337 replies to this topic

[eon]

Is the new prescription product called Deplin just a fancier and mega dose version of l-methylfolate (which is an active form of OTC folate)? I read about this product a few months ago and I think it's out now. I forgot where I read the article but it was something about pharmaceuticals patenting (allegedly) l-methylfolate to make it prescription only when it has been OTC for years. I think the story is untrue and more likely conspiracy theory.

 

http://www.deplin.co...for-depression/

Edited by eon, 10 February 2015 - 11:39 AM.

[Thew]

Thank you for the very useful information you have shared. I'll take my time to read them.

 

As for my dad's condition who is made his depression lot worse is by binging alcohol. Quitting on his own is difficult, he can't cope with his withdrawal symptoms very well. Asking for help is necessary so a relative suggested different alcohol addiction program that can treat his addiction alongside with his depression. (I made a link to serve an example of the treatments mention to my dad) Taking a CBT (cognitive behavioral therapy) thought him identify ways to manage his emotions. I've seen improvements with our relationship with him since he did his therapy.  

[Galaxyshock]

As for my dad's condition who is made his depression lot worse is by binging alcohol. Quitting on his own is difficult, he can't cope with his withdrawal symptoms very well.

 

Baclofen has been successfully used to withdrawal from alcohol and preventing relapse.

[Thew]

 

As for my dad's condition who is made his depression lot worse is by binging alcohol. Quitting on his own is difficult, he can't cope with his withdrawal symptoms very well.

 

Baclofen has been successfully used to withdrawal from alcohol and preventing relapse.

 

Thanks for the suggestion Galaxyshock. I've heard it also from my friends that it was effective.

[Flex]

Stumbled upon this in my herb recherche:

Declinol, a Complex Containing Kudzu, Bitter Herbs (Gentian, Tangerine Peel) and Bupleurum, Significantly Reduced Alcohol Use Disorders Identification Test (AUDIT) Scores in Moderate to Heavy Drinkers: A Pilot Study

http://www.ncbi.nlm....les/PMC3835486/

Edited by Flex, 12 February 2015 - 05:39 PM.

[Flex]

Found this:

Combining two types of antidepressants produces stronger effect; mouse study may help patients for whom existing antidepressants are not effective

http://www.scienceda...01116102126.htm

 

Picciotto and her colleagues found that combining the SSRI fluoxetine (Prozac) with cytisine, a drug that limits the effects of acetylcholine, produced greater antidepressant-like properties in mice than when the drugs were used alone..

 

cytisine = Tabex

http://en.wikipedia.org/wiki/Cytisine

[Joe Monroe]

Is the new prescription product called Deplin just a fancier and mega dose version of l-methylfolate (which is an active form of OTC folate)? I read about this product a few months ago and I think it's out now. I forgot where I read the article but it was something about pharmaceuticals patenting (allegedly) l-methylfolate to make it prescription only when it has been OTC for years. I think the story is untrue and more likely conspiracy theory.

 

http://www.deplin.co...for-depression/

 

You can buy l-methyfolate on amazon, it's just kinda expensive... they work around the patented version of l-methyfolate by... I forget exactly what they do but it's basically made a little bit differently but still the same thing. 

 

I've bought it a few times.. I'm not sure, I mean I think it helps? lol. Nothing significant for me unfortunately. 

[Milkyway]

I think Deplin has been available for a while.  From what I understand it is a mega dose of a vitamin.

[ILIkeBeer]

I found a new drug that is just starting to be researched so there is very little knowledge about it.  I will keep updating as I find it.   It is called  ALKS 7119... it is being made by the same company making ALKS 5461

 

http://www.fiercebio...zheimers-agitat

 

[FeelsNumbMan]

Thanks OP! You're a good guy for doing this. I only hope that one of these things will become available soon enough and prove to be effective. More so than your "antidepressants" that take time to find out the proper dose, time in general to find out whether or not it will work, and then the "right" one 

 

One would have to live to see the day... I hope I can make it. It's already tough as it is.

[eon]

Psychiatrists have finally discovered how to better treat depression

 

"Depression isn't all the same."

 

"Despite its ubiquity, the disease is complex to understand, and to treat. The latest family of antidepressants was developed in the 1980s and drugs today, while improved, haven’t changed substantially since then."

 

"A new study, which Hasler co-authored with his colleague Philipp Homan and published in Nature’s Journal of Translational Psychiatry, may shed light on the nature of two of the most common types of depression and could help dramatically improve the accuracy of drug prescription. These two forms of depression are linked to two chemical imbalances: serotonin deficiency and lack of noradrenaline. "

 

“More psychological symptoms are related to serotonin,” Hasler told Quartz, while “more somatic symptoms—short breath, sweating, feeling of chocking are all bought by [lack of noradrenaline].”

 

Reducing serotonin in the study subjects, says Hasler, led to what is more commonly recognized as a “depressive mood,” nicknamed a lack of “New-York-type happiness” (positive energy).  On the other hand, a reduction of noradrenaline did not cause sadness, but rather a lack of motivation and concentration difficulties, or lack of “Eastern-type” happiness (calmness).

 

http://qz.com/369385...eat-depression/

 

There was a time when depression was more of a lack of serotonin so now noradrenaline is involved. I would think my self medication with St. John's Wort, 5-htp, SAMe, led to me having too much serotonin (serotonin syndrome). What could have been had I been supplementing with herbals that may have increased noradrenaline (which I don't really know much).

 

 

Fasting[edit]

 

 

A study has shown that fasting leads to increased levels of norepinephrine (NE) in the blood for up to 4 days of fasting.^[29]

 

Macronutrient intake[edit]

 

Glucose intake was found to significantly increase plasma NE levels. In contrast, protein and fat intake was found to have no effect.^[30]

 

Receptor binding modulators[edit]

 

Examples include alpha blockers for the α-receptors, and beta blockers for the β-receptors.

 

"Norepinephrine is synthesized from tyrosine as a precursor, and packed into synaptic vesicles. It performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine or by uptake by surrounding cells."

 

"The synthesis of norepinephrine depends on the presence of tyrosine, an amino acid found in proteins such as meat, nuts, and eggs. Dairy products such as cheese also contain high amounts of tyrosine (the amino acid is named for "tyros", the Greek word for cheese). However, adult humans readily synthesize tyrosine from phenylalanine, an essential amino acid. Tyrosine is the precursor to dopamine, which in turn is a precursor to epinephrine and norepinephrine."

 

http://en.wikipedia..../Norepinephrine

 

So the answer is in amino acids: tyrosine and phenylalanine, one or the other?

Edited by eon, 26 March 2015 - 10:02 AM.

[Al Capacino]

I don't get it...I am clearly serotonin deficient due to my utter miserable feelings and positive reaction to some serotonin acting drugs as well as st John's wort.

But I also have incredible fatigue, low motivation and basically all symptoms of low noradrenaline...but when I take wellbutrin or lofepramine, two pills with strong affinity for noradrenaline, I'm stupidly anxious. Like physically uncomfortable anxiety. Although mirtazapine was amazing for motivation, best I've ever felt motivation wise. It also has strong noradrenaline affinity but much more as well I suppose which may have been the source of my positive reaction in terms of motivation, energy etc.
I think above study is oversimplified just like the way they believe antidepressants etc work

[eon]

Anxiety is part of the symptom of serotonin syndrome. I think you're taking too much serotonergics. If you're mixing SSRIs with St. John's wort you're making a mistake.

 

 

[Al Capacino]

No I don't mean I mixed ssris and st John's wort. I only ever took one thing at a time when it came to serotonin products.

Anxiety can't be serotonin syndrome when I was only taking wellbutrin at the time, which acts on norepinephrine and dopamine.

[Flex]

Anxiety is part of the symptom of serotonin syndrome. I think you're taking too much serotonergics. If you're mixing SSRIs with St. John's wort you're making a mistake.

 

Would second that about the anxiety, I believe to read that the downregulation of Serotonergic receptors is anxiolytic.

I cant remeber any 5-ht receptor execpt the 5-ht1 ones that are anxiolytic.

 

mao-A inhibition (passionflower or rhodiola rosea) + St.john´s wort could be also problematic as well as too much sole 5-htp.

Though I think that small ammounts of the combination could be helpful to bypass the down of a beginning.

 

In regards of (synthethic) SSRI´s; watch out for PSSD, the percentage is afaik(?) moderate but it can affect anybody !

http://en.wikipedia....ual_dysfunction

http://wp.rxisk.org/...ring-from-pssd/

 

[eon]

The Most Popular Antidepressants Are Based On An Outdated Theory

 

http://io9.com/the-m...eory-1686163236

 

 

The Myth Of The Chemical Imbalance Theory

 

"There is no question that the chemical imbalance theory has spurred chemists to invent new anti-depressants, or that these anti-depressants have been shown to work; but proof that low serotonin is to blame for depression – and that boosting serotonin levels is the key to its treatment – has eluded researchers."

 

"For starters, it is impossible to directly measure brain serotonin levels in humans. You can’t sample human brain tissue without also destroying it. A crude work-around involves measuring levels of a serotonin metabolite, 5-HIAA, in cerebrospinal fluid (CSF), which can only be obtained with a spinal tap."

 

"The corollary to the chemical imbalance theory, which implies that raising brain serotonin levels alleviates depression, has also been hard to prove. As mentioned previously, the serotonin-depleting drug reserpine was itself shown to be an effective anti-depressant in the 1950s, the same decade in which other studies claimed that reserpine caused depression-like symptoms. At the time, few psychiatrists acknowledged these conflicting reports, as the studies muddled a beautiful, though incorrect, theory. Tianeptine is another drug that decreases serotonin levels while also serving as a bona-fide anti-depressant. Tianeptine does just the opposite of SSRIs – itenhances serotonin reuptake. Wellbutrin is a third anti-depressant that doesn’t increase serotonin levels. You get the picture."

 

"If you prefer your data to be derived more accurately, but less relevantly, from rodents, you might consider a recent meta-analysis carried out by researchers led by McMaster University psychologist Paul Andrews. Their investigation revealed that, in rodents, depression was usually associated with elevated serotonin levels. Andrews argues that depression is therefore a disorder of too much serotonin, but the ambiguous truth is that different experiments have shown“activation or blockage of certain serotonin receptors [to improve] or worsen depression symptoms in an unpredictable manner.”

 

"Other problems with the chemical imbalance model of depression have been well documented elsewhere. For instance, if low serotonin levels were responsible for symptoms of depression, it stands to reason that boosting levels of serotonin should alleviate symptoms more or less immediately. In fact, antidepressants can take more than a month to take effect. Clearly, something here just doesn’t add up."

 

"In a joint e-mail, Lacasse and Leo told me that the public portrayal of the chemical imbalance theory has dropped off noticeably in the past few years. Though TV commercials promoted SSRIs using the chemical imbalance theory in the early 2000s, “we noticed these advertisements came to a screeching halt around 2006-07,” they said. It’s not entirely clear why these advertisements disappeared, but the researchers speculate it’s because the underlying science had failed to corroborate the theory, and finally come to the attention of advertising execs who had knowingly skipped their homework."

 

"But Lacasse and Leo say depressed patients are still routinely told by their GPs and psychiatrists that they have a chemical imbalance, in spite of criticisms from prominent academic psychiatrists like Ronald Pies, who “states that no knowledgable, well-trained clinician would say such a thing."

 

"Videbech also mentioned several new therapies that could gain traction in coming years.Ketamine, for example, shows promise, but must be given at regular intervals; transcranial magnetic stimulation, in which magnets are used to non-invasively manipulate brain activity, and wake therapy, in which patients are kept awake for prolonged periods, are two other options backed by reams of scientific evidence. In the future, we may even see psychedelicsreturn to the psychiatric clinic; a number of psychedelic compounds – including psilocybin, the hallucinogen found in magic mushrooms – have shown promise as antidepressants in recent years, a fact that has led many to call for an end to bans on psychoactive drug research."

 

I think "wake therapy" sounds interesting since it's the first time I've heard it. 

 

Edited by eon, 06 April 2015 - 01:48 PM.

[Flex]

Dont want to oppose that but found this considerable:

 

This is what I said the last time this was posted, by lightfiend 19 days ago.

"I'm not impressed by the paper overall. It reads to me like the author over-enjoys the role of being a gadfly. So he is prone to make simplifying generalizations about what the current paradigm is, and that gives him plenty of room to poke holes in it, because he stated the paradigm in a too-simplified and too-generalized way to begin with. A straw man. I just don't think it's true that the "reigning paradigm" is based on a "low serotonin" hypothesis - that's too broadly stated and too simplified. There are clearly alterations in certain specific neurotransmitters in certain specific circuits - some up, some down, - and the neurotransmitter list of interest includes serotonin, dopamine, norepinephrine, acetyl choline, histamine, glutamate, GABA, endogenous opioids, endogenous cannabinoids. I think everybody in the field realizes it's very complex, and next to nobody is clinging to a reductionistic notion of "low serotonin" or "high serotonin." My background = MD, biological psychiatrist, have been treating depression for many years now."

 

http://www.reddit.co...science_behind/

 

This was a response to:

 

Science behind commonly used anti-depressants appears to be backwards, researchers say

http://www.scienceda...50217114119.htm

Edited by Flex, 06 April 2015 - 03:05 PM.

[eon]

Well what compound could possibly "hit" all the neurotransmitter? I couldn't remember the name for it but I thought I read someone making a comment that if this one particular neurotransmitter or "part" of the brain is given medicine it affects the entire "system". Not sure if that's sci-fi or simply assumption. The outcome I don't know could be good or bad. If anyone knows chime in.

[Flex]

Would be quiet interresting. Please post the name or link if You remeber it.

[eon]

I wish I could remember it but I'll look for it possibly on this forum or reddit. I would think it was more assumption by someone but if such thing existed or possible then I would think everyone would have heard of it by now.

 

But here's more bad news regarding a common antidepressant/SSRI called Zoloft:

 

Common antidepressant increased coronary atherosclerosis in animal model

 

http://medicalxpress...sis-animal.html

 

 

Would be quiet interresting. Please post the name or link if You remeber it.

 

[eon]

I may have found it. I think it's called Orexin/Orexinergics. While I have little understanding how it works, I think someone "assumed" that if you look into orexinergics the rest of the neurotransmitters will follow. Sort of like it's the "main" one to "attack" and everything will benefit from it. If someone else can explain better go ahead. But below are some information from wikipedia:

 

"Orexin, also called hypocretin, is a neurotransmitter that regulates arousal, wakefulness, and appetite."

 

"Orexin seems to promote wakefulness. Recent studies indicate that a major role of the orexin system is to integrate metabolic, circadian and sleep debt influences to determine whether an animal should be asleep or awake and active. Orexin neurons strongly excite various brain nuclei with important roles in wakefulness including the dopamine, norepinephrine, histamine and acetylcholine systems[8][9] and appear to play an important role in stabilizing wakefulness and sleep."

 

"Many scientists believe that orexin-based drugs could increase alertness in the brain without the side effects of substituted amphetamines."

 

"High levels of orexin-A have been associated with happiness in human subjects, while low levels have been associated with sadness.[25] The finding suggests that boosting levels of orexin-A could elevate mood in humans, being thus a possible future treatment for disorders like depression. Likewise, it helps explain the incidence of depression associated with narcolepsy.

 

"Orexinergic neurons have been shown to be sensitive to inputs from Group III metabotropic glutamate receptors,[31] adenosine A1 receptors,[32] muscarinic M3 receptors,[33] serotonin 5-HT1A receptors,[34] neuropeptide Y receptors,[35] cholecystokinin A receptors,[36] and catecholamines,[37][38] as well as to ghrelin, leptin, and glucose.[39] Orexinergic neurons themselves regulate release of acetylcholine,[40][41] serotonin and noradrenaline,[42] so despite the relatively small number of orexinergic neurons compared to other neurotransmitter systems in the brain, this system plays a key regulatory role and extensive research will be required to unravel the details. "

 

 

 

Would be quiet interresting. Please post the name or link if You remeber it.

 

[ILIkeBeer]

Thanks OP! You're a good guy for doing this. I only hope that one of these things will become available soon enough and prove to be effective. More so than your "antidepressants" that take time to find out the proper dose, time in general to find out whether or not it will work, and then the "right" one 

 

One would have to live to see the day... I hope I can make it. It's already tough as it is.

 

 

I feel your pain friend!  I really appreciate your comments!  I hope this does give some people hope! 

[ILIkeBeer]

I have made so many posts I don't know if I posted these already but if so then I guess I will just remind people

 

Nitrous Oxide -  This apparently works very quickly and is highly available now.

 

http://www.biologica...0910-X/abstract

 

 

and a new microchip - this to me sounds awesome because it feels more like a cure then other things... if it works... not that I could ever afford it :(

 

http://www.dailymail...treat-PTSD.html

 

 

 

 

 

 

[eon]

Isn't nitrous oxide some type of gas? So how is this "available" product used? Is it inhaled? I've read about another gas supposedly great for depression (considering its neuroprotectant activity) and other things explained below. The gas is called xenon.

 

I have read that nitrous oxide can be neurotoxic:

 

Medical[edit]

 

Anesthesia[edit]

 

Xenon has been used as a general anesthetic. Although it is expensive, anesthesia machines that can deliver xenon are about to appear on the European market, because advances in recovery and recycling of xenon have made it economically viable.^[131][132]

 

Xenon interacts with many different receptors and ion channels and like many theoretically multi-modal inhalation anesthetics these interactions are likely complementary. Xenon is a high-affinity glycine-site NMDA receptor antagonist.^[133] However, xenon distinguishes itself from other clinically used NMDA receptor antagonists in its lack of neurotoxicity and its ability to inhibit the neurotoxicity of ketamine and nitrous oxide.^[134][135] Unlike ketamine and nitrous oxide, xenon does not stimulate a dopamine efflux from the nucleus accumbens.^[136] Like nitrous oxide and cyclopropane, xenon activates the two-pore domain potassium channel TREK-1. A related channel TASK-3 also implicated in inhalational anesthetic actions is insensitive to xenon.^[137] Xenon inhibits nicotinic acetylcholine α₄β₂ receptors which contribute to spinally mediated analgesia.^[138][139] Xenon is an effective inhibitor of plasma membrane Ca²⁺ ATPase. Xenon inhibits Ca²⁺ ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations.^[140]

 

Xenon is a competitive inhibitor of the serotonin 5-HT₃ receptor. While neither anesthetic nor antinociceptive this activity reduces anesthesia-emergent nausea and vomiting.^[141]

 

Xenon has a minimum alveolar concentration (MAC) of 72% at age 40, making it 44% more potent than N₂O as an anesthetic.^[142] Thus it can be used in concentrations with oxygen that have a lower risk of hypoxia. Unlike nitrous oxide (N₂O), xenon is not a greenhouse gas and so it is also viewed as environmentally friendly.^[143] Xenon vented into the atmosphere is being returned to its original source, so no environmental impact is likely.

 

Neuroprotectant[edit]

 

Xenon induces robust cardioprotection and neuroprotection through a variety of mechanisms of action. Through its influence on Ca2+, K+, KATP\HIF and NMDA antagonism xenon is neuroprotective when administered before, during and after ischemic insults.^[144][145] Xenon is a high affinity antagonist at the NMDA receptor glycine site.^[133] Xenon is cardioprotective in ischemia-reperfusion conditions by inducing pharmacologic non-ischemic preconditioning. Xenon is cardioprotective by activating PKC-epsilon & downstream p38-MAPK.^[146] Xenon mimics neuronal ischemic preconditioning by activating ATP sensitive potassium channels.^[147] Xenon allosterically reduces ATP mediated channel activation inhibition independently of the sulfonylurea receptor1 subunit, increasing KATP open-channel time and frequency.^[148] Xenon upregulates hypoxia inducible factor 1 alpha (HIF1a).

 

Xenon gas was added as an ingredient of the ventilation mix for a newborn baby at St. Michael's Hospital, Bristol, England, whose life chances were otherwise very compromised, and was successful, leading to the authorisation of clinical trials for similar cases.^[149] The treatment is done simultaneously with cooling the body temperature to 33.5 °C.^[150]

 

Doping[edit]

 

Inhaling a xenon/oxygen mixture activates production of the transcription factor HIF-1-alpha, which leads to increased production of erythropoietin. The latter hormone is known to increase red blood cell production and athletes' performance. Xenon inhalation has been used for this purpose in Russia since at least 2004.^[151] On August 31 2014 the World Anti Doping Agency (WADA) added Xenon (and Argon) to the list of prohibited substances and methods, although at this time there is no reliable test for abuse.^[152]

 

http://en.wikipedia.org/wiki/Xenon

 

There are precautions to take when using xenon. Read the wikipedia site. Now, the question is who would sell xenon and has anyone here tried it? It is a very expensive gas. I've read of it being $150 per hour (I would assume this is from a medical treatment setting?).

Edited by eon, 11 April 2015 - 02:45 AM.

[Flex]

Found this:

 

Uncoupling the dopamine D1-D2 receptor complex exerts antidepressant-like effects.

http://www.ncbi.nlm....pubmed/21113156

 

Dopamine D1-D2 receptor heteromer signaling pathway in the brain: emerging physiological relevance

and that the mobilization of intracellular calcium was in fact a unique signaling pathway resulting from the activation of this D1-D2 heteromeric receptor complex

http://www.molecular.../content/4/1/26

 

seems to me that Clozapine is able to attenuate it:

 

Mechanism of action of clozapine in the context of dopamine D1-D2 receptor hetero-dimerization--a working hypothesis

Further investigation confirmed the idea that high affinity binding sites exist when the receptor is coupled with G protein, and also that clozapine attenuates the hetero-oligomerization of a high affinity pool of dopamine D1-D2 receptors.

http://www.ncbi.nlm....pubmed/19066405

 

 

 

 

Edited by Flex, 11 April 2015 - 01:20 PM.

[eon]

Link between serotonin and depression is a myth, says top psychiatrist

 

http://medicalxpress...ychiatrist.html

 

The widely held belief that depression is due to low levels of serotonin in the brain - and that effective treatments raise these levels - is a myth, argues a leading psychiatrist in The BMJ this week.

 

David Healy, Professor of Psychiatry at the Hergest psychiatric unit in North Wales, points to a misconception that lowered serotonin levels in depression are an established fact, which he describes as "the marketing of a myth."

 

The serotonin reuptake inhibiting (SSRI) group of drugs came on stream in the late 1980s, nearly two decades after first being mooted, writes Healy. The delay centred on finding an indication.

 

After concerns emerged about tranquilliser dependence in the early 1980s, drug companies marketed SSRIs for depression, "even though they were weaker than older tricyclic antidepressants, and sold the idea that depression was the deeper illness behind the superficial manifestations of anxiety," he explains. The approach was an astonishing success, "central to which was the notion that SSRIs restored serotonin levels to normal, a notion that later transmuted into the idea that they remedied a chemical imbalance."

 

In the 1990s, no one knew if SSRIs raised or lowered serotonin levels, he writes; they still don't know. There was no evidence that treatment corrected anything, he argues.

 

He suggests that the myth "co-opted" many, including the complementary health market, psychologists, and journals. But above all the myth co-opted doctors and patients, he says. "For doctors it provided an easy short hand for communication with patients. For patients, the idea of correcting an abnormality has a moral force that can be expected to overcome the scruples some might have had about taking a tranquilliser, especially when packaged in the appealing form that distress is not a weakness."

 

Meanwhile more effective and less costly treatments were marginalised, he says.

 

He stresses that serotonin "is not irrelevant" but says this history "raises a question about the weight doctors and others put on biological and epidemiological plausibility." Does a plausible (but mythical) account of biology and treatment let everyone put aside clinical trial data that show no evidence of lives saved or restored function, he asks? Do clinical trial data marketed as evidence of effectiveness make it easier to adopt a mythical account of biology?

 

These questions are important, he says. "In other areas of life the products we use, from computers to microwaves, improve year on year, but this is not the case for medicines, where this year's treatments may achieve blockbuster sales despite being less effective and less safe than yesterday's models."

 

"The emerging sciences of the brain offer enormous scope to deploy any amount of neurobabble. We need to understand the language we use. Until then, so long, and thanks for all the serotonin," he concludes.

 

[Michael Rian]

Extremely fascinating thread!  Thank you all so much for sharing all this! 

[BarbCat]

Do you know if Tocris will sell to individuals, or does it have to be a legitimate research institution?

I've found that Tocris .com has many interesting compounds available but the small amounts that they sell are extremely expensive, prohibitively so.  What I wonder is if the amounts are extra potent and you don't need much.  The question then is, how much to administer?  What's the dosage?  The dilution ratio?  I can't find any helpful conversion info out there.

[eon]

Tocris sells to the general public? Powdercity should be able to get them produced in China for less? Just make a request...

[eon]

I'm sure everyone here has read about the use of the hallucinogenic DMT for depression so I'm curious about this drug if it has any relations to it:

 

αMT (alpha-methyltryptamine), an anti-depressant from the tryptamine family; first developed in the Soviet Union and marketed under the brand name Indopan.

 

It is a schedule 1 drug in the U.S. along with heroin, etc. I don't know why an anti-depressant would be scheduled that way but I'm assuming since the hallucinogenics DMT, psilocybin, LSD, etc. all belong in the same drug schedule level, that may be the reason. But I doubt Indopan is hallucinogenic, but I don't get the scheduling level it belongs to. Maybe it's effective? One person on this forum mentioned that DMT is all you need for depression but of course anyone who likes something will boast about it. LOL I have to find that person's name again and ask him what he thinks of Indopan.

Edited by eon, 25 May 2015 - 02:47 AM.