous side effects certain drugs have and inflating the positive effects. Or by stating a drug is clinically effective, when the effects are in fact, only slightly statistically significant.



Deprenyl has been immensely helpful for me in attenuating the depressive symptoms I've had for the past 9 years.

Deprenyl, secondary to being a MAO-B and to some extent, a MAO-A inhibitor, also possesses catchecholamine and serotonin activity enhancing effects. This means that, whenever a neuron is stimulated by an adjacent neuron, a larger amount of the neurotransmitters dopamine or serotonin is released.

Deprenyl was recently approved by the FDA for treatment of major depressive disorder, using a transdermal delivery system named "Ensam".

Combined with less than or equal to 500 mgs of l-tryptophan and vitamin B6, which you should be getting anyways, more l-tryptophan should convert into 5-HTP rather than kyurenine.

Deprenyl is an aphrodisiac, mediated in part by its' effects on the mesolimbic dopamine pathway, by secreting more mesolimbic dopamine (DA). This hasn't been conclusively shown in humans yet, but from my own experience, yes it is a true aphrodisiac. Also, recall that deprenyl is a CAS activity enhancer, in theory this would cause larger amounts of dopamine to be secreted, and reinforce natural reward seeking behaviours such as sex and food.

I take 5-HTP, tyrosine and DLPA in small dosages throughout the day. It is highly effective.

Deprenyl purpotedly enhances various neurotrophic factors in the CNS. These neurotrophic factors could theoretically speed recovery, if the theory holds that certain SSRI's work by enhancing hippocampal neurogenesis. It also has neuroprotective effects.

Rapid treatment of depression with selegiline-phenylalanine combination.
http://www.ncbi.nlm..../pubmed/1900832

L-deprenyl plus L-phenylalanine in the treatment of depression.
http://www.ncbi.nlm..../pubmed/6425455

The aphrodisiac effect of low doses of (-) deprenyl in male rats.
http://www.ncbi.nlm..../pubmed/6821215

***
Despite possessing weak MAO-A affinity, you should absolutely not mix deprenyl and tramadol. Tramadol lowers the seizure threshold, and may cause brain jolts and other nasty side effects. Moreover, tramadol doesn't only affect the mu opiod receptors, but also other opiod receptors and has SNRI activity.

So that's another problem if you go down this route.

Cooperative opioid and serotonergic mechanisms generate superior antidepressant-like effects in a mice model of depression.
http://www.ncbi.nlm....pubmed/19341511

Edited by Deep Thought, 06 December 2013 - 07:49 PM.

[Tom_]

Selegiline at doses below 6-8mg don't inhibit MAO-A and hence give no antidepressant activity. At doses above this both are inhibited requiring avoidance of serotonergic or dopamine/noradenergic drugs (in general). Oral dosing requires an MAOI diet and as such isn't approved in doses smaller than 6mg/24 hours. Furthermore there is no evidence that it improves sex drive beyond that of lifting depressive symptoms and has been associated with sexual dysfunction.

Taking 6mg+ of selegiline a day alongside L-tryptophan puts you at high risk for serotonin toxidromes.

[Deep Thought]

Selegiline at doses below 6-8mg don't inhibit MAO-A and hence give no antidepressant activity. At doses above this both are inhibited requiring avoidance of serotonergic or dopamine/noradenergic drugs (in general). Oral dosing requires an MAOI diet and as such isn't approved in doses smaller than 6mg/24 hours. Furthermore there is no evidence that it improves sex drive beyond that of lifting depressive symptoms and has been associated with sexual dysfunction.

Taking 6mg+ of selegiline a day alongside L-tryptophan puts you at high risk for serotonin toxidromes.

Selegiline is free from the cheese effect when given in oral dosages less than 10 mg/day, and with a diet that has less than 200 mg of tyramine.

Short-term treatment with the emsam patch had a small positive effect in treating the symptoms of sexual dysfunction: http://www.ncbi.nlm....pubmed/18162016

[nowayout]

What are the results of an increased dose. You can't have global GABA insensitivity, you'd die from a constant seizure.

I am afraid of experimenting any more with this since it left me very nauseated since last night.

[Tom_]

Likely a coincidence. Up for one more trial?

[Deep Thought]

Selegiline at doses below 6-8mg don't inhibit MAO-A and hence give no antidepressant activity. At doses above this both are inhibited requiring avoidance of serotonergic or dopamine/noradenergic drugs (in general). Oral dosing requires an MAOI diet and as such isn't approved in doses smaller than 6mg/24 hours. Furthermore there is no evidence that it improves sex drive beyond that of lifting depressive symptoms and has been associated with sexual dysfunction.

Taking 6mg+ of selegiline a day alongside L-tryptophan puts you at high risk for serotonin toxidromes.

Selegiline is free from the cheese effect when given in oral dosages less than 10 mg/day, and with a diet that has less than 200 mg of tyramine.

Short-term treatment with the emsam patch had a small positive effect in treating the symptoms of sexual dysfunction: http://www.ncbi.nlm....pubmed/18162016

To elaborate.

Cheese effect:

"It wasn’t until the development of two novel MAOIs that the mechanisms behind the cheese effect became elucidated. In 1964, Knoll developed l-deprenyl, a potent and irreversible MAOI (5). Unlike traditional MAOIs, deprenyl selectively inhibited the deanimation of only certain amines, most notably dopamine, phenylethylamine and benzylamine. What made l-deprenyl particularly remarkable was its freedom from tyramine interactions. Not only was it free from such interactions, but l-deprenyl also had the ability to block the hypertensive effects of tyramine (8)."
8. Magyar K, Vizi ES, Ecseri Z, Knoll J. Comparative pharmacological analysis of the optical isomers of phenyl-isopropyl-methyl-propinylamine (E-250). Acta Physiol Acad Sci Hung. 1967;32(4):377-87.

The antidepressant effect:

"Formed from the decarboxylation of phenylalanine, PEA is a naturally occurring trace amine found in the brain that has amphetamine-like activity. Patients with major depression often have low levels of PEA metabolites in the urine, while manic and schizophrenic patients demonstrate elevated levels (36). While the intake of phenylalanine can improve depression, supposedly by increased PEA formation (35), PEA is rapidly metabolized by MAO-B, limiting its effect. However, when MAO-B is inhibited with l-deprenyl, PEA levels rapidly and substantially increase (37). When PEA is administered along with l-deprenyl to humans, there is a potent and rapid antidepressant effect on par with amphetamine, but without tolerance (38)."
38. Sabelli H, Fink P, Fawcett J, Tom C. Sustained antidepressant effect of PEA replacement. J Neuropsychiatry Clin Neurosci. 1996 Spring;8(2):168-71.

Comment: PEA might be too dangerous. I suggested DLPA.

Sexual Function:

"Given the intimate relationship between dopamine and sexual function, l-deprenyl can act as an aphrodisiac in male rats (62), turning sexually low performing rats into high performing ones (63). Male rats on l-deprenyl also experience increased erectile potency (64) probably due to enhancement of nitric oxide, which can dilate blood vessels (65).
Hypersexuality is not uncommon in Parkinson’s patients receiving l-deprenyl and other dopaminergic drugs (66), and there is at least one case of a patient on l-deprenyl who developed transvestic fetishism (67). The man’s impulse to wear women’s clothing ceased when the drug was discontinued."

Comment: I meant only to theorize that deprenyl is an aphrodisiac, not stating it as a fact. (I'll reread my post later for other errors.)

Sources taken from:
http://www.mindandmu...-andrew-novick/
http://www.mindandmu...-andrew-novick/

**

I suggest reading those two articles, if anyone reading this is curious about deprenyl. Deprenyl is an interesting molecule. Since I'm not educated in epidemiology, I cannot tell you which parts are bullshit and which parts are true.

Especially, read the part about "CAE". Also, the fact that BPAP is similar in action to deprenyl, but more than 120 times more potent in several modes of its' actions is fascinating.

**

Serotonin toxidrome.

I need to further elaborate this.
5-HTP might be too dangerous despite the fact that deprenyl doesn't seem to have much MAO-A inhibition at low dosages.

Edited by Deep Thought, 07 December 2013 - 03:39 PM.