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

Photo
- - - - -

serotonin receptor regeneration nootropics?


  • Please log in to reply
60 replies to this topic

#1 jama

  • Guest
  • 10 posts
  • 1

Posted 12 May 2010 - 01:18 AM


hey everyone,

A while back I, unwittingly, used MDMA, a drug with neurotoxic potential. Over the course of the 18 months I used approximately 5-10 times, not more than a pill each time (probably totaled around 5-7 pills). I know this wasn't the intelligent thing to do and I'm certainly not pleased with the decision, but such is life sometimes. Prior to that, I used marijuana and alcohol throughout that time period. Since about 6 months ago I've stopped all drug use; things have gotten better. Currently, I'm a university student and I do pretty well, but I'm looking for some help. My main concern is not so much immediate cognitive improvement, but long-term health and repair--at the very least, attenuation. If anyone on this thread has any experience on the topic of serotonergic regeneration (the damage, if present, is not extensive), and particular nootropics/herbal supplements that may encourage such a process, I'd be very grateful. A few considerations of my own: St John's Wort, Ashwagandha, Gotu Kola, Bacopa. I'm already taking fish oil and exercising. Thanks.

#2 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 12 May 2010 - 04:40 AM

Its higly unlikely you did any damage with that small MDMA use. Blame alcohol and weed instead.

sponsored ad

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

#3 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 12 May 2010 - 04:11 PM

To go further in my previous reply, was in a hurry this morning:

However, recent studies have found that the relationship between ecstasy use and psychological symptoms was no longer significant after controlling for marijuana use (e.g., Morgan et al., 2002).

CONCLUSIONS: These results revealed that, although ecstasy users demonstrate elevated levels of psychological symptoms and executive dysfunction, these symptoms are not statistically associated with their ecstasy consumption. Instead, other drug use (alcohol, marijuana, opioids, and inhalants) significantly predict psychological symptoms in this sample of polydrug users.

High prevalence psychiatric symptomatology in ecstasy polydrug users may be associated with polydrug rather than ecstasy use.

J Psychoactive Drugs. 2007 Mar;39(1):31-9.Links
Is recreational ecstasy (MDMA) use associated with higher levels of depressive symptoms?
Guillot C.

University of Southern Mississippi Hattiesburg, MS, USA. casey.guillot@usm.edu

Due to potential serotonergic deficits, 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) may cause long-term mood disruptions in recreational Ecstasy users. The purpose of this review is to evaluate the evidence for a relationship between recreational Ecstasy use and higher levels of depressive symptoms. Eleven out of 22 studies initially have reported significantly higher depression scores in Ecstasy users in comparison to control participants. However, only three studies ultimately have revealed significantly higher depression scores in comparison to cannabis or polydrug controls. Furthermore, most studies have suffered from methodological weaknesses, and the levels of depressive symptoms that have been found in Ecstasy users have not been shown to be much higher than those found in normative groups. The evidence for an association specifically between Ecstasy use and higher levels of depressive symptoms is currently unconvincing, but the frequent concomitant use of Ecstasy and other illicit drugs has been shown to be associated with higher levels of depressive symptoms. Possible causes include polydrug use in general, MDMA-induced serotonergic deficits, individual effects of illicit drugs besides Ecstasy, combined effects of MDMA and other illicit drugs, and preexisting differences in the levels of depressive symptoms in Ecstasy users.

PMID: 17523583 [PubMed - indexed for MEDLINE]



#4 jama

  • Topic Starter
  • Guest
  • 10 posts
  • 1

Posted 12 May 2010 - 06:27 PM

To go further in my previous reply, was in a hurry this morning:

However, recent studies have found that the relationship between ecstasy use and psychological symptoms was no longer significant after controlling for marijuana use (e.g., Morgan et al., 2002).

CONCLUSIONS: These results revealed that, although ecstasy users demonstrate elevated levels of psychological symptoms and executive dysfunction, these symptoms are not statistically associated with their ecstasy consumption. Instead, other drug use (alcohol, marijuana, opioids, and inhalants) significantly predict psychological symptoms in this sample of polydrug users.

High prevalence psychiatric symptomatology in ecstasy polydrug users may be associated with polydrug rather than ecstasy use.

J Psychoactive Drugs. 2007 Mar;39(1):31-9.Links
Is recreational ecstasy (MDMA) use associated with higher levels of depressive symptoms?
Guillot C.

University of Southern Mississippi Hattiesburg, MS, USA. casey.guillot@usm.edu

Due to potential serotonergic deficits, 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) may cause long-term mood disruptions in recreational Ecstasy users. The purpose of this review is to evaluate the evidence for a relationship between recreational Ecstasy use and higher levels of depressive symptoms. Eleven out of 22 studies initially have reported significantly higher depression scores in Ecstasy users in comparison to control participants. However, only three studies ultimately have revealed significantly higher depression scores in comparison to cannabis or polydrug controls. Furthermore, most studies have suffered from methodological weaknesses, and the levels of depressive symptoms that have been found in Ecstasy users have not been shown to be much higher than those found in normative groups. The evidence for an association specifically between Ecstasy use and higher levels of depressive symptoms is currently unconvincing, but the frequent concomitant use of Ecstasy and other illicit drugs has been shown to be associated with higher levels of depressive symptoms. Possible causes include polydrug use in general, MDMA-induced serotonergic deficits, individual effects of illicit drugs besides Ecstasy, combined effects of MDMA and other illicit drugs, and preexisting differences in the levels of depressive symptoms in Ecstasy users.

PMID: 17523583 [PubMed - indexed for MEDLINE]


More recent studies (Schilt 2007, 2008, 2009; Cowan 2003, 2007; V. Raj 2010) have found otherwise. Schilt conducted a naturalistically designed prospective study--the only of its kind and to date the most reputable--showing memory (verbal) deficits in ecstasy users after an average lifetime dosage of 3 pills; concurrent brain scans from the study showed sustained regional brain flow changes after a few months abstinence and possible evidence of axonal damage in the thalamus. Cowan conducted brain imaging (voxel-based morphometry) showing reduced cerebral grey volume in ecstasy users for low, moderate, and heavy lifetime dosages; reduced volume was correlated with cumulative lifetime dosage. V. Raj conducted a brain activation study showing changes in semantic retrieval after a mean period of abstinence of shortly over 1 year; changes were correlated with cumulative lifetime dosage and may be representative of compensatory mechanisms employed by the brain in the presence of damage. Impairment, while potentially unapparent in current neuropsychological testing measures, may surface upon engagement of sufficiently complex tasks. Moreover, no brain imaging study to date has detected normalization of brain activation patterns with abstinence.

Thus, I'm looking to encourage normalization through rehabilitative action. Part of this will be include nootropic/herbal supplementation over an extended period of time (as of yet indefinite). I'm not looking to debate whether damage has been sustained (this is a health forum, not illicit drug forum), I'm looking to encourage a healthy lifestyle and be good to my brain given my past. Anything specific (or even general for that matter--I know little about nootropics) in mind to help?
  • like x 1

#5 chrono

  • Member, Moderator
  • 2,444 posts
  • 801
  • Location:New England

Posted 13 May 2010 - 07:40 AM

The withanolide molecules in ashgawandha have been shown to promote axonal and dendritic regeneration. Probably the best bet for what we're talking about here. Substances which induce or mimic NGF are very promising for neuroprotection and genesis. ALCAR, lion's mane, lithium, etc. Other than that, just looking out for brain health in the same general way anyone else might is your best bet.

See these threads for previous discussion of this problem:

Need Help With Specialized Supplement Regimen

best regimen for healing the brain after multi-substance abuse/mdma

Trying to "repair" brain after drug use

Edited by chrono, 13 May 2010 - 07:41 AM.


#6 outsider

  • Guest
  • 396 posts
  • 9

Posted 13 May 2010 - 09:53 AM

Ginkgo biloba has been known to increase acetylcholine and serotonin receptor numbers in animal models.

It has been suggested that the bilobalides may aid the regrowth of damaged neurons in the central nervous system.

Edited by outsider, 13 May 2010 - 09:58 AM.


#7 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 13 May 2010 - 11:26 AM

I'l check those studies out, but has poly drug use been investigated next to MDMA use? It seems that poly drug use potentiates the damage done my MDMA wich in case of single MDMA use inst a significant problem. Atleast those studies didnt pick up any cognitive problems. And the studies looking at the difference between poly drug and mdma use cant be dismissed. I will look into those studies you mentioned.

#8 ooooouuuuuuuu

  • Guest
  • 31 posts
  • 0

Posted 13 May 2010 - 11:56 AM

I once read that Rhodiola Rosea brought the MDMA magic back to what is was for someone. So I assume it would work for that. It has many other health benefits too.
Inositol also reverses desensitization of serotonin receptors.

#9 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 13 May 2010 - 12:09 PM

I once read that Rhodiola Rosea brought the MDMA magic back to what is was for someone. So I assume it would work for that. It has many other health benefits too.
Inositol also reverses desensitization of serotonin receptors.

Yes, but tolerance doesnt have to be corrolated with long term problems. If there indeed is damage, things like ALCAR, ashwaghanda, lions mane?, etc are off more benefit.

#10 jama

  • Topic Starter
  • Guest
  • 10 posts
  • 1

Posted 14 May 2010 - 06:01 PM

I'll definitely take a look at everything mentioned, and thanks for the links. Apart from theoretical benefit, is there anyone in my position whose had real success with any of these? I see a lot of suggestions on the web, but more often than not the people that have allegedly 'healed' over time/effort still have apparent difficulties, e.g., terrible grammar, simple sentences, etc. Just wondering whether there is actually a chance that I might restore my brain to its pre-drug state, or is it that at this point I should be looking to optimize what's left? I've read that people that have sustained brain damage generally don't recover 100% but sometimes are close--is this me?

#11 matter_of_time

  • Guest
  • 135 posts
  • -8

Posted 14 May 2010 - 06:16 PM

Cerebrolysin does help a lot for this kind of problems.

I'll definitely take a look at everything mentioned, and thanks for the links. Apart from theoretical benefit, is there anyone in my position whose had real success with any of these? I see a lot of suggestions on the web, but more often than not the people that have allegedly 'healed' over time/effort still have apparent difficulties, e.g., terrible grammar, simple sentences, etc. Just wondering whether there is actually a chance that I might restore my brain to its pre-drug state, or is it that at this point I should be looking to optimize what's left? I've read that people that have sustained brain damage generally don't recover 100% but sometimes are close--is this me?



#12 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 14 May 2010 - 06:44 PM

I'll definitely take a look at everything mentioned, and thanks for the links. Apart from theoretical benefit, is there anyone in my position whose had real success with any of these? I see a lot of suggestions on the web, but more often than not the people that have allegedly 'healed' over time/effort still have apparent difficulties, e.g., terrible grammar, simple sentences, etc. Just wondering whether there is actually a chance that I might restore my brain to its pre-drug state, or is it that at this point I should be looking to optimize what's left? I've read that people that have sustained brain damage generally don't recover 100% but sometimes are close--is this me?

Yeah, EGCG completely reversed the small memory problem i got from a stupid combo of research chemicals i took. (I took 1 gram 4FMP, 500mg mephedrone, 500mg MDAI and 1 liter of wine, downright stupidity) and was left with sometimes not coming up with certain words, like my mind stayed blank while trying to remember the name of something, or a certain word.

EGCG completely reversed this within a few days.

#13 dilenja

  • Guest
  • 89 posts
  • 33

Posted 14 May 2010 - 09:06 PM

That is fascinating, and glad to hear that it worked for you. How much EGCG did you consume during this period?

I'll definitely take a look at everything mentioned, and thanks for the links. Apart from theoretical benefit, is there anyone in my position whose had real success with any of these? I see a lot of suggestions on the web, but more often than not the people that have allegedly 'healed' over time/effort still have apparent difficulties, e.g., terrible grammar, simple sentences, etc. Just wondering whether there is actually a chance that I might restore my brain to its pre-drug state, or is it that at this point I should be looking to optimize what's left? I've read that people that have sustained brain damage generally don't recover 100% but sometimes are close--is this me?

Yeah, EGCG completely reversed the small memory problem i got from a stupid combo of research chemicals i took. (I took 1 gram 4FMP, 500mg mephedrone, 500mg MDAI and 1 liter of wine, downright stupidity) and was left with sometimes not coming up with certain words, like my mind stayed blank while trying to remember the name of something, or a certain word.

EGCG completely reversed this within a few days.



#14 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 14 May 2010 - 09:11 PM

400mg: 200mg egcg/80% catechins from now foods. In a matter of days my memory problems were gone.

Also check this study:

Low Dosage of Rasagiline and Epigallocatechin Gallate Synergistically Restored the Nigrostriatal Axis in MPTP-Induced Parkinsonism.
Reznichenko L, Kalfon L, Amit T, Youdim MB, Mandel SA.

Eve Topf Center for Neurodegenerative Diseases Research and Department of Molecular Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.
Abstract
Background: The anti-Parkinson monoamine oxidase B inhibitor rasagiline appears to be the first neuroprotective disease-modifying therapy in early-stage Parkinson's disease (PD). Objective: Using a polypharmacy paradigm, we tested whether the distinct neuroprotective pharmacological profile of rasagiline would complement that of (-)-epigallocatechin-3-gallate (EGCG), the main antioxidant/iron chelator polyphenol constituent of green tea, and restore the neuronal loss and molecular targets damaged in animal parkinsonism. Methods/Results: We show by high-performance liquid chromatography, immunohistochemistry and Western blot analyses that the combination of rasagiline and EGCG, at subliminal doses which have no profound protective effect, acts synergistically to restore the nigrostriatal axis in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. A detailed analysis revealed a complementary action of these drugs, differentially acting at MPTP-injured molecules/targets in the substantia nigra (SN): induction of brain-derived neurotrophic factor by rasagiline, increased membranal levels of the protein kinase C alpha-isoform by EGCG and a synergistic replenishment of their downstream effector, the serine/threonine kinase Akt/protein kinase B, suggesting that this kinase might represent one point of convergence of the distinct mechanisms of action of the drug cocktail. Conclusion: These results provide molecular evidence that activation of multiple brain targets by the combination of rasagiline and EGCG may synergistically contribute to the rescue of the dopamine neurons in the SN and replenishment of striatal dopamine. This may have important implications for rasagiline-treated PD patients who could further benefit from an adjunct administration of EGCG. Copyright © 2010 S. Karger AG, Basel.

While i didnt take this combo, it seems that EGCG has potent neurorestorative effects.

#15 dilenja

  • Guest
  • 89 posts
  • 33

Posted 15 May 2010 - 12:48 AM

Interesting study, I wonder if the effects could be further enhanced with memantine as this has also been shown to upregulate dopamine 2 receptors in the striatum. Thanks, I appreciate you posting!

400mg: 200mg egcg/80% catechins from now foods. In a matter of days my memory problems were gone.

Also check this study:

Low Dosage of Rasagiline and Epigallocatechin Gallate Synergistically Restored the Nigrostriatal Axis in MPTP-Induced Parkinsonism.
Reznichenko L, Kalfon L, Amit T, Youdim MB, Mandel SA.

Eve Topf Center for Neurodegenerative Diseases Research and Department of Molecular Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.
Abstract
Background: The anti-Parkinson monoamine oxidase B inhibitor rasagiline appears to be the first neuroprotective disease-modifying therapy in early-stage Parkinson's disease (PD). Objective: Using a polypharmacy paradigm, we tested whether the distinct neuroprotective pharmacological profile of rasagiline would complement that of (-)-epigallocatechin-3-gallate (EGCG), the main antioxidant/iron chelator polyphenol constituent of green tea, and restore the neuronal loss and molecular targets damaged in animal parkinsonism. Methods/Results: We show by high-performance liquid chromatography, immunohistochemistry and Western blot analyses that the combination of rasagiline and EGCG, at subliminal doses which have no profound protective effect, acts synergistically to restore the nigrostriatal axis in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. A detailed analysis revealed a complementary action of these drugs, differentially acting at MPTP-injured molecules/targets in the substantia nigra (SN): induction of brain-derived neurotrophic factor by rasagiline, increased membranal levels of the protein kinase C alpha-isoform by EGCG and a synergistic replenishment of their downstream effector, the serine/threonine kinase Akt/protein kinase B, suggesting that this kinase might represent one point of convergence of the distinct mechanisms of action of the drug cocktail. Conclusion: These results provide molecular evidence that activation of multiple brain targets by the combination of rasagiline and EGCG may synergistically contribute to the rescue of the dopamine neurons in the SN and replenishment of striatal dopamine. This may have important implications for rasagiline-treated PD patients who could further benefit from an adjunct administration of EGCG. Copyright © 2010 S. Karger AG, Basel.

While i didnt take this combo, it seems that EGCG has potent neurorestorative effects.


Edited by dilenja, 15 May 2010 - 12:49 AM.


#16 dilenja

  • Guest
  • 89 posts
  • 33

Posted 15 May 2010 - 12:48 AM

duplicate post - delete

Edited by dilenja, 15 May 2010 - 12:49 AM.


#17 Animal

  • Guest
  • 689 posts
  • 158
  • Location:UK

Posted 15 May 2010 - 01:14 AM

What is your primary focus, supplements or pharmaceuticals? How easily can you acquire psychotropic medication? I.e. do you have an agreeable GP or psychiatrist? To what extent are you willing to experiment with substances which have potentially undesirable side effects?

Just a few questions before I put some any effort into making some suggestions, personally after many years of experimentation I tend to gravitate towards the pharmaceutical solution to physiological problems, rather then naturopathic supplements and the like. Though there are a minority of effective supplements out there.

#18 jama

  • Topic Starter
  • Guest
  • 10 posts
  • 1

Posted 15 May 2010 - 05:58 AM

What is your primary focus, supplements or pharmaceuticals? How easily can you acquire psychotropic medication? I.e. do you have an agreeable GP or psychiatrist? To what extent are you willing to experiment with substances which have potentially undesirable side effects?

Just a few questions before I put some any effort into making some suggestions, personally after many years of experimentation I tend to gravitate towards the pharmaceutical solution to physiological problems, rather then naturopathic supplements and the like. Though there are a minority of effective supplements out there.


I initially decided on supplements but I haven't really considered pharmaceuticals. At this point I'm not sure that I can acquire a psychotropic medication, though I'm not sure and wouldn't rule it out. I am willing to test medicines and determine a benefit/risk profile; and I might be inclined to agree with you on an intuitive basis, factoring in concentrations and additives. Many herbs are for very general use it seems. I would certainly be interested in hearing your suggestions, including the supplements you've found most effective.

#19 chrono

  • Member, Moderator
  • 2,444 posts
  • 801
  • Location:New England

Posted 15 May 2010 - 10:32 AM

Just a few questions before I put some any effort into making some suggestions, personally after many years of experimentation I tend to gravitate towards the pharmaceutical solution to physiological problems, rather then naturopathic supplements and the like. Though there are a minority of effective supplements out there.

I would be extremely interested in hearing about any pharmaceuticals that have the potential to address this kind of damage. Both out of sheer curiosity about neural regeneration in general, but also because this question comes up a lot here, and in the threads I linked to we seem to be collecting progressively better answers. And I have several friends who have ranged between single and excessive constant use of MDMA, some of whom are noticing cognitive deficits and trying to recover mental faculties to varying degrees.

My suggestion of withanolide's axonal regeneration capability is unproven in vivo, but in my research about neuroregenerative agents I haven't come across any others with this specific ability (does an increase in neurotrophic factors in general have any effect on this type of damage, do you think?). I for one would be extremely grateful for your opinion on the matter.


Here's a few of the imaging studies jama mentioned. I was unaware of some of the research from the past 5 years (esp. the NeXT study), which is quite compelling.

J Psychopharmacol. 2010 Feb;24(2):187-201. Epub 2009 Mar 20.
MDMA (ecstasy) use is associated with reduced BOLD signal change during semantic recognition in abstinent human polydrug users: a preliminary fMRI study.
Raj V, Liang HC, Woodward ND, Bauernfeind AL, Lee J, Dietrich MS, Park S, Cowan RL.

During semantic recognition, lifetime MDMA use was associated with decreased activation in left BA 9, 18 and 21/22 but not 45. This was partly influenced by contributions from cannabis and cocaine use. MDMA exposure was not associated with accuracy or response time during the semantic recognition task. During semantic recognition, MDMA exposure was associated with reduced regional brain activation in regions mediating verbal memory.

Drug Alcohol Depend. 2003 Dec 11;72(3):225-35.
Reduced cortical gray matter density in human MDMA (Ecstasy) users: a voxel-based morphometry study.
Cowan RL, Lyoo IK, Sung SM, Ahn KH, Kim MJ, Hwang J, Haga E, Vimal RL, Lukas SE, Renshaw PF.

Structural magnetic resonance imaging (MRI) scans of 31 MDMA polydrug users versus 29 non-MDMA users were compared using voxel-based morphometry (VBM) to assess regional brain gray and white matter concentration. VBM employs gray/white matter segmentation and statistical parametric mapping (SPM) analysis to calculate a voxel-wise comparison of regional gray or white matter concentration. Using this method, we consistently found several brain regions having decreased gray matter concentration in MDMA polydrug users. These regions were localized to neocortex in bilateral Brodmann area (BA) 18, left BA 21, and left BA 45, as well as bilateral cerebellum, and midline brainstem. Overall, these preliminary findings suggest that MDMA polydrug users have multiple regions of gray matter reduction, potentially accounting for previously reported neuropsychiatric impairments in MDMA users.

Brain. 2008 Nov;131(Pt 11):2936-45. Epub 2008 Oct 7.
Sustained effects of ecstasy on the human brain: a prospective neuroimaging study in novel users.
de Win MM, Jager G, Booij J, Reneman L, Schilt T, Lavini C, Olabarriaga SD, den Heeten GJ, van den Brink W.

Decreased FA and increased ADC in the thalamus may reflect ecstasy-induced axonal damage, because axonal cell membranes are known to be responsible for most of the restriction of water diffusion and axonal damage lead to decreased FA and increased ADC. This finding of ecstasy-induced brain pathology in the thalamus corroborates findings from previous studies showing decreased thalamic SERT densities in (heavy) ecstasy users, most probably reflecting damage to terminals of serotonergic axons...As the thalamus is important for neurocognitive processes, one can speculate that ecstasy-induced thalamic damage is (partly) responsible for decreased verbal memory performance frequently reported in heavy ecstasy users and recently also shown in the current prospective cohort of low-dose ecstasy users (Schilt et al., 2007).
...
In line with this, a previous study showed a positive relation between mean FA and age in young adults up to 39.5 years, suggesting that structural changes in the brain continue in normal young adults, especially in areas with low anisotropy (Yoshiura et al., 2005). Therefore, we speculate that this normal maturation did occur in the persistent ecstasy-naives; whereas, this failed to occur in the group of novel ecstasy users.

Br J Psychiatry. 2008 Oct;193(4):289-96.
Neurotoxic effects of ecstasy on the thalamus.
de Win MM, Jager G, Booij J, Reneman L, Schilt T, Lavini C, Olabarriaga SD, Ramsey NF, Heeten GJ, van den Brink W.

The most interesting finding is that different imaging techniques all showed a specific effect of ecstasy on the thalamus. Even after adjustment for amphetamine, cocaine, cannabis and other relevant potential confounders, a significant effect of ecstasy, and no effects of any of the other drugs, was found on [123I]β-CIT binding (reduced), fractional anisotropy (reduced) and rrCBV (increased) in the thalamus. As [123I]β-CIT SPECT was previously validated to assess in vivo binding to serotonin transporters, the finding of decreased [123I]β-CIT binding probably reflects lower serotonin transporter densities in ecstasy users. Moreover, the thalamus is a serotonin transporter-rich area and previous studies showed that [123I]β-CIT binding in the thalamus is mainly related to transporter binding, although the thalamus also contains noradrenaline transporters. Diffusion tensor imaging measures diffusional motion of water molecules in the brain which is normally restricted in amplitude and direction by cellular structures such as axons. When axons are damaged, extracellular water content increases and fractional anisotropy decreases. Therefore, it is likely that the observed decreased fractional anisotropy is related to ecstasy-induced axonal injury.
...
Taken together, it seems that these measurements in the thalamus converge in the direction of decreased serotonergic function, with decreased serotonin transporter binding and decreased fractional anisotropy values probably reflecting damage to serotonergic axons and increased rrCBV due to decreased vasoconstriction caused by depletion of serotonin. Previous studies in animals also showed ecstasy-induced axonal damage to the serotonergic axons of the thalamus, although signs of re-innervation after a period of recovery were also observed. As the thalamus plays a key role in awareness, attention and neurocognitive processes such as memory and language, one can speculate that ecstasy-induced serotonergic damage to the thalamus is (partly) responsible for reduced verbal memory performance frequently reported in ecstasy users.


And some cognition studies (though in this context I think addressing the neurological damage should have greater priority than trying to improve verbal memory directly, unless some agent specifically obviates deficits caused by damage to the regions mentioned above):

Arch Gen Psychiatry. 2007 Jun;64(6):728-36.
Cognition in novice ecstasy users with minimal exposure to other drugs: a prospective cohort study.
Schilt T, de Win MM, Koeter M, Jager G, Korf DJ, van den Brink W, Schmand B.

At the initial examination, there were no statistically significant differences in any of the neuropsychological test scores between persistent Ecstasy-naive subjects and future Ecstasy users. However, at follow-up, change scores on immediate and delayed verbal recall and verbal recognition were significantly lower in the group of incident Ecstasy users compared with persistent Ecstasy-naive subjects. There were no significant differences on other test scores. CONCLUSIONS: Our findings suggest that even a first low cumulative dose of Ecstasy is associated with decline in verbal memory. Although the performance of the group of incident Ecstasy users is still within the normal range and the immediate clinical relevance of the observed deficits is limited, long-term negative consequences cannot be excluded.

Psychopharmacology (Berl). 2010 Jan;207(4):583-91. Epub 2009 Oct 13.
Long-term neuropsychological effects of ecstasy in middle-aged ecstasy/polydrug users.
Schilt T, Koeter MW, Smal JP, Gouwetor MN, van den Brink W, Schmand B.

Moderate to heavy ecstasy/polydrug users performed significantly worse on a verbal memory task than none or very mild ecstasy using polydrug users and drug naives. Moderate and heavy ecstasy/polydrug users also differed significantly from drug-naives on measures of depression, sensation-seeking and impulsivity but not from none or very mild ecstasy-using polydrug users.

Psychol Med. 2008 Sep;38(9):1309-17. Epub 2007 Nov 8.
Specific effects of ecstasy and other illicit drugs on cognition in poly-substance users.
Schilt T, de Win MM, Jager G, Koeter MW, Ramsey NF, Schmand B, van den Brink W.

Ecstasy use [mean 327 (S.D.=364) tablets in lifetime] had a specific significant dose-related negative effect on verbal delayed recall after adjusting for the use of other drugs.

Neuropsychopharmacology. 2008 Jan;33(2):247-58. Epub 2007 Apr 25.
Assessment of cognitive brain function in ecstasy users and contributions of other drugs of abuse: results from an FMRI study.
Jager G, de Win MM, van der Tweel I, Schilt T, Kahn RS, van den Brink W, van Ree JM, Ramsey NF.

Multiple regression analysis showed that associative memory performance was affected by amphetamine much more than by ecstasy. Both drugs affected associative memory-related brain activity, but the effects were consistently in opposite directions, suggesting that different mechanisms are at play. This could be related to the different neurotransmitter systems these drugs predominantly act upon, that is, serotonin (ecstasy) vs dopamine (amphetamine) systems.


And finally, here's a monkey study which is highly relevant. The results section of this paper details specific areas and types of 5-HT injury, and the discussion analyzes factors which may have been involved in the healing which took place over the 7 years. Way too much info to post here, but very technical and highly recommended.

J Neurosci. 1999 Jun 15;19(12):5096-107.
Altered serotonin innervation patterns in the forebrain of monkeys treated with (+/-)3,4-methylenedioxymethamphetamine seven years previously: factors influencing abnormal recovery.
Hatzidimitriou G, McCann UD, Ricaurte GA.

In summary, the present results indicate that MDMA-induced 5-HT neural injury in nonhuman primates lasts for at least 7 years and may well be permanent. In addition, the present results point to several factors that appear to influence axonal recovery after MDMA injury, including the distance of the damaged terminal field from its nerve cell body of origin, the size or severity of the initial lesion, and the proximity of the injured axons to myelinated fiber tracts. Additional studies are needed to assess the relative importance of each of these factors and to identify other variables that may influence recovery of 5-HT axons after MDMA injury. Finally, it will be important to use newly developed positron emission tomography imaging techniques (McCann et al., 1998) to determine whether the present findings generalize to humans with a history of recreational MDMA use.


Edited by chrono, 03 August 2010 - 05:42 PM.


#20 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 15 May 2010 - 04:39 PM

Interesting study, I wonder if the effects could be further enhanced with memantine as this has also been shown to upregulate dopamine 2 receptors in the striatum. Thanks, I appreciate you posting!

400mg: 200mg egcg/80% catechins from now foods. In a matter of days my memory problems were gone.

Also check this study:

Low Dosage of Rasagiline and Epigallocatechin Gallate Synergistically Restored the Nigrostriatal Axis in MPTP-Induced Parkinsonism.
Reznichenko L, Kalfon L, Amit T, Youdim MB, Mandel SA.

Eve Topf Center for Neurodegenerative Diseases Research and Department of Molecular Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.
Abstract
Background: The anti-Parkinson monoamine oxidase B inhibitor rasagiline appears to be the first neuroprotective disease-modifying therapy in early-stage Parkinson's disease (PD). Objective: Using a polypharmacy paradigm, we tested whether the distinct neuroprotective pharmacological profile of rasagiline would complement that of (-)-epigallocatechin-3-gallate (EGCG), the main antioxidant/iron chelator polyphenol constituent of green tea, and restore the neuronal loss and molecular targets damaged in animal parkinsonism. Methods/Results: We show by high-performance liquid chromatography, immunohistochemistry and Western blot analyses that the combination of rasagiline and EGCG, at subliminal doses which have no profound protective effect, acts synergistically to restore the nigrostriatal axis in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. A detailed analysis revealed a complementary action of these drugs, differentially acting at MPTP-injured molecules/targets in the substantia nigra (SN): induction of brain-derived neurotrophic factor by rasagiline, increased membranal levels of the protein kinase C alpha-isoform by EGCG and a synergistic replenishment of their downstream effector, the serine/threonine kinase Akt/protein kinase B, suggesting that this kinase might represent one point of convergence of the distinct mechanisms of action of the drug cocktail. Conclusion: These results provide molecular evidence that activation of multiple brain targets by the combination of rasagiline and EGCG may synergistically contribute to the rescue of the dopamine neurons in the SN and replenishment of striatal dopamine. This may have important implications for rasagiline-treated PD patients who could further benefit from an adjunct administration of EGCG. Copyright © 2010 S. Karger AG, Basel.

While i didnt take this combo, it seems that EGCG has potent neurorestorative effects.

Well, D2 upregulation is only usefull regarding drug tolerance, memantine is very usefull in preventing rapid tolerance to opiates, amphetamine's, nicotine and the sedative effect of benzo's. It however most likely wont restore any neurotoxic damage (altough it does increase BDNF).

#21 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 15 May 2010 - 04:40 PM

I have taken a full botle of now foods ashwaghanda before but it didnt reverse my cognitive problems after that RC overdose, unlike EGCG.
  • dislike x 1

#22 chrono

  • Member, Moderator
  • 2,444 posts
  • 801
  • Location:New England

Posted 15 May 2010 - 05:05 PM

I have taken a full botle of now foods ashwaghanda before but it didnt reverse my cognitive problems after that RC overdose, unlike EGCG.

How long was it between when you took this esoteric combo, and when you took the EGCG that might have cleared it up? If it worked within a matter of days, it probably wasn't correcting neural damage. Neural repair and reintegration take much longer than a few days. It seems more likely that it helped to quickly correct some other kind of imbalance still present from the event.

Anyway, I don't think your experience with the RC combo and EGCG can be used to predict the kind of structural repair needed for MDMA-related impairment. Though as you said, EGCG is an awesome compound, with potent neuroprotective and other benefits (and may be capable of improving certain types of memory in general).


This paper suggests that the pattern of regrowth of serotonin axons is non-uniform. This should be considered along with the last paper in my previous post when predicting the efficacy of a substance-based regeneration therapy.

Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy").
Fischer C, Hatzidimitriou G, Wlos J, Katz J, Ricaurte G.

The recreational drug (+/)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is a methamphetamine derivative that selectively destroys central 5-HT axons and axon terminals in animals and, possibly, humans. The fate of 5-HT neurons following MDMA injury is uncertain. In particular, while it is known that central 5-HT axons can undergo regenerative sprouting after MDMA injury, it has not been determined whether they reestablish the original innervation pattern. To address this question, the present studies examined 5-HT innervation patterns in animals lesioned with MDMA 12-18 months previously. Both rodents (rats) and nonhuman primates (squirrel monkeys) were examined, since there is indication that serotonergic recovery after MDMA injury may be species dependent. 5-HT axon projections were studied neurochemically, autoradiographically and immunocytochemically. In both rodents and nonhuman primates previously lesioned with MDMA, substantial serotonergic axonal sprouting was observed. However, in a few rats and in most squirrel monkeys, the reinnervation pattern was highly abnormal: distant targets (e.g., dorsal neocortex) remained denervated, while some proximal targets (e.g., amygdala, hypothalamus) were reinnervated or hyperinnervated. Although the specific determinants of axonal recovery after MDMA injury remain to be identified, it appears that axons which initially sustain more severe damage, are longer, or are more highly arborized have low probability of recovering. The observation that some brain regions remain denervated, while others are reinnervated or hyperinnervated suggests that, under some circumstances, MDMA injury can lead to a lasting reorganization of ascending 5-HT axon projections. Such lasting changes in brain innervation, documented here in MDMA-treated animals, may have implications for humans using MDMA recreationally.

PMID: 7643196 [PubMed - indexed for MEDLINE]


Edited by chrono, 03 August 2010 - 05:43 PM.


#23 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 15 May 2010 - 05:56 PM

Been taking the EGCG for 5 weeks now, and the RC combo i took last year in december. I dont exactly know how long it took for EGCG to restore the damage, but i do know that i no longer have the cognitive problems as before.

Edited by medievil, 15 May 2010 - 05:57 PM.


#24 jama

  • Topic Starter
  • Guest
  • 10 posts
  • 1

Posted 16 May 2010 - 12:36 AM

I have taken a full botle of now foods ashwaghanda before but it didnt reverse my cognitive problems after that RC overdose, unlike EGCG.

How long was it between when you took this esoteric combo, and when you took the EGCG that might have cleared it up? If it worked within a matter of days, it probably wasn't correcting neural damage. Neural repair and reintegration take much longer than a few days. It seems more likely that it helped to quickly correct some other kind of imbalance still present from the event.

This paper suggests that the pattern of regrowth of serotonin axons is non-uniform. This should be considered along with the last paper in my previous post when predicting the efficacy of a substance-based regeneration therapy.
[indent=1]

Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy").
Fischer C, Hatzidimitriou G, Wlos J, Katz J, Ricaurte G.


I'd agree that it's unlikely the EGCG would have short-term restorative effects but it possibly resulting in a corrected imbalance could make a world of difference--not to mention that over time, this corrected imbalance could facilitate a neurotrophic environment sufficient for modest neural repair. Also, ahwaghanda could have had an effect.

The paper cited above of regrowth of serotonin axons, while pertinent to the general neurotoxic potential of mdma, may not be the debilitating factor in human recreational use. For instance, the areas cited in the Schilt paper (NEXT) note that sustained damage was detected in the thalamus; the thalamus is a brain region known to fully innervate or hyperinnervate after abstinence from MDMA damage. Thus, rather than a structural abnormality, the difference could lie in receptor function changes, axonal dysfunction, or loss of brain coupling of serotonin with neurotrophic factors. Considering this last mechanism of brain dysfunction (as suggested in Cowan 2003) the brain could be 'shrinking' in various areas in accordance with a less rich neurotrophic environment; in this regard then nootropics seem especially hopeful taken over the long-term and in conjunction with other brain-supporting actions. It of course is also quite possible that there is a real axonal loss and reorganization involved in human recreational use. If this is the case, recovery seems more distant and less robust, taking more time to regrow rather than 're-feed' or restabilize. Of course the noted alterations in semantic retrieval is an interesting study, mainly remarking that BA 9 (dorsolateral prefronal cortex) is an area showing greater brain activation in abstinent MDMA users for the same task; this agrees with the Schilt study (NEXT), noting increased blood flow in abstinent users 4 months after use limited to BA 9.

It is important to note that cognitive deficits in the Schilt study were apparent only in specific polymorphisms (roughly 75% of the population). Schilt did a follow up study in 2009 remarking that the val/val polymorphism on a particular codon was far less susceptible to cognitive impairment than the val/met or met/met polymorphism. Interesting that after light use, no neuropsychological impairments were discovered (something to do with dopamine interaction in the prefrontal cortex).

All in all, I'm not sure what to make of this. I figured I'd briefly explain a possible disruptive mechanism at play but apart from this forum, I have limited knowledge of specific courses of action. But perhaps this overview can stimulate/guide discussion? In my own case, as I've mentioned before, I don't believe that the damage sustained is extensive whether or not it is irremediable. I haven't noticed any particular cognitive deficit, but if I were to really press myself (at the risk of psychosomatic production of deficit) I might say that I've encountered a slight reduction in verbal learning and memory. I don't think, given this, that addressing this symptom directly is the best route--though if it doesn't conflict with long-term remedy, I wouldn't be opposed to a little help in the mean time. And pharmaceutical suggestions welcome!

#25 Advanc3d

  • Guest
  • 283 posts
  • 2
  • Location:Sydney

Posted 17 May 2010 - 09:56 AM

Interesting study, I wonder if the effects could be further enhanced with memantine as this has also been shown to upregulate dopamine 2 receptors in the striatum. Thanks, I appreciate you posting!

400mg: 200mg egcg/80% catechins from now foods. In a matter of days my memory problems were gone.

Also check this study:

Low Dosage of Rasagiline and Epigallocatechin Gallate Synergistically Restored the Nigrostriatal Axis in MPTP-Induced Parkinsonism.
Reznichenko L, Kalfon L, Amit T, Youdim MB, Mandel SA.

Eve Topf Center for Neurodegenerative Diseases Research and Department of Molecular Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.
Abstract
Background: The anti-Parkinson monoamine oxidase B inhibitor rasagiline appears to be the first neuroprotective disease-modifying therapy in early-stage Parkinson's disease (PD). Objective: Using a polypharmacy paradigm, we tested whether the distinct neuroprotective pharmacological profile of rasagiline would complement that of (-)-epigallocatechin-3-gallate (EGCG), the main antioxidant/iron chelator polyphenol constituent of green tea, and restore the neuronal loss and molecular targets damaged in animal parkinsonism. Methods/Results: We show by high-performance liquid chromatography, immunohistochemistry and Western blot analyses that the combination of rasagiline and EGCG, at subliminal doses which have no profound protective effect, acts synergistically to restore the nigrostriatal axis in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. A detailed analysis revealed a complementary action of these drugs, differentially acting at MPTP-injured molecules/targets in the substantia nigra (SN): induction of brain-derived neurotrophic factor by rasagiline, increased membranal levels of the protein kinase C alpha-isoform by EGCG and a synergistic replenishment of their downstream effector, the serine/threonine kinase Akt/protein kinase B, suggesting that this kinase might represent one point of convergence of the distinct mechanisms of action of the drug cocktail. Conclusion: These results provide molecular evidence that activation of multiple brain targets by the combination of rasagiline and EGCG may synergistically contribute to the rescue of the dopamine neurons in the SN and replenishment of striatal dopamine. This may have important implications for rasagiline-treated PD patients who could further benefit from an adjunct administration of EGCG. Copyright © 2010 S. Karger AG, Basel.

While i didnt take this combo, it seems that EGCG has potent neurorestorative effects.

Well, D2 upregulation is only usefull regarding drug tolerance, memantine is very usefull in preventing rapid tolerance to opiates, amphetamine's, nicotine and the sedative effect of benzo's. It however most likely wont restore any neurotoxic damage (altough it does increase BDNF).


NMDA antagonists also reduce the high considerbally. Its almost like taking a GABA agonist except with control of excitation rather then inhibitory

#26 Animal

  • Guest
  • 689 posts
  • 158
  • Location:UK

Posted 17 May 2010 - 04:40 PM

NMDA antagonists also reduce the high considerbally. Its almost like taking a GABA agonist except with control of excitation rather then inhibitory


Yeah well if you're taking the substance to get high then you've got bigger problems then burgeoning tolerance.
  • like x 1
  • dislike x 1

#27 jama

  • Topic Starter
  • Guest
  • 10 posts
  • 1

Posted 20 May 2010 - 04:36 AM

I'l check those studies out, but has poly drug use been investigated next to MDMA use? It seems that poly drug use potentiates the damage done my MDMA wich in case of single MDMA use inst a significant problem. Atleast those studies didnt pick up any cognitive problems. And the studies looking at the difference between poly drug and mdma use cant be dismissed. I will look into those studies you mentioned.



I'm not sure to what extent poly drug use potentiates MDMA neurotoxicity. I do know that recent studies have consistently linked MDMA-related impairment to specific regions in the brain and that the NeXT project included one study attempting to evaluate this very problem; the title of the study is "Cognition in Novice Ecstasy Users With Minimal Exposure to Other Drugs". It seems that poly drug use may indeed potentiate MDMA-related impairment but it isn't necessary. I know other studies attempt to statistically factor out the influence of other drug use on measurement results, but this is a difficult and controversial maneuver.

If this isn't in fact true, that is that MDMA alone isn't the culprit but rather recreational drug use, is there anyone with suggestions on how to improve general brain function after poly substance use?

#28 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 20 May 2010 - 12:27 PM

I havent looked at those studies yet.

But i beleive that other drugs then MDMA cause the body's antioxidant enzymes to go down, wich would cause the body to be less defensive to the oxidative stress MDMA causes.

We know that:
- Damage corrolates with the consumption of E in the example of poly drug users (so it seems that mdma is the "offender")
- Long term problems are corrolated with poly drug use and not MDMA use itself.

For example, it seems that GHB decreases some antioxidant enzyme's:

Gamma-hydroxybutyric acid induces oxidative stress in cerebral cortex of young rats.
Sgaravatti AM, Sgarbi MB, Testa CG, Durigon K, Pederzolli CD, Prestes CC, Wyse AT, Wannmacher CM, Wajner M, Dutra-Filho CS.

Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600 Anexo, CEP 90035-003 Porto Alegre, RS, Brazil.
GHB is a naturally occurring compound in the central nervous system (CNS) whose tissue concentration are highly increased during drug abuse and in the inherited deficiency of succinic semialdehyde dehydrogenase (SSADH) activity. SSADH deficiency is a neurometabolic-inherited disorder of the degradation pathway of gamma-aminobutyric acid (GABA). It is biochemically characterized by increased concentrations of gamma-hydroxybutyric acid (GHB) in tissues, cerebrospinal fluid (CSF), blood and urine of affected patients. Clinical manifestations are variable, ranging from mild retardation of mental, motor, and language development to more severe neurological symptoms, such as hypotonia, ataxia and seizures, whose underlying mechanisms are practically unknown. In the present study, the in vitro and in vivo effects of GHB was investigated on some parameters of oxidative stress, such as chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR), as well as the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in homogenates from cerebral cortex of 15-day-old Wistar rats. In vitro, GHB significantly increased chemiluminescence and TBA-RS levels, while TRAP and TAR measurements were markedly diminished. In contrast, the activities of the antioxidant enzymes SOD, CAT and GPX were not altered by GHB in vitro. Acute administration of GHB provoked a significant enhance of TBA-RS levels and a decrease of TRAP and TAR measurements. These results indicate that GHB induces oxidative stress by stimulating lipid peroxidation and decreasing the non-enzymatic antioxidant defenses in cerebral cortex of young rats. If these effects also occur in humans, it is possible that they might contribute to the brain damage found in SSADH-deficient patients and possibly in individuals who consume GHB or its prodrug gamma-butyrolactone.

While also increasing oxidative stress, this would lead to cumulative oxidative stress while at the same time being less protected from this.

#29 jama

  • Topic Starter
  • Guest
  • 10 posts
  • 1

Posted 21 May 2010 - 03:39 PM

But i beleive that other drugs then MDMA cause the body's antioxidant enzymes to go down, wich would cause the body to be less defensive to the oxidative stress MDMA causes.


Sure, I'd agree that some drugs have the potential to decrease total antioxidant availability, increasing the risk of oxidative assault caused by MDMA--but I don't think that MDMA by itself can't either 1) both decrease antioxidative defense and increase oxidative assault or 2) overwhelm antioxidative defense and thus cause oxidative assualt; although, it is difficult to find strictly MDMA users and hence the lack of formal research. Other neurotoxins, e.g., alcohol, chemotherapy, methamphetamine, all cause neurotoxicity without potentiation from other substances. MDMA in animal models is the same.

We know that:
- Damage corrolates with the consumption of E in the example of poly drug users (so it seems that mdma is the "offender")
- Long term problems are corrolated with poly drug use and not MDMA use itself.


This claim is not supported by any research whatsoever. The closest thing I have read to it is a recent study suggesting that "MDMA alone is not the sole culprit" for cognitive dysfunction. Even this is scant evidence for your claim. MDMA use itself very likely causes long-term problems in humans; it does in all animal models and human anecdotal reports. I think I read that you take 2 pills a week? Even veteran MDMA users will tell you that this is not a good idea. On a side note, the first thing I usually notice about heavy MDMA users is extremely poor grammar.

But again, I'm not writing this to defend MDMA toxicity theory or anything else for that matter, I just figured medievel needed some advice. If anyone has a stack they've had great luck with I'm planning to see a neurologist soon and it'd be great to have them evaluate it.
  • dislike x 1

sponsored ad

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

#30 medievil

  • Guest Guest
  • 3,750 posts
  • 20
  • Location:Belguim

Posted 21 May 2010 - 04:20 PM

On a side note, the first thing I usually notice about heavy MDMA users is extremely poor grammar.

If your referring to me, id like to see how good your dutch is ?

This claim is not supported by any research whatsoever. The closest thing I have read to it is a recent study suggesting that "MDMA alone is not the sole culprit" for cognitive dysfunction. Even this is scant evidence for your claim. MDMA use itself very likely causes long-term problems in humans; it does in all animal models and human anecdotal reports. I think I read that you take 2 pills a week? Even veteran MDMA users will tell you that this is not a good idea. On a side note, the first thing I usually notice about heavy MDMA users is extremely poor grammar.

My own use doesnt matter, i took alot more. However this isnt any evidence as anecdotal reports are rubbish when it comes to this, just like those anecdotal reports saying they got braindamaged.

J Psychoactive Drugs. 2007 Mar;39(1):31-9.Links
Is recreational ecstasy (MDMA) use associated with higher levels of depressive symptoms?
Guillot C.

University of Southern Mississippi Hattiesburg, MS, USA. casey.guillot@usm.edu

Due to potential serotonergic deficits, 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) may cause long-term mood disruptions in recreational Ecstasy users. The purpose of this review is to evaluate the evidence for a relationship between recreational Ecstasy use and higher levels of depressive symptoms. Eleven out of 22 studies initially have reported significantly higher depression scores in Ecstasy users in comparison to control participants. However, only three studies ultimately have revealed significantly higher depression scores in comparison to cannabis or polydrug controls. Furthermore, most studies have suffered from methodological weaknesses, and the levels of depressive symptoms that have been found in Ecstasy users have not been shown to be much higher than those found in normative groups. The evidence for an association specifically between Ecstasy use and higher levels of depressive symptoms is currently unconvincing, but the frequent concomitant use of Ecstasy and other illicit drugs has been shown to be associated with higher levels of depressive symptoms. Possible causes include polydrug use in general, MDMA-induced serotonergic deficits, individual effects of illicit drugs besides Ecstasy, combined effects of MDMA and other illicit drugs, and preexisting differences in the levels of depressive symptoms in Ecstasy users.

PMID: 17523583 [PubMed - indexed for MEDLINE]

Drug Alcohol Depend. 2007 Mar 16;87(2-3):303-11. Epub 2006 Oct 30.Click here to read Click here to read Links
Anxiety, depression, and behavioral symptoms of executive dysfunction in ecstasy users: contributions of polydrug use.
Medina KL, Shear PK.

Department of Psychiatry, University of California at San Diego, 3350 La Jolla Village Drive (151B), San Diego, CA 92161, USA. klmedina@ucsd.edu

BACKGROUND: Given ecstasy's (MDMA) potential serotonergic neurotoxicity, it is plausible that regular ecstasy users would have an elevated prevalence of behavioral executive dysfunction or mood symptoms. However, recent studies have found that the relationship between ecstasy use and psychological symptoms was no longer significant after controlling for marijuana use (e.g., Morgan et al., 2002). The goal of the present study was to examine the relationship between ecstasy exposure and self-reported executive functioning and psychological symptoms after controlling for gender, ethnicity, and other drug use. METHODS: Data were collected from 65 men and women with a wide range of ecstasy use (including 17 marijuana-using controls). Participants were administered the Frontal Systems Behavioral Scale, State-Trait Anxiety Inventory for adults, and the Beck Depression Inventory-2nd edition. RESULTS: Although 19-63% of the ecstasy users demonstrated clinically elevated psychological symptoms, frequency of ecstasy use did not predict the psychological symptoms. No gender differences or interactions were observed. CONCLUSIONS: These results revealed that, although ecstasy users demonstrate elevated levels of psychological symptoms and executive dysfunction, these symptoms are not statistically associated with their ecstasy consumption. Instead, other drug use (alcohol, marijuana, opioids, and inhalants) significantly predict psychological symptoms in this sample of polydrug users.

PMID: 17074449 [PubMed - indexed for MEDLINE]

Ecstasy (MDMA) and high prevalence psychiatric symptomatology: somatic anxiety symptoms are associated with polydrug, not ecstasy, use.
Bedi G, Van Dam NT, Redman J.

School of Psychology, Psychiatry and Psychological Medicine, Monash University, Melbourne, Australia. gbedi@bsd.uchicago.edu
Abstract
Although previous studies have examined anxiety and depression in ecstasy (+/-3,4-methylenedioxymethamphetamine; MDMA) users, it remains unclear whether symptoms are associated specifically with ecstasy or with polydrug use in general. We compared mean symptomatology and clinically significant symptoms in 45 ecstasy polydrug, 48 cannabis polydrug and 40 legal drug users, who completed standardised self-report anxiety and depression symptom measures. We further examined whether group differences were secondary to increased somatic symptom reporting, which may reflect acute/subacute drug effects. Anxiety and depression scores were higher in polydrug than legal drug users, with no difference between ecstasy and cannabis groups. There was no difference in numbers meeting criteria for clinically significant depression or 'moderate' or 'severe' anxiety, but the polydrug group contained more individuals reporting at least 'mild' anxiety symptoms than the legal drug control. Multivariate analyses indicated that anxiety alone was sufficient to discriminate groups. Polydrug users reported more somatic anxiety symptoms than legal drug users, but endorsed equivalent numbers of non-somatic symptoms. High prevalence psychiatric symptomatology in ecstasy polydrug users may be associated with polydrug rather than ecstasy use. Higher ratings in polydrug users appear to be secondary to increased somatic symptom reporting, suggesting possible impacts of drug effects on symptom endorsement.

If you have studies suporting your claims, (where polydruguse has been seperated from MDMA use) feel free to post them.

Edited by medievil, 21 May 2010 - 04:41 PM.





0 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users