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Author: Subject: Tinnitus treatment via 3,4-methylenedioxy-phenethylamine?
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[*] posted on 13-4-2018 at 14:03
Tinnitus treatment via 3,4-methylenedioxy-phenethylamine?


Quote:

QUALITATIVE COMMENTS: (with 200 mg) It was taken twice at different times in a dosage of 200 milligrams each time, without the slightest peripheral or central effects. 

(with 300 mg) My tinnitus had disappeared. Probably nothing.  -PIHKAL


I'm sure this is probably nothing.

Shulgin comments:
Quote:

How strange. Even more than DMPEA, this cyclic analogue MDPEA is a potential prodrug to dopamine, and would be a prime candidate for central activity. So why is this drug not active? The usual reason advanced by the pharmacologists is that the body is full of potent enzymes known as monoamine oxidases, and this is a monoamine, and so the body simply chews away on it in an oxidative manner, inactivating it before it ever makes it to some target receptor. 

That is the pitch given in the textbooks. Phenethylamines are subject to easy enzymatic oxidation, hence they are not active. The presence of an alpha-methyl group (the corresponding amphetamines) blocks the compound from easy access to the enzyme, and since that protects them from oxidative destruction, they are active. The oft-quoted exception is mescaline, and even it is largely destroyed, as evidenced by the large amount needed for activity (a fraction of a gram). Sorry, I can't buy it. This entire book is peppered with phenethylamines that are active at the few-milligram area. Why aren't they also destroyed as well? The textbooks simply are not right. -PIHKAL


Despite shulgin's comments on the matter I still think that the exposed amine nitrogen on these compounds makes them far more amenable to oxidative deamination through mono amine oxidase enzymes in vivo, and that the reason why the alpha methylated homologues of these compounds are nearly doubled in potency is because that methyl grouping on the alpha carbon of the ethylamine side chain is serving to protect the amine nitrogen from these enzymes to some degree, however, that's not the subject of this post.

I do not know very much about the treatment of tinnitus or the pharmacology of currant tinnitus treatments, but I was quite interested when I saw the comment in PIHKAL relating to this compound eliminating tinnitus in one subject, and while yes, it was probably nothing, there is also a small chance that shulgin had stumbled onto a pharmacological application for the compound. The compound really doesn't overtly do anything psychologically and it appears to be physically benign, if it had a potential medical application I can not imagine why shulgin did not at least explore the possibility...

It probably was a coincidence that the subjects tinnitus diminished during the experiment, or it was probably a fluke of some sort, or some type of psychosomatic or placebo reaction, and maybe I just get overly enthusiastic over potential medical applications of these compounds, but if were shulgin I would have at least tried to repeat the experiment or find another subject who suffered from tinnitus to participate in an experiment with the compound just to be sure...


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[*] posted on 14-4-2018 at 07:03


Hmm...

I was wondering if this post was appropriate for this forum.

Not much interest.

I would not mind if an administrator wanted to take it down. These topics can be hit or miss, and sometimes a topic will simply flop. Seems like that's what happened here. Sorry.

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[*] posted on 14-4-2018 at 07:19


This book claims to remove all diseases simply by "not eating" or in long term changin eating and living habits.
http://www.web.ms11.net/~drbass/orthopathy/index.html

While all people say there's no cure for my hay fever and 100 other diseases i have, this book makes sense:

HAY FEVER

Definition: This is an acute, usually recurrent, and distinctly seasonal inflammation of the nasal mucous membrane sometimes extending to the conjunctiva of the eye, and the membranes of the pharynx, bronchial tubes and Eustachian tubes.

Symptoms: While defined as an acute inflammation which is subject to recurrent and seasonal acute exacerbations, the catarrh is continuous but is peculiarly subject to, pronounced increase in severity of symptoms in the months of May, June, July and August. In the South it may last all the year. Nasal obstruction with rhinorrhea and much sneezing are accompanied by congestion of the conjunctive, watering of the eyes, itching of the eyelids, nose and palate. There is headache and lassitude and, occasionally, paroxysms of asthma. It may be described as a severe cold running on day after day, with no let-up, and often growing worse, for the longer it persists in the acute stage, the more sensitive the mucous membrane becomes.

Etiology: Hay fever, being seasonal, develops largely in the spring (rose-cold) and in the autumn (autumnal catarrh) and is said to be excited or evoked by inhaling the pollens of certain plants and grasses — ragweed, goldenrod, cedar, timothy grass, etc. The condition of hypersensitiveness to the toxalbumin of pollen is called anaphylaxis or allergy. Since, however, allergy does not cause itself this theory of cause does not go deep enough. It fails to account for the local hypersensitiveness to normal elements of man's natural environment.
Although it is true that dust, pollen, emanations from horses, cats, dogs, birds, etc., and even cold air, will drive hay-fever sufferers into intolerable suffering, this does not prove them to be causes of hay fever. Anything that irritates a sensitive mucous membrane occasions a rush of blood to the point of irritation and the pouring out of an exudation to flush away the irritant.
Within recent years enterprising doctors have discovered that some hay fever subjects are allergic to their sweet-hearts and suffer an exacerbation (aggravation) of symptoms every time they visit their lovers. In a few instances the source of irritation was found in the lip-stick, rouge, and face powder, or even in the perfume, but in other instances emanations from the lover's hair were blamed.
The mistake has been made of considering normal elements in man's environment — pollen, and emanations from animals — as causes of hay fever; whereas, the true cause, the basic cause, is the cause of the sensitization of membranes which normally are not sensitive to pollens, etc.
Hay fever is simply a peculiar type of chronic catarrh, which only a small percentage of catarrhal subjects develop. Two people have catarrh to the same extent; one develops hay fever, the other does not. The sensitive individual is neurotic, the other is not. Hay fever is chronic catarrh in a neurotic subject.
Only neurotic individuals — those subject to nervous diseases —will develop the individualizing sensitization that distinguishes hay fever from ordinary catarrh. The non-neurotic sufferer from catarrh will be influenced little or none by the inhalation of dust, pollen, smoke, pungent odors, or cold air. "Hot dogs" are the only dogs of which I know that may help to cause hay fever.
Hay fever rests on a basis of enervation and toxemia. The hay fever sufferer is made highly toxic by his enervating habits which inhibit full elimination of normal body waste. The subject builds his disease daily by keeping his stomach deranged with his meats, potatoes, breads, pies, cakes, pastries, butter, breakfast foods, and even with his luscious fruits covered with cream and sugar. These things over-stimulate him and produce a toxic state of his blood which further adds to his enervation and produces nervousness and sensitiveness as well as catarrh.

Prognosis: Complete recovery may be expected in six weeks or less in the vast majority of cases. A few cases persist longer than this time.

Care of the Patient: Running away from the external sources of irritation is merely a palliative measure. Going to dustless, pollenless, ragweedless, catless, horseless, chickenless, gooseless, sweatheartless and senseless resorts does not correct the underlying constitutional perversion — toxemia and its resulting catarrh. Hoping for the hurried coming of the old charlatan, practicing without a license, Jack Frost, to put an end to pollens, wastes a lot of valuable time and causes the sufferer to endure a lot of misery. Searing the nose, wearing air-filters, staying all summer long in air-conditioned rooms, going on sea voyages, etc., do not remove cause. Most of these palliatives are for the well-to-do only.
A fast for the removal of toxemia will end the catarrh in a very short time and remove all sensitiveness to pollen, dust, sweetheart, etc. Rest for the nervous system and a healthful mode of living will build up a high degree of health and prevent all future recurrence of hay fever. Following the elimination of toxemia, restoration of normal nerve energy and correction of the mode of living, the evolution into good health is sure and rapid.

Maybe there's something about tinnitus and all diseases too... Best of all they are categorized by chapters, that is by locations on body. Hay fever is "respiratory organs". Only this and one book by J.H.Tilden claimed to cure my hay fever.

Wikipedia defines many diseases as "no cure" and "unknown cause".

I still can't test Shelton's books as I eat sugar and salt and cookies and cola....even worse than that. Luckily no alcohol and tobacco and drugs. :(

Oh, I forgot what is fruits and vegetables. Haven't seen one in months.

[Edited on 14-4-2018 by RawWork]
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[*] posted on 14-4-2018 at 12:15


Shulgin's note is indeed probably nothing, but having said that.... Tinnitus often seems to be a matter of auditory nerves firing too easily. Many phenethylamines have varying degrees of affinity for serotonin receptors. And serotonin receptors (broadly speaking) tend to have an inhibitory effect on neuron firing.

So, it's not a crazy idea that this class of drugs could have an effect on suppressing tinnitus.

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[*] posted on 16-4-2018 at 06:08


Quote: Originally posted by Reboot  
Shulgin's note is indeed probably nothing, but having said that.... Tinnitus often seems to be a matter of auditory nerves firing too easily. Many phenethylamines have varying degrees of affinity for serotonin receptors. And serotonin receptors (broadly speaking) tend to have an inhibitory effect on neuron firing.

So, it's not a crazy idea that this class of drugs could have an effect on suppressing tinnitus.



That's what I was thinking. Probably nothing.

I have not looked into serotonin receptor agonism in relation to tinnitus, but it seems reasonable, though we know that the compound is not acting at 5-HT2a/c receptor sites or it would be psychoactive, but it's possible that it has some type of serotonin receptor affinity.

Its also possible that due to oxidative deamination from mono amine oxidase enzymes in vivo that the compound is never fully reaching the system, in which case the perceived effect would have had to have been psychosomatic, as I do not see the deaminated metabolite as acting in this fashion.

If the compound was being enzamatically deaminated, it's possible that consumption with a monoamine oxidase inhibitor could result in activity... if the compound did show activity when consumed with an MAOI it could confirm that the exposed amine nitrogen at the end of the ethylamine side chain is making the molecule amenable to deamination...

Again, I apologize, the subject matter here really was not deserving of it's own thread, it's interesting stuff, but doesn't seem to be very good conversation.

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[*] posted on 16-4-2018 at 17:03


Dunno. If you wanna develop tinnitus, just take a lot of aspirin. Works for a lot of people.
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[*] posted on 16-4-2018 at 18:07


it could also be a fluke in that maybe that the drug does have the desired effect but it might not be easily repeatable because the specific individual had less active MAO enzymes or took a MAO-Inhibitor unknown to the investigation?

its 100% speculation but other drugs have "race" related efficacy from the genetics of the populations.
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[*] posted on 17-4-2018 at 09:08


I can understand that individuals might have differing biochemistry, though I am not certain that this was the issue here. I have not looked into genetics or race affecting the pharmacological outcome of a specific compound, but I can't imagine that it would apply here. Though I will note that my focus is on organic chemistry, so it would not surprise me if some pharmacological information slipped past me.

As shulgin noted, it's a surprise that this compound is not active, it could potentially serve as a pro-drug to 3,4-dihydroxy-phenethylamine, and If one were to substitute a methyl grouping onto the alpha carbon of the ethylamine side chain you would obtain 3,4-methylenedioxy-alpha-methyl-phenethylamine (MDA), a highly active entactogen/empathogen.

My guess is that the compound is highly amenable to oxidative deamination by mono-amine oxidase enzymes in vivo, meaning the amine nitrogen is being enzamatically removed before the compound can enter the system, hence inactivity. It would be interesting if the deaminated metabolite was actually responsible for the tinnitus relief, however, in reality we can't even confirm that there was any tinnitus relief, a single entry from a single patient is an interesting note, but ultimately means very little.

I'm not sure why shulgin chose not to explore this compound with an MAOI, I don't see serotonin syndrome or hypertension becoming an issue with that particular combination.

I also don't understand why shulgin did not seek out at least one other research patient who suffered from tinnitus, the note could have been confirmed as a fluke or as a potential medicine simply by incorporating other research patients. I think shulgin should have at least passed the idea to Darrell Lemaire if he himself was not willing to do the work, but hey, it's far too late now.
Its possible that tinnitus and its treatment are not well understood, and that treatments are not a viable option for one reason or another hence the idea would ultimately not be worth shulgin pursuing.

I myself do not suffer from tinnitus, and I do not think I know anyone who does, so I have really never looked into it until contemplating this compound as a potential treatment.

Like I said, not a very good topic, not much besides speculation can be achieved. Though I would be willing to bet that consuming this compound with an MAOI would give some sort of central activity.

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[*] posted on 17-4-2018 at 09:37


It would certainly be active on a large enough scale, at least 500mg; take beta-phenylethylamine for instance which is active at doses ranging from 1-2 grams - I myself use it with profound effects despite being considered inactive - whereas the alpha-methylated derivative (Adderall for discussion and legality sake) is active below 20mg for medical doses. All you need to do is saturate the MAO enzymes so enough active compound can get through to bind to receptors. Taking MAOIs simply reduces the required dose for mentioned reasons, as it does for other phenylethylamines.

[Edited on 17-4-2018 by LearnedAmateur]




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[*] posted on 23-4-2018 at 06:13


Quote: Originally posted by LearnedAmateur  
It would certainly be active on a large enough scale, at least 500mg; take beta-phenylethylamine for instance which is active at doses ranging from 1-2 grams - I myself use it with profound effects despite being considered inactive - whereas the alpha-methylated derivative (Adderall for discussion and legality sake) is active below 20mg for medical doses. All you need to do is saturate the MAO enzymes so enough active compound can get through to bind to receptors. Taking MAOIs simply reduces the required dose for mentioned reasons, as it does for other phenylethylamines.

[Edited on 17-4-2018 by LearnedAmateur]


Hmmm...

I'm not sure it would be active on any scale.

You are suggesting that if you consume enough of the compound to occupy the entirety of your monoamine oxidase enzymes that some could slip into the system, no?

If so ill elaborate on that matter.

"Beta-phenethylamine" is a synonym for phenethylamine, which is not active.
Quote:

DOSAGE: greater than 1600 mg. 

DURATION: unknown. 

QUALITATIVE COMMENTS: (with 200, 400, 800 and 1600 mg) No effects. 

(with 500 mg) No effects. 

(with 800 and 1600 mg) No effects. 

(with 25 and 50 mg i.v.) RNo effects. 

EXTENSIONS AND COMMENTARY: Here is the chemical that is central to this entire book. This is the structural point of departure for every compound that is discussed here. It is the RPS in PIHKAL. It is without activity in man! Certainly not for the lack of trying, as some of the dosage trials that are tucked away in the literature (as abstracted in the "Qualitative Comments" given above) are pretty heavy duty. Actually, I truly doubt that all of the experimenters used exactly that phrase, "No effects," but it is patently obvious that no effects were found. It happened to be the phrase I had used in my own notes.  -PIHKAL


If you were speaking about "beta-methyl-phenethtlamine" you must keep in mind that the methyl grouping on the beta-carbon of the ethylamine side chain still prevents mono amine oxidase enzymes from chewing off the amine nitrogen.

Beta-methyl-phenethylamine is a positional isomer of amphetamine (alpha-methyl-phenethylamine), and as the name suggests there is a methyl grouping connected to the beta carbon of the ethylamine side chain. These methyl substitutions to this side chain serve to block the amine nitrogen from mono amine oxidase enzymes in vivo to some degree.

...shulgin was discussing phenethylamines which are not substituted on the ethylamine side chain in regards to monoamine oxidase enzymes.

...any way, it gets kind of complex, though I would love to elaborate if needed.
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[*] posted on 26-4-2018 at 07:34


I have the time to do some research with this compound, but have not decided if it's a waste of time or not, in all honesty there are other compounds which I am far more interested in...
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[*] posted on 26-4-2018 at 14:01


Yes, it’s the MAO enzymes which inhibit activity of a lot of phenylethylamines because they’re broken down so quickly - take enough to saturate the enzymes and it will produce effects as long as it can cross the BBB. Of course, their duration is very short because the enzymes won’t be ‘locked up’ for long, but providing enough molecules have access to the receptors then you will get effects.

PEA certainly is active, I can personally attest to that because I have put over a kilogram of the stuff through my body over the past two years, with predictable dosing, tolerance, and duration. The molecule I’m referring to is what you think, the benzene molecule with an aminoethyl group - nothing else apart from that except for the HCl salt since the freebase is liquid and highly basic.

From my experience, dosing with no tolerance is as follows:
1-1.5g orally taken in 2-3 lots of 500mg encapsulated and ground salt.
Onset of action is approximately 20 minutes and requires a completely or near empty stomach otherwise no effects are experienced.
Duration lasts between 30 and 45 minutes with after effects lasting up to two hours, mood is altered for several hours.
Effects: potential stomach discomfort before manifestation of effects rapid increase in amphetamine like stimulation peaking within 10 minutes, tingling extremities (not pins and needles but like you can feel the blood moving; vasoconstriction), pressure in sinuses, intense ability to focus/greater ignorance of distractions but attention can still be consciously diverted easily. Even with a mild overdose (200mg+ more than standard dose), the intense psychological effects may cause vomiting and induce strong anxiety.

Overall, PEA is not addictive or dependence forming, even when tolerance leads to doses of 2-2.5g, there is no withdrawal or cravings when discontinuing usage. Dose decreases back down to baseline within two weeks. I like to use it when gaming because it increases focus and I seem to play a LOT better than without it, but outside of that and for maybe studying, it’s pretty useless. No euphoria is experienced so it has little value as a recreational substance, and the short duration and high dose means that it isn’t great medicinally. As a pure TAAR1/TAAR2 agonist, PEA obviously has no psychedelic effects, only stimulant like its methylated cousins.

[Edited on 26-4-2018 by LearnedAmateur]




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[*] posted on 28-4-2018 at 07:15


Quote: Originally posted by LearnedAmateur  
Yes, it’s the MAO enzymes which inhibit activity of a lot of phenylethylamines because they’re broken down so quickly - take enough to saturate the enzymes and it will produce effects as long as it can cross the BBB. Of course, their duration is very short because the enzymes won’t be ‘locked up’ for long, but providing enough molecules have access to the receptors then you will get effects.

PEA certainly is active, I can personally attest to that because I have put over a kilogram of the stuff through my body over the past two years, with predictable dosing, tolerance, and duration. The molecule I’m referring to is what you think, the benzene molecule with an aminoethyl group - nothing else apart from that except for the HCl salt since the freebase is liquid and highly basic.

From my experience, dosing with no tolerance is as follows:
1-1.5g orally taken in 2-3 lots of 500mg encapsulated and ground salt.
Onset of action is approximately 20 minutes and requires a completely or near empty stomach otherwise no effects are experienced.
Duration lasts between 30 and 45 minutes with after effects lasting up to two hours, mood is altered for several hours.
Effects: potential stomach discomfort before manifestation of effects rapid increase in amphetamine like stimulation peaking within 10 minutes, tingling extremities (not pins and needles but like you can feel the blood moving; vasoconstriction), pressure in sinuses, intense ability to focus/greater ignorance of distractions but attention can still be consciously diverted easily. Even with a mild overdose (200mg+ more than standard dose), the intense psychological effects may cause vomiting and induce strong anxiety.

Overall, PEA is not addictive or dependence forming, even when tolerance leads to doses of 2-2.5g, there is no withdrawal or cravings when discontinuing usage. Dose decreases back down to baseline within two weeks. I like to use it when gaming because it increases focus and I seem to play a LOT better than without it, but outside of that and for maybe studying, it’s pretty useless. No euphoria is experienced so it has little value as a recreational substance, and the short duration and high dose means that it isn’t great medicinally. As a pure TAAR1/TAAR2 agonist, PEA obviously has no psychedelic effects, only stimulant like its methylated cousins.

[Edited on 26-4-2018 by LearnedAmateur]


Phenethylamine is an endogenous monoaminergic neuromodulator. Phenethylamine does induce a very mild release of norepinephrine and dopamine, and through a glutamate-mediated mechanism some acetylcholine release does occur. The human trace amine-associated receptor agonism is associated with neuromodulation, for example the taar1 receptor acts as a regulator of the neurotransmission relating to 3,4-hydroxy-phenethylamine, norepinephrine, and serotonin neurons.

So in this sense it could be considered pharmacologically active, however, I do not consider the compound to be psychoactive, even with its incredibly mild stimulant properties. These stimulant properties should also be far too brief to be perceptible, below Shulgin elaborates:
Quote:

Phenethylamine is intrinsically a stimulant, although it doesn't last long enough to express this property. In other words, it is rapidly and completely destroyed in the human body. It is only when a number of substituent groups are placed here or there on the molecule that this metabolic fate is avoided and pharmacological activity becomes apparent.  -Shulgin;PIHKAL


The compound is rapidly metabolized to phenylacetic acid, and to some tyramine by aldehyde dehydrogenase and mono amine oxidase B. These are all endogenous products in humans.

I have also taken phenethylamine through many routes of administrations and doses, and ultimately my conclusions were near identical to Shulgin's:
Quote:

PHENETHYLAMINE:
DOSAGE: greater than 1600 mg. 
DURATION: unknown. 
QUALITATIVE COMMENTS: (with 200, 400, 800 and 1600 mg) No effects. 

(with 500 mg) No effects. 

(with 800 and 1600 mg) No effects. 

(with 25 and 50 mg i.v.) No effects.
-shulgin;PIHKAL


Every experiment I have participated in with phenethylamine has provided the same results in terms of psychoactivity...nothing.

...Though I suppose I can understand what you are saying, even though I have never been able to feel any perceptible effect from consumption of the compound.

Moving on:

It's not just being able to enter the system that constitutes activity, the compound has to play a specific role at a receptor site. I picture the alpha helical proteins of the receptor site to be analogous to the pins in a tumbler lock, and the molecule being analogous to a key, the molecule has to move each alpha-helical protein into a specific shape to produce the desired effect. So without going into any greater detail I will sum things up by saying that just getting into the system is only the first of the obstacles for a molecule.

Miscellaneous note:

If you orally consumed serotonin, it would be inactive, the hydroxyl grouping at position 5 acts as a large hydrophilic mass and is too polar to allow passage beyond the blood brain barrier, and, the exposed amine nitrogen at the end of the ethylamine side makes the compound amenable to enzymatic deamination by mono amine oxidase enzymes in vivo, however, if one were to place methyl groupings at these two positions one would obtain 5-methoxy-alpha-methyl-tryptamine, an orally active psychedelic.

With phenethylamine we do not have a hydroxyl grouping to worry about, but we have the same ethylamine side chain, and the same issue with amenability to oxidative deamination by mono amine oxidase enzymes...

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[*] posted on 28-4-2018 at 09:12


It’s one of those hit and miss compounds, for the lucky some like myself it works well at the doses I listed and is quite intense at the peak. You can find instances of people getting strong stimulant effects from PEA; whilst I do look up to Shulgin, I don’t agree with the statement that it is ‘without activity in man’ - it’s all well and good sharing his particular experiences but what happens to one person may not happen to another.* We also don’t know what personal circumstances there were surrounding his trials, like I said you need a near empty stomach to experience any effects (morning is preferable, at least 3-5 hours since the last meal) otherwise the absorption is too slow. Oral dosing is so predictable for me that I could comfortably measure out my starting dose despite not having taken it for a few months now, and be happy with the level of effects I feel, but I wouldn’t attempt this with intranasal or IV administration.

* Take codeine for instance, which a lot of people take to get high but many people lack a good amount of CYP2D6 enzymes required for adequate metabolism to morphine, like myself, so to me codeine has no effects at all, not even analgesic.

We’re starting to get a bit on the bad side of the site rules now so I wouldn’t be surprised if a mod puts a stop to this thread at some point in the near future. It’s just that I stand by PEA having a massively perceptible effect, having taken it at least weekly (usually around five days with 2-4 redoses a day) with a couple of breaks lasting a few months each.

https://erowid.org/experiences/subs/exp_Phenethylamine.shtml




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[*] posted on 2-5-2018 at 01:26


Quote: Originally posted by LearnedAmateur  
It’s one of those hit and miss compounds, for the lucky some like myself it works well at the doses I listed and is quite intense at the peak. You can find instances of people getting strong stimulant effects from PEA; whilst I do look up to Shulgin, I don’t agree with the statement that it is ‘without activity in man’ - it’s all well and good sharing his particular experiences but what happens to one person may not happen to another.* We also don’t know what personal circumstances there were surrounding his trials, like I said you need a near empty stomach to experience any effects (morning is preferable, at least 3-5 hours since the last meal) otherwise the absorption is too slow. Oral dosing is so predictable for me that I could comfortably measure out my starting dose despite not having taken it for a few months now, and be happy with the level of effects I feel, but I wouldn’t attempt this with intranasal or IV administration.

* Take codeine for instance, which a lot of people take to get high but many people lack a good amount of CYP2D6 enzymes required for adequate metabolism to morphine, like myself, so to me codeine has no effects at all, not even analgesic.

We’re starting to get a bit on the bad side of the site rules now so I wouldn’t be surprised if a mod puts a stop to this thread at some point in the near future. It’s just that I stand by PEA having a massively perceptible effect, having taken it at least weekly (usually around five days with 2-4 redoses a day) with a couple of breaks lasting a few months each.

https://erowid.org/experiences/subs/exp_Phenethylamine.shtml


I was not attempting to claim that you were incorrect, simply that my experience has matched shulgin's.

I once read that the phenethylamine in chocolate caused some type of brief euphoria or had antidepressant effect, and decided to experiment, with chocolate as well as a fairly pure form of phenethtlamine. Maybe something happened, but nothing beyond a +/-.

You are right though, we should probably agree to disagree, as my experience and information says one thing, and yours says another.

When shulgin says "not active in man" he means it is not "psychoactive", not that it is not pharmacologically active.

But again, I guess we would have to agree to disagree.

[Edited on 2-5-2018 by PhenethylamineMachine]
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[*] posted on 22-7-2018 at 18:51


Tinnitus has no defined treatment so far, and the disease is curently associated with several stemming neurological regional and neurotransmitter imbalances.
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JJay
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[*] posted on 22-7-2018 at 19:38


Not to harsh anyone's buzz, but it's not clear from the description whether the drug caused his tinnitus. In general, tinnitus is regarded as a very bad side effect not only because people don't like it but because it is a fairly specific (though unselective) indicator of neurotoxicity. Doctors don't prescribe drugs that might cause tinnitus without a very good reason.



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