Edited by eon, 02 November 2014 - 09:37 AM.

#1
Posted 02 November 2014 - 09:30 AM
#2
Posted 02 November 2014 - 07:11 PM
Well ... yes pretty much anything similar to heroin in effect will help against pretty much any mental disorder. Schizophrenia: cured, depression: cured, anxiety: cured. You know the drill.
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#3
Posted 03 November 2014 - 11:46 AM
The paracetamol in the percocet will destroy your liver, if you take too much (which you almost certainly will).
#4
Posted 03 November 2014 - 05:11 PM
wow, everyone got -1, what's up with that? This is a legitimate topic. Percocet is helpful to those suffering from pains. It's not meant to be abused just like everything else.
#5
Posted 03 November 2014 - 05:36 PM
#6
Posted 04 November 2014 - 08:07 AM
so high dopamine lowers serotonin and is one of the possible culprit behind OCD?
#7
Posted 04 November 2014 - 12:25 PM
so high dopamine lowers serotonin and is one of the possible culprit behind OCD?
No. Increasing/decreasing single neurotransmitters doesn't cause any mental disorders. All it can do is cause certain and rather physical than mental defects (like seizures, apathy/fatigue/spasms/agitation/tremors and such).
#8
Posted 05 November 2014 - 03:24 AM
so high dopamine lowers serotonin and is one of the possible culprit behind OCD?
I should have been more precise; low serotonin tends to exacerbate the symptoms of OCD.
Edit: Anyway, toxo is more strongly implicated in schizophrenia; there may be something to the "crazy cat lady" stereotype
Edited by StevesPetRat, 05 November 2014 - 03:26 AM.
#9
Posted 21 December 2014 - 02:19 PM
but high serotonin leads to serotonin syndrome?
"OCD has been linked to abnormalities with the neurotransmitter serotonin, although it could be either a cause or an effect of these abnormalities. Serotonin is thought to have a role in regulating anxiety." Wiki
so high dopamine lowers serotonin and is one of the possible culprit behind OCD?
I should have been more precise; low serotonin tends to exacerbate the symptoms of OCD.
Edit: Anyway, toxo is more strongly implicated in schizophrenia; there may be something to the "crazy cat lady" stereotype
Edited by eon, 21 December 2014 - 02:28 PM.
#10
Posted 21 December 2014 - 03:33 PM
Edited by Ark, 21 December 2014 - 03:34 PM.
#11
Posted 21 December 2014 - 04:11 PM
Considering the Zoloft I took then is an SSRI but didn't work, what does that tell me?
All it tells you is that Zoloft doesn't work for you.
(That's assuming you took it for long enough to give it a real go).
It doesn't mean a different SSRI wouldn't be helpful for your OCD.
Do you have access to a physician or psychiatrist, or are you self-prescribing?
From wikipedia:
... many OCD patients benefit from the use of selective serotonin reuptake inhibitors (SSRIs), a class of antidepressant medications that allow for more serotonin to be readily available to other nerve cells...
Behavioral therapy (BT), cognitive behavioral therapy (CBT), and medications are first-line treatments for OCD...
... Medications as treatment include selective serotonin reuptake inhibitors (SSRIs) and the tricyclic antidepressants, in particular clomipramine...
#12
Posted 22 December 2014 - 09:55 AM
I tried all those separately not at the same but never used Memantine yet. I've tried Inositol as well. I just tried OTC lithium that has 50 mcg elemental lithium in it, after 1 dose I dumped the whole bottle. I felt like I had Alzheimer's with all the hand trembling and unsteadiness with standing up, my legs felt unstable. It wasn't for me.
What I was getting at was since OCD is linked to the serotonin receptor (for the most part right?), should I be looking into:
Considering adding these three to your OCD regiment. Memantine, Pregnenolone and low dose Psilocybin. Also make sure your keeping your vitamin d levels up, plus if you have time look into lithium off label it has been used somewhat successfully in conjunction with other drugs/supplements treating anxiety orders.
#13
Posted 22 December 2014 - 12:46 PM
Considering the Zoloft I took then is an SSRI but didn't work, what does that tell me?
All it tells you is that Zoloft doesn't work for you.
(That's assuming you took it for long enough to give it a real go).
It doesn't mean a different SSRI wouldn't be helpful for your OCD.
Do you have access to a physician or psychiatrist, or are you self-prescribing?
From wikipedia:... many OCD patients benefit from the use of selective serotonin reuptake inhibitors (SSRIs), a class of antidepressant medications that allow for more serotonin to be readily available to other nerve cells...
Behavioral therapy (BT), cognitive behavioral therapy (CBT), and medications are first-line treatments for OCD...
... Medications as treatment include selective serotonin reuptake inhibitors (SSRIs) and the tricyclic antidepressants, in particular clomipramine...
#14
Posted 22 December 2014 - 03:42 PM
so high dopamine lowers serotonin and is one of the possible culprit behind OCD?
I should have been more precise; low serotonin tends to exacerbate the symptoms of OCD.
Edit: Anyway, toxo is more strongly implicated in schizophrenia; there may be something to the "crazy cat lady" stereotype
OCD is not based on low serotonin, or high serotonin, its based off of central glutamatergic neuron dysfunction and specifically, a strange cAMP-adenosine disinhibition that causes very high calcium channel activity leading to central overstimulation.....however, there are also instances where cAMP is much lower in OCD individuals - and it tends to follow either biphasic histaminergic action e.g action starting with excessive H1 activation and then being exascerbated by H3 activation which reduces cAMP, but also reduces GABA and serotonin as well as other NT's.
NMDA-glutamate receptors are usually distinctively different in OCD, generally being hypoactive (underactive) but not to the point or level of schizophrenia, and interestingly, unlike schizophrenics, OCD sufferers don't have a net lower glutamate tone and tend to have higher at the kainate and AMPA receptors..if this were exchanged and OCD sufferers were to somehow re-map this networking issue, where NMDA-glutamate receptors are favored over kainate and AMPA, that would be expected to help the situation.....
Lowering glutamate may not be the best therapy either, but it can help in many individuals, however, it's interesting to note that there are some OCD sufferers who have actually been noted with LOW GLUTAMATE, and the patterns in these individuals tend to be less compulsive but far more obsessive.
Dopamine has a role , but it's the cross-interactions with serotonin that play a bigger role , when dopamine cross-reacts and activates serotonin 2X family, this is expected to worsen OCD symptoms as these serotonin receptors would worsen the calcium / IP3 pathway which is usually already excessive in these individuals.
Dopamine doesn't directly worsen nor help OCD, but it may alter the tone of OCD or intensity of thoughts, depending on how much is converting into noradrenaline...and how much at which receptor for both catecholamines.
D2R activation in moderate amounts may reduce OCD symptoms if the 5-HT2X serotonin complex is also blocked, and glutamate is under control , because then the contributions to AMPA reactivity by D2R would be reduced, so therefore D2R would raise GABA and hopefully alleviate some excessive stimulation.
Serotonin 1A is a weird one, the pre-synaptic autoreceptors receptors are most probably over-active, and the post-synaptic is either under-active or unchanged....however, antagonizing both 1A and 1B receptors would also alter the tone of OCD, possibly reducing some of the more intense and broad OCD symptoms but possibly increasing more externalized symptoms.
**SOURCES/REFERENCES**
http://www.mayoclinic.org/diseases-conditions/ocd/basics/causes/con-20027827
http://www.sciencedirect.com/science/article/pii/S0301008204000280
http://en.wikipedia.org/wiki/Biology_of_obsessive%E2%80%93compulsive_disorder
#15
Posted 22 December 2014 - 08:17 PM
I'm not so sure that serotonin doesn't have a role in OCD. I had miserable, intrusive, obsessive fears since I was a kid until I was put on Effexor. Effexor completely obliterated the obsessive fears. The problem; Effexor was way too serotogenic for me, it caused so many miserable side-effects that I never felt like celebrating being rid of, what I once thought, was the bane of my existence.
#16
Posted 22 December 2014 - 08:58 PM
I'm not so sure that serotonin doesn't have a role in OCD. I had miserable, intrusive, obsessive fears since I was a kid until I was put on Effexor. Effexor completely obliterated the obsessive fears. The problem; Effexor was way too serotogenic for me, it caused so many miserable side-effects that I never felt like celebrating being rid of, what I once thought, was the bane of my existence.
I didn't say it didn't have a role, I said it's not specifically about high or low levels, it's about what receptors are / aren't being activated and the overall influence on glutamate mediated currents......
Serotonergic activity can increase obsessive fears in some cases, and even facilitate paranoia depending on which receptor it binds to, let's not forget that LSD (Acid) has affinity for multiple serotonin subtypes and in addition, many other addictive drugs; cocaine even, have pronounced effects on serotonin receptors, especially the 5-HT1A receptor, 2A and type 3 through which they are known to produce some degree of euphoria.
On the other hand, most other serotonin receptors can be emotionally blunting / anhedonic.
It seems to depend on the person.
Eur J Pharmacol. 2003 Jan 17;459(2-3):167-9.
Cocaine inhibits 5-HT3 receptor function in neurons from transgenic mice overexpressing the receptor.AbstractStudies have shown that cocaine alters the function of recombinant 5-HT(3) receptors and that behavioral responses to cocaine are affected by 5-HT(3) receptor ligands. However, the actions of cocaine on brain 5-HT(3) receptors have not been characterized because these receptors are not abundantly expressed in most neuronal populations. We examined the effect of cocaine on 5-HT(3) receptor function in cultured hippocampal neurons from transgenic mice overexpressing the receptor. Cocaine competitively inhibited 5-HT(3) receptors with an IC(50) of approximately 4 microM, indicating that brain 5-HT(3) receptors are important targets for the actions of this commonly abused substance.
PMID: 12524142 [PubMed - indexed for MEDLINE]
Abstract
Cocaine induced locomotor stimulant effects are generally attributed to cocaine effects on brain dopamine. In this report, we present evidence that the 5-hydroxytryptamine1A (5-HT1A) agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT) and the 5-HT1A antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinyl-cycylhexanecarboxaminde maleate (WAY 100635) can enhance or block, respectively, the locomotor stimulant effects induced by cocaine. In two separate experiments, rats administered cocaine (10 mg/kg) exhibited a locomotor stimulant effect and decreased grooming behavior compared to saline treated rats. Pretreatment with the 5-HT1A agonist, 8-OHDPAT (0.2 mg/kg) enhanced and pretreatment with the 5-HT1A antagonist, WAY 100635 (0.4 mg/kg) eliminated the locomotor stimulant effect of cocaine. Neither the 8-OHDPAT nor WAY 100635 effects were attributable to effects on the behavioral baseline. The 8-OHDPAT and WAY 100635 had opposite effects on grooming behavior. 8-OHDPAT decreased and WAY 100635 increased grooming. Neither treatment, however, affected the grooming suppression induced by cocaine. Ex vivo biochemical measurements indicated that neither 8-OHDPAT or WAY 100635 affected brain dopamine metabolism or cocaine availability in brain. Both treatments affected 5-HT metabolism and altered the effect of cocaine on 5-HT metabolism. 8-OHDPAT increased and WAY 100635 decreased cocaine effects on 5-HT metabolism. Cocaine and 8-OHDPAT but not WAY 100635 increased corticosterone. Altogether, these findings indicate that the 5-HT1A receptor site may be an important target for the development of pharmacotherapies for the treatment of cocaine abuse.
#17
Posted 23 December 2014 - 11:41 AM
name drop some drug compounds regarding your last 2 paragraphs...
so high dopamine lowers serotonin and is one of the possible culprit behind OCD?
I should have been more precise; low serotonin tends to exacerbate the symptoms of OCD.
Edit: Anyway, toxo is more strongly implicated in schizophrenia; there may be something to the "crazy cat lady" stereotype
OCD is not based on low serotonin, or high serotonin, its based off of central glutamatergic neuron dysfunction and specifically, a strange cAMP-adenosine disinhibition that causes very high calcium channel activity leading to central overstimulation.....however, there are also instances where cAMP is much lower in OCD individuals - and it tends to follow either biphasic histaminergic action e.g action starting with excessive H1 activation and then being exascerbated by H3 activation which reduces cAMP, but also reduces GABA and serotonin as well as other NT's.
NMDA-glutamate receptors are usually distinctively different in OCD, generally being hypoactive (underactive) but not to the point or level of schizophrenia, and interestingly, unlike schizophrenics, OCD sufferers don't have a net lower glutamate tone and tend to have higher at the kainate and AMPA receptors..if this were exchanged and OCD sufferers were to somehow re-map this networking issue, where NMDA-glutamate receptors are favored over kainate and AMPA, that would be expected to help the situation.....
Lowering glutamate may not be the best therapy either, but it can help in many individuals, however, it's interesting to note that there are some OCD sufferers who have actually been noted with LOW GLUTAMATE, and the patterns in these individuals tend to be less compulsive but far more obsessive.
Dopamine has a role , but it's the cross-interactions with serotonin that play a bigger role , when dopamine cross-reacts and activates serotonin 2X family, this is expected to worsen OCD symptoms as these serotonin receptors would worsen the calcium / IP3 pathway which is usually already excessive in these individuals.
Dopamine doesn't directly worsen nor help OCD, but it may alter the tone of OCD or intensity of thoughts, depending on how much is converting into noradrenaline...and how much at which receptor for both catecholamines.
D2R activation in moderate amounts may reduce OCD symptoms if the 5-HT2X serotonin complex is also blocked, and glutamate is under control , because then the contributions to AMPA reactivity by D2R would be reduced, so therefore D2R would raise GABA and hopefully alleviate some excessive stimulation.
Serotonin 1A is a weird one, the pre-synaptic autoreceptors receptors are most probably over-active, and the post-synaptic is either under-active or unchanged....however, antagonizing both 1A and 1B receptors would also alter the tone of OCD, possibly reducing some of the more intense and broad OCD symptoms but possibly increasing more externalized symptoms.
**SOURCES/REFERENCES**
http://www.mayoclinic.org/diseases-conditions/ocd/basics/causes/con-20027827
http://www.sciencedirect.com/science/article/pii/S0301008204000280
http://en.wikipedia.org/wiki/Biology_of_obsessive%E2%80%93compulsive_disorder
#18
Posted 23 December 2014 - 02:04 PM
name drop some drug compounds regarding your last 2 paragraphs...
would taking a calcium channel blocker be worth looking into? Nimodipine comes to mind as it is one and is listed in "Smart Drug 2" (book).Nimodipine (Nimotop) - This substance can pass the blood-brain barrier and is used to prevent cerebral vasospasm. - WikiFrom the book regarding nimodipine: "by blocking calcium channels on the nerve cell membranes, nimodipine slows the entry of calcium into those cells. This has the effect of increasing the magnesium/calcium ratio. Would a magnesium supplement have some of the effects of nimodipine? Maybe."Although I do not have severe OCD anymore, I do supplement with magnesium glycinate. Not sure if that is enough. I only become OCD when I forgot to become OCD as if having such ritualistic habits needed to be done.I don't quite get the whole calcium thing, is this regarding calcium we consume daily? I do not supplement with calcium. Would a calcium deficient diet be enough not to use a calcium channel blocker?
No and Yes; it's regarding calcium ions that are triggered by glutamate. histamine, serotonin ,adrenaline , etc
(visualize the mineral calcium being taken into an electrical stream of energy and that this energy activates glutamate , GABA, norepinephrine)
The more calcium channels and calmodulin-kinase-channels/Ca2+ the less uptake of calcium into the bones the more in the brain , the less calcium channels as with 5-HT1B activation, beta blockade etc, the calcium retracts from the nerves and gets into the bones and other tissues, low calcium channel can be dangerous as well because it can pre-dispose one to kidney stones and other calcium related issues such as over-methylation.
It should all make sense now.
Calcium channels are an important modulator of homeostasis, and they are needed for blood pressure maintenance; if they rise too high they will cause BP issues due to central norepinephrine/glutamate overload..and even though glutamate stimulates nitric oxide, it also has an effect on the efflux of norepinephrine, and due to it's effects through cortisol, it can also raise blood pressure.
You want to minimize cortisol, but you don't want to eliminate glutamate, because glutamate is needed for calcium channels and for proper energy production as well as some is needed in the balance of keeping your blood pressure stable.
http://www.ecmjourna...pdf/v007a02.pdf
http://hmg.oxfordjou...11/20/2377.full
See comment in PubMed Commons below
Cell. 2008 Nov 28;135(5):825-37. doi: 10.1016/j.cell.2008.09.059.Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum.Yadav VK1, Ryu JH, Suda N, Tanaka KF, Gingrich JA, Schütz G, Glorieux FH, Chiang CY, Zajac JD, Insogna KL, Mann JJ, Hen R, Ducy P, Karsenty G.AbstractLoss- and gain-of-function mutations in the broadly expressed gene Lrp5 affect bone formation, causing osteoporosis and high bone mass, respectively. Although Lrp5 is viewed as a Wnt coreceptor, osteoblast-specific disruption of beta-Catenin does not affect bone formation. Instead, we show here that Lrp5 inhibits expression of Tph1, the rate-limiting biosynthetic enzyme for serotonin in enterochromaffin cells of the duodenum. Accordingly, decreasing serotonin blood levels normalizes bone formation and bone mass in Lrp5-deficient mice, and gut- but not osteoblast-specific Lrp5 inactivation decreases bone formation in a beta-Catenin-independent manner. Moreover, gut-specific activation of Lrp5, or inactivation of Tph1, increases bone mass and prevents ovariectomy-induced bone loss. Serotonin acts on osteoblasts through the Htr1b receptor and CREB to inhibit their proliferation. By identifying duodenum-derived serotonin as a hormone inhibiting bone formation in an Lrp5-dependent manner, this study broadens our understanding of bone remodeling and suggests potential therapies to increase bone mass.
Comment in
- When the gut talks to bone. [Cell. 2008]
PMID: 19041748 [PubMed - indexed for MEDLINE] PMCID: PMC2614332 Free PMC Article
Edited by Area-1255, 23 December 2014 - 02:09 PM.
#19
Posted 24 December 2014 - 12:12 PM
Edited by eon, 24 December 2014 - 12:19 PM.
#20
Posted 25 December 2014 - 11:23 AM
#21
Posted 29 December 2014 - 08:18 AM
Edited by eon, 29 December 2014 - 08:22 AM.
#22
Posted 30 December 2014 - 02:32 PM
is not knowing how to let go (i.e. obsessing) a form of OCD and or obsession? Say you had a falling out with a family member over what the person did and you refuse to let the problem go (whatever it may be) and has become an obsession as a form of holding a grudge. I'm trying to learn how to let go but it seems difficult as if this compulsion to obsess about something that had already happened has been preventing me from letting something that happened in the past be the past. In other words, I need to learn how to move on, but find it difficult, especially if it's a relative, but not so much with a stranger (because a stranger is really just that).
#23
Posted 03 January 2015 - 03:28 AM
is not knowing how to let go (i.e. obsessing) a form of OCD and or obsession? Say you had a falling out with a family member over what the person did and you refuse to let the problem go (whatever it may be) and has become an obsession as a form of holding a grudge. I'm trying to learn how to let go but it seems difficult as if this compulsion to obsess about something that had already happened has been preventing me from letting something that happened in the past be the past. In other words, I need to learn how to move on, but find it difficult, especially if it's a relative, but not so much with a stranger (because a stranger is really just that).
I'm not sure if this will be helpful to you or not, but I'll explain my own experience with holding and not letting go of grudges. I suffered from mildly to moderately severe obsessive fears for most of my life. Then I was put on the snri Effexor and in just a few weeks these obsessive thoughts were just obliterated. Unfortunately effexor was just too seretonongenic for me and caused a host of nasty side effects. One of the side effects was increased anger and holding grudges. I would get mad at someone for a genuinely good reason, but I simply could not let go of my anger and would obsessively ruminate about how mad I was at this person and on and on forever. I finally got off snri's and went back to tca's and within a few days almost all of my long standing grudges just melted away. It did take about 8 months total to be rid of all grudges and a great deal of my anger, but I'm pretty normal now when it comes to getting mad at someone and then letting it go when it's over.
I'm not sure if any of this pertains to your situation, but in my case not letting go of grudges was not part of the obsessive/compulsive spectrum, but rather too much serotonin causing too much NE firing, at least in specific parts of my brain, and this led to increased anger and holding grudges forever.
#24
Posted 03 January 2015 - 04:43 AM
Lots of drugs that are serotonergic and TCAs are considered to cause serotonin syndrome. Not sure how the TCA you took worked for you. I think I know what you mean by being angrier and holding more grudges than you really had. I think it's too much serotonin. SSRIs, TCAs, and SNRIs I would think would exacerbate the symptoms.
I took herbals: 5htp, SAMe, and St. John's Wort in combination. 5htp and St. John's Wort are listed as the herbals that can cause serotonin syndrome. I think too much adrenaline makes one vigilant. It's good when you're in battle but if you're with loved ones or co-workers being obsessively watchful may cause problems add to that the OCD.
A serotonin antagonist would work for the situation you described, not sure how a TCA helped you, but I guess it depends on what type of action the medicine you took had. Which one was it?
Thinking about the grudges or something small and blown out of proportion by the mind is somewhat obsessive I think as it keeps repeating in one's mind similar to an OCD. I was already OCD before I took the meds/herbals so upon taking them I guess gave me too much serotonin and exacerbated my OCD symptoms.
Edited by eon, 03 January 2015 - 05:10 AM.
#25
Posted 04 January 2015 - 12:44 AM
It's not true of all tca's, but many don't inhibit SERT as strongly as the snri's/ssri's. So with those tca's that are less inhibiting you don't have as much serotonin floating around in your brain, so less potential for triggering anger. The downside is that physical side-effects (dry mouth, constipation, etc,) are worse with tca's and also with less serotonin obsessive/compulsive symptoms can worsen. I do agree with you that the inability to let go of anger does feel obsessive, but for me it was almost as if I enjoyed being angry and didn't want to drop my grudges, rather than being unable to.
#26
Posted 04 January 2015 - 10:27 AM
U noobs nothing helpful did ever come from this neurotransmitter pseudoscience esotericism talk. Better embrace some REAL shamanism with real hallucinogenic drugs or continue to go by your "mitochondrial support" (hahahhahaha) placebos for less risky stuff.
#27
Posted 04 January 2015 - 11:15 AM
I know what you mean, as if anger is a "gift", enjoying much of it would not allow you to drop the grudges, so it goes round and round. Like I said, it's fine if you're in battle but not in the "real world".
It's not true of all tca's, but many don't inhibit SERT as strongly as the snri's/ssri's. So with those tca's that are less inhibiting you don't have as much serotonin floating around in your brain, so less potential for triggering anger. The downside is that physical side-effects (dry mouth, constipation, etc,) are worse with tca's and also with less serotonin obsessive/compulsive symptoms can worsen. I do agree with you that the inability to let go of anger does feel obsessive, but for me it was almost as if I enjoyed being angry and didn't want to drop my grudges, rather than being unable to.
Don't get me started with hallucinogenics! Do not call yourself a shaman if you haven't tried Datura. Off topic...
U noobs nothing helpful did ever come from this neurotransmitter pseudoscience esotericism talk. Better embrace some REAL shamanism with real hallucinogenic drugs or continue to go by your "mitochondrial support" (hahahhahaha) placebos for less risky stuff.
#28
Posted 13 March 2015 - 08:32 AM
#29
Posted 13 March 2015 - 01:40 PM
but high serotonin leads to serotonin syndrome?
Not really.
Serotonin Syndrome refers to a syndrome of acute and extremely high levels of Synaptic Serotonin most commonly caused specifically by drugs/foods/herbs that inhibit Monamine oxidase (MAOIs) in combination with drugs/foods/herbs that suppress the re-uptake of serotonin (SSRIs, SSNRIs).
Monoamine oxidase braks down serotonin and other neurotransmitters -- MAOIs stop that process -- leaving more Serotonin available at the synapse.
SSRIs/SSNRIs --- inhibit the reuptake of Serotonin into the presynaptic cell.
Or by intentional or unintentional overdose of said drugs
That said, it can also be caused by a combination of any drug or metabolite that significantly raises levels of serotonin -- and concomitant (simultaneous) use of drugs that limit re-uptake, inhibit monoamine oxidase -- or affect the cytochrome pathway for clearance of said drugs.
Libby Zion apparently died from SS because of the metabolite of pethidine -- norpethidine which apparently raises serotonin -- used in combination with phenelzine an IRREVERSIBLE MAOI -- meaning it binds to MAOI permanently, rendering the MAOI ineffective -- resulting in reduced MAOI activity in the CNS until the body can make more.
Moral of Serotonin Syndrome -- IRREVERSIBLE MAOIs are bad news unless you absolutely need to use them because other psychotropics fail to work.
That said, It is not a common syndrome.
Millions of people are taking said drugs -- without causing boatloads Serotonin Syndrome
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#30
Posted 22 March 2015 - 06:41 AM
Edited by eon, 22 March 2015 - 06:43 AM.
Also tagged with one or more of these keywords: ocd
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