• N&PD Moderators: Skorpio

Is alcohol a drug?

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Thanks for all the info.

The reason I posted this in ADD, was because I know you guys know your stuff. There have been some 'advanced' replies, just a basic question. This is the person who I was debating with, he still has his ideas on his website: http://recoveredalcoholic.blogspot.com/search/label/Drug is a Drug
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Someone asked...I was heroin, methadone, benzos, alcohol addict. I am now clean 7 months.
 
It is the official toxicological definition of narcosis.
It's a bitch to find a good reference for this, but I can guarantee you that the original definition of a narcotic was any substance that disrupts neuronal functioning by destabilizing the cell membrane.

Absolutely, completely false. The term "narcotic" was originally coined by Galen something like 1800 years ago. The root, obviously, is "narc" (I've seen it spelled "narke" as well, but I haven't bothered to see which, if either, is actually correct) which means "stupor."

The term narcosis refers to a sedated, stuporous, numbed state. It was applied to opioids originally because that's what they produce.

Whether there's some area of research that uses the same definition you're claiming as the original, I don't know, but I think you may have read a very old explanation of what narcotics do. We already know that these drugs aren't causing their effects through destabilizing the cell membranes- they're binding to various receptors and causing those receptors to do various things.

With the advent of opiates and opioids, these substances with a different MOA were also called narcotics.

No, they were the original narcotics- some poppy preparation was actually included when Galen originally coined the term.

And then at some point, it was decided that narcotics would be the new term for all drugs of abuse that cause anasthesia (Probably American idea with their gallons and miles and what-not...).

Again, not true. The term was applied to all of these drugs that produced a numbed, stuporous state. I'd have to look around, but I'd be surprised if ethanol wasn't described as a narcotic long before our modern anaesthesia was even developed.

You also know that gallons and miles weren't developed in the US, right? They're British in origin


Which is really annoying, since narcosis is still the official name for the phenomenon mentioned previously.

Except that it's not, so it's not annoying. The reason you can't find documentation is because that doesn't seem to be an accepted definition anywhere- and indeed, I can't find evidence that it ever was, even as jargon in some area of research. Yet you can find the definition everyone is repeating here everywhere.


Is that so?
Can you please clarify what chloroform and diethyl ether have in common - judged by MOA - with a modern day anasthetic like propofol or thiopental?

Yeah, they're both NMDA antagonists and diethyl ether at least has some GABAergic activity. Comparing them to propofol and thiopental doesn't make much sense, they're more like nitrous oxide or ketamine in terms of effects.

I respect the fact that no one knows everything and all.
But please don't try to make these kind of bold statements unless you have a certain degree of expertise in this area.

I like how you mildly chastise him for "boldly" making claims, like you're his benevolent grandfather. It's made more hilarious by you asking him to shut up if he doesn't know what he's talking about! LOL You're getting all sorts of things screwed up. You apparently believed that volatile anaesthetics like chloroform didn't bind to receptors!

(a ref for instance, showing that they do: Biochem Pharmacol. 1995 Mar 15;49(6):809-17)

However, I understand why you don't see a place for kerosene in my list.
If you purely look at MOA, then chloroform and ethyl ether should be on the same list as kerosene, acetone, toluene and most other 'solvents of abuse'.
But you are more looking at application; substances that were used as anasthetics can be considered narcotics by your definition, but substances that have exactly the same physiological effects can not.

Kerosene doesn't belong because it's not a chemical, it's a mix of chemicals. The last bit I don't understand at all. Inhaling fumes from kerosene may produce some intoxication, but we're talking about how chemicals interact with receptors, which makes discussing kerosene pointless- individual compounds within it, sure, but a complex mix? No way

That's exactly the big issue when putting labels on classes of chemicals.
'Oh, LSD is a drug of abuse...so it can never be used as a medicine, no way!'
You tell me what makes more sense: Grouping chemicals by MOA or by any other attribute?

I don't see how this developed from what came before it, it doesn't seem relevant at all. No one suggested that because something is a drug of abuse it can't be a medicine. The opposite is obviously true. LSD won't be used medicinally because it's far too long acting and won't make for a good therapy drug. There are definitely psychedelics that would make excellent therapy drugs.

If we're going to group chemicals there are lots of other classes to organize by. Structural relationships is the most obvious. Target receptor makes more sense than a much vaguer "mode of action."

Excuse me from strolling off the topic, but at least this post is 'advanced'...which makes it on-topic again. ;)

That's a huge stretch, it's full of obviously inaccurate information you could have found through Google even.
 
I'm not ashamed to say you are absolutely right about the etymology of narcotics.
I also did some more research on the stuff mentioned previously (before reading your post actually), since I was also wondering if my explanation was correct or not.
I found a textbook reference for the toxicological definition of narcosis HERE.
Turns out that sometimes you can better use Google than PubMed. ;)
As you can see this edition is a publication from 2004, so it was not some ancient misunderstanding about the MOA of narcotics.

Again, not true. The term was applied to all of these drugs that produced a numbed, stuporous state. I'd have to look around, but I'd be surprised if ethanol wasn't described as a narcotic long before our modern anaesthesia was even developed.
I think the truth lies somewhere in the middle here...
If you look at the American legal definition of narcotics, I believe it is limited to all opiates/opioids and cocaine.
But there is possibly also a pharmacological definition, though I wouldn't be surprised if the term 'narcotic' is somewhat outdated, just like antipsychotics are now usually called neuroleptics.

Haha, must say you got me on the Imperial system.
But then again...the Americans were stupid enough to keep it after they kicked the British out.

You apparently believed that volatile anaesthetics like chloroform didn't bind to receptors!
It was never my intention to say that they do not bind to receptors.
I am very aware they bind to receptors, receptors are proteins after all and fi chloroform is widely used for the precipitation of proteins.
I just don't think that the main effect of inhaling solvents is produced by interaction with a receptor.
Of course there will be a few exceptions, but if you try to look at it through the above definition of narcosis, perhaps you'll understand what I mean.
All solvent cause this narcosis, because they are by nature highly soluble in the lipid bilayer.
So I made a list of a few well-known solvent, but if chloroform merely acts by recepter interaction I must say I wasn't aware of that.
But looks to me like it's a combination between narcosis, starting at threshold levels, and receptor activation/inhibition when concentrations are high enough.

we're talking about how chemicals interact with receptors
You (plural) were talking about how chemical interact with receptors.
I, on the other hand, was talking about how chemicals interact with the cell membrane.
Perhaps that's part of the mutual misunderstanding here?

I don't see how this developed from what came before it, it doesn't seem relevant at all.
It was more a general frustration towards the excessive labeling of chemicals (mostly by governmental agencies).
Something is a narcotic or a class XYZ drug.
I think it's bullshit, something is a partial 5HT2C-agonist or an inverse NMDA-agonist.
You should not group chemicals because they all cause your skin to turn blue (for instance), but you could group all chemicals that cause pain relieve because they interact with a subtype of opiate receptor.
Luckily, this change is already in progress in pharmaceutical science, where most drugs are classified by their receptor affinity.
BTW, I wonder what your definition of 'mode of action' is, because my definition of MOA is the whole array of receptors that are influenced by a compound.

Classification of chemicals based on structural relationships is more logical from a physicochemical point of view.
But pharmacologically speaking I think receptor affinities should get more attention than structural relationships. :)
 
I am very aware they bind to receptors, receptors are proteins after all and fi chloroform is widely used for the precipitation of proteins.
I just don't think that the main effect of inhaling solvents is produced by interaction with a receptor.[2]
Of course there will be a few exceptions, but if you try to look at it through the above definition of narcosis [1], perhaps you'll understand what I mean.
All solvent cause this narcosis, because they are by nature highly soluble in the lipid bilayer.
So I made a list of a few well-known solvent, but if chloroform merely acts by recepter interaction I must say I wasn't aware of that.
But looks to me like it's a combination between narcosis, starting at threshold levels, and receptor activation/inhibition when concentrations are high enough.

[1] I need to look a little more into this, and the value of that book (that's not a definition I've seen before, and while it's not uncommon for a single word to have multiple meanings, and between various jargons a single word may have multiple, but closely related definitions.

[2] Maybe I'm wrong. I can honestly say I don't know all that much about how solvent inhalants produce their effects, but I have a hard time believing that their strong ability to dissolve lipids can be relevant at the sorts of concentrations that are achieved through inhalation.
 
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[2] Maybe I'm wrong. I can honestly say I don't know all that much about how solvent inhalants produce their effects, but I have a hard time believing that their strong ability to dissolve lipids can be relevant at the sorts of concentrations that are achieved through inhalation.
Their effect is not achieved by dissolving the lipids, but by disrupting the membrane that consists largely of these lipids. Imagine the membrane as a sheet consisting of little magnetic balls, that bind eachother magnetically. If you start replacing the magnetic balls with plastic balls, the strength of the sheet as a whole will be influenced.

The cell membrane is of course a tiny bit more complicated; this is just a simplification for the sake of clarification (I could give a better explanation if desired, just ask). Now, the cell membrane also contains all kinds of proteins, that form pores to exchange ions between the interior and exterior of a cell. Some proteins also function as a receptor; if a molecule binds on the extracellular part of this protein, the conformation of the whole protein will change, and inside the cell something else will happen to convert the extracellular signal to an intracellular effect. Again, there is much more to it than this short version, but it will suffice to clarify the MOA.

Solvents can influence the above process in a few ways, most importantly:
1) They bind to certain spots on the protein, thereby causing a conformational change or interfering with binding of the 'normal' signalling molecule.
2) They nest inside the cell membrane - just as the plastic balls mentioned above - and thus influence the stability of the membrane. This means that the membrane might not be able to support the receptors (which are large and heavy proteins), so their 'anchor' inside the membane alters and they cannot function properly.
3) They will also change the polarity of the membane. Some messenger molecules do not bind to extracellular receptors, but can diffuse through the membrane and bind intracellulary (to the DNA or an intrecellular receptor, for instance). Solvents function a bit like a soap-molecule: They cover a portion of a messenger molecule, which can make it easier for that molecule to cross the membrane.

Hope this post helps understand the mechanism behind the effects of solvent inhalation instead of making it all-that-much more complicated. :p
 
'Narcosis' defined as the disruption of membrane lipid bilayers in the central nervous system? Ohhhhh, I dunno. That sounds like a really long strech to me.
I'd expect that this leads to a decrease in receptor function, followed by denaturation of proteins intra- and extracellularly, lysis of the cell, necrosis resp. irreversible tissue damage, death. In this order, roughly summarized.
The term 'narcotics', with respect to its historical, judicial and nowadays common day application does not refer to eg. gasoline as a 'narcotic'; that was actually one of the examples declared as a 'class 1 narcotic' in the book that you linked ("The aliphatic hydrocarbon (C5 to C8 )...").

I recommend to read the chapter "Outdated lipid hypotheses of general anaesthetic action" of this Wiki-article: http://en.wikipedia.org/wiki/Theories_of_general_anaesthetic_action
This extremely broadly phrased (and actually uncommon and rather misleading) definition could stem from one of the older theories. The main effect of practically all of what we declare nowadays as being 'a narcotic' stems from receptor-mediated interactions. That's a damn broad definition, too, but at least a correct one.


Edit: I've just read the second-last post #65. Really entertaining but in large parts nonsense. ---> "Their effect is not achieved by dissolving the lipids, but by disrupting the membrane that consists largely of these lipids." WRONG! True on the other hand are the protein-mediated effects listed under 1).
...
And do you really think you need to explain Hammilton how a membrane is build, with all those fancy "little magnetic balls, that bind eachother magnetically"?
 
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The term 'narcotics', with respect to its historical, judicial and nowadays common day application does not refer to eg. gasoline as a 'narcotic'; that was actually one of the examples declared as a 'class 1 narcotic' in the book that you linked ("The aliphatic hydrocarbon (C5 to C8 )...").
Guess you should mail the publisher then! Be sure to include a reference to this thread, so they can correct their mistake in the next edition and give you credit where it's due.

In the meanwhile, perhaps you could also try to reread the last 25 posts. I have never said that the MOA of drugs that are narcotics by legal definition is the same as what are considered narcotics by the toxicological definition. And neither will any page in the book I referenced. It really looks like you mistake shortsightedness with acting intelligent. There must be thousands of terms that have a different definition, depending on the context.

The main effect of practically all of what we declare nowadays as being 'a narcotic' stems from receptor-mediated interactions. That's a damn broad definition, too, but at least a correct one.
True, but none of those narcotics cause narcosis on the cellular level. Are you still not respecting the fact that we're talking different concepts here? My entire post had nothing to do with the MOA of anasthetics, it was entirely devoted to solvents - which cause narcosis on the cellular level. It's rather awkward: You denounce my defintion of narcosis, but you act like you are more familiar with it's MOA at the same time. Please go on educating me, I'll be sure to let the four professors of my department know that all their knowledge on narcosis is a giant heap of bullshit. Finally my chance to clear some office space around here and secure myself an academic position. You don't mind me taking advantage of all your knowledge, do you? You seem to have so much of it...

And do you really think you need to explain Hammilton how a membrane is build, with all those fancy "little magnetic balls, that bind eachother magnetically"?
Oh, you are so right! How dare I give a good explanation when there's a chance the person I'm adressing has the same level of knowledge on the subject as me. Must be so awkward for Hammilton too... I guess you need me to spell it out for you, that it's really professional to take these kind of 'arguments' into a discussion on a scientific level? My whole story must be bogus, since I give a simplified explanation to someone that might not need it.
 
If the effect is purely mediated by receptor action, does that explain the fact that (theoretically-speaking) any volatile gas has a "narcotic" effect given the right gas pressure? At specific pressures, gasses like argon and nitrogen begin to have a "narcotic" effect. Theoretically, any gas can do this. It just so happens that simple hydrocarbons and anaesthetic gasses do this at low pressures and more effeciently.

seep posted a neat chart a few months back about the relative effectiveness of gasses in a ratio to pressure or something, I can`t remember the details. But it had things like helium and even hydrogen at the tail end of the chart, and things like enflurane at the other side. Or something. I think it`s available on Wiki; I`m on my cell and can`t find it quickly.

So again, if the anaesthetic effects of volatile gasses are purely receptor driven, does this still explain how any gas is theoretically narcotic at certain pressures and concentrations? I`m just curious, I don`t profess to be an expert.
 
How could it be any thing else!! Foods are also drugs. Look at the obese society in America.
As others have pointed out it is obvious. Anything you put in your mouth in my opinion is a drug. Damn- I'm going to have another beer and/or have another something or other. My refrigerator is empty! God Damn it!!
 
Back on topic...

You know, some of the most heated, enflamed debates are over semantics. I mean, what it comes down to is that there`s a right answer and there`s a wrong answer, and that can be deduced by picking up a dictionary/encyclopaedia. That pretty much solves the question of the topic. It`s not a matter of opinion.
 
Back on topic...

You know, some of the most heated, enflamed debates are over semantics. I mean, what it comes down to is that there`s a right answer and there`s a wrong answer, and that can be deduced by picking up a dictionary/encyclopaedia. That pretty much solves the question of the topic. It`s not a matter of opinion.

that is what happens when people let language determine reality. It's a very seductive fallacy. The 4th gospel begins, "In the beginning was the word, and the word was with God, and the word was God."
 
If the effect is purely mediated by receptor action, does that explain the fact that (theoretically-speaking) any volatile gas has a "narcotic" effect given the right gas pressure? At specific pressures, gasses like argon and nitrogen begin to have a "narcotic" effect. Theoretically, any gas can do this. It just so happens that simple hydrocarbons and anaesthetic gasses do this at low pressures and more effeciently.

seep posted a neat chart a few months back about the relative effectiveness of gasses in a ratio to pressure or something, I can`t remember the details. But it had things like helium and even hydrogen at the tail end of the chart, and things like enflurane at the other side. Or something. I think it`s available on Wiki; I`m on my cell and can`t find it quickly.

So again, if the anaesthetic effects of volatile gasses are purely receptor driven, does this still explain how any gas is theoretically narcotic at certain pressures and concentrations? I`m just curious, I don`t profess to be an expert.

Yeah, that's actually the only thing that's making me question.


with regard to 3rd_I_blind's response: dissolve wasn't the right word, I apologize, in the late AM hours I'm hardly at my peak, but we are talking about the same thing.
 
Back on topic...

You know, some of the most heated, enflamed debates are over semantics. I mean, what it comes down to is that there`s a right answer and there`s a wrong answer, and that can be deduced by picking up a dictionary/encyclopaedia. That pretty much solves the question of the topic. It`s not a matter of opinion.

truth is a consensus reality (i made that up and i think it sounds good, but maybe i'm just being silly)

but anyway alcohol is a drug- it changes your mood, your heartrate, etc. and that is what drugs do, exert a biological response. most foods have drug like effects its just that the boundary that separates a food from a drug is how much it affects you physiologically compared to how important it is in terms of sustenance. thc is a fat, alcohol is very simlar to sugar (which exerts drug like effects), there must be more that transcend the gap...

check out this shit http://en.wikipedia.org/wiki/Casomorphine
 
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