Didn't you originally want to use snus instead of a pharmaceutical antidepressant?
- Status
Didn't you originally want to use snus instead of a pharmaceutical antidepressant?
God no. I was looking into it as a means to suppress the cravings I get for cigarettes I get while depressed. When I'm in a particularly low mood I get cigarette (not nicotine) cravings. So I figured snus might be a way of sating these.
I'm posting this for another member. From tceight:
information for "what are we missing" thread
greetings all. A long time lurker, and vaping for a couple months. I've been following the 'what are we missing' , 'beta carbolines' and 'WTA' associated threads.
Followers of these threads may be interested in these articles I found, and if so could you repost in the appropriate thread as I am unable to as a new poster.
Science News, may 7 1994
".....When pressing the lever delivered only saltwater, the animals gave themselves about 8 doses a day. But when it delivered 8 micrograms of acetaldehyde per kilogram of body weight ([mu]g/kg) -- the rat equivalent of what a person could receive from smoking one cigarette -- the animals upped their daily intake to some 240 doses. When offered nicotine, the rats gave themselves 90 doses a day. However, when given the choice of a cigarette's worth of nicotine and acetaldehyde, the animals self-administered 400 doses a day."
and this one from Neuropsychopharmacol, 2007
"This review evaluates the presumed contribution of acetaldehyde to tobacco smoke addiction. In rodents, acetaldehyde induces reinforcing effects, and acts in concert with nicotine. Harman and salsolinol, condensation products of acetaldehyde and biogenic amines, may be responsible for the observed reinforcing effect of acetaldehyde. Harman and salsolinol inhibit monoamine oxidase (MAO), and some MAO-inhibitors are known to increase nicotine self-administration and maintain behavioural sensitization to nicotine. Harman is formed in cigarette smoke, and blood harman levels appear to be 2-10 times higher compared to non-smokers. Since harman readily passes the blood-brain barrier and has sufficient MAO-inhibiting potency, it may contribute to the lower MAO-activity observed in the brain of smokers. In contrast, the minor amounts of salsolinol that can be formed in vivo most likely do not contribute to tobacco addiction. Thus, acetaldehyde may increase the addictive potential of tobacco products via the formation of acetaldehyde-biogenic amine adducts in cigarette smoke and/or in vivo, but further research is necessary to substantiate this hypothesis."
This is probably nothing 'new' to the experts out there, but does tend to support the harman alkaloid approach by those experimenting with Passion Flower extracts.
Thanks to all those researching and sharing their results in these areas!
information for "what are we missing" thread
greetings all. A long time lurker, and vaping for a couple months. I've been following the 'what are we missing' , 'beta carbolines' and 'WTA' associated threads.
Followers of these threads may be interested in these articles I found, and if so could you repost in the appropriate thread as I am unable to as a new poster.
Science News, may 7 1994
".....When pressing the lever delivered only saltwater, the animals gave themselves about 8 doses a day. But when it delivered 8 micrograms of acetaldehyde per kilogram of body weight ([mu]g/kg) -- the rat equivalent of what a person could receive from smoking one cigarette -- the animals upped their daily intake to some 240 doses. When offered nicotine, the rats gave themselves 90 doses a day. However, when given the choice of a cigarette's worth of nicotine and acetaldehyde, the animals self-administered 400 doses a day."
and this one from Neuropsychopharmacol, 2007
"This review evaluates the presumed contribution of acetaldehyde to tobacco smoke addiction. In rodents, acetaldehyde induces reinforcing effects, and acts in concert with nicotine. Harman and salsolinol, condensation products of acetaldehyde and biogenic amines, may be responsible for the observed reinforcing effect of acetaldehyde. Harman and salsolinol inhibit monoamine oxidase (MAO), and some MAO-inhibitors are known to increase nicotine self-administration and maintain behavioural sensitization to nicotine. Harman is formed in cigarette smoke, and blood harman levels appear to be 2-10 times higher compared to non-smokers. Since harman readily passes the blood-brain barrier and has sufficient MAO-inhibiting potency, it may contribute to the lower MAO-activity observed in the brain of smokers. In contrast, the minor amounts of salsolinol that can be formed in vivo most likely do not contribute to tobacco addiction. Thus, acetaldehyde may increase the addictive potential of tobacco products via the formation of acetaldehyde-biogenic amine adducts in cigarette smoke and/or in vivo, but further research is necessary to substantiate this hypothesis."
This is probably nothing 'new' to the experts out there, but does tend to support the harman alkaloid approach by those experimenting with Passion Flower extracts.
Thanks to all those researching and sharing their results in these areas!
Thanks to you both. I might have seen the first paper before - can't be sure without looking it up, which I will do later; it's all good info.
I think both angles of approach are interesting both in terms of research (understanding) and potentially practical benefit : whole tobacco extraction and nicotine liquid additions.
Incidentally, I wonder if there is some measure of correlation between those in the 'something missing' camp and being drinkers (regular tipplers or who would smoke most when out for a drink?
~~~
Also of interest :
Acetaldehyde may modulate the interaction of nicotine and stress via increased production of corticosterone (which interestingly also regulates the body's fuel to energy conversion). Effects some of the same receptrs as benzodiazepines such as Valium.
http://www.nature.com/npp/journal/v32/n9/full/1301327a.html
A variety of studies suggests that natural tobacco polysaccharides, including cellulose, are the primary precursors of acetaldehyde in MS smoke rather than mono- and disaccharides (sugars) used as additives.
The same paper also concludes: MS [main-stream] smoke acetaldehyde deposits primarily in the upper respiratory tract, including the mouth, of the smoker. Acetaldehyde is rapidly metabolized by aldehyde dehydrogenase in the blood and elsewhere in the body, including at the blood−brain barrier. Tobacco sugar-derived MS smoke acetaldehyde from commercial cigarettes is unlikely to result in direct central nervous system effects on the smoker.
The sudy is from 2002 though.
http://pubs.acs.org/doi/abs/10.1021/tx020069f
As the first product formed during the body's breakdown of alcohol, acetaldehyde may be responsible for the addictive properties leading to alcohol addiction.
Acetaldehyde is somewhat carcinogenic. Cysteine (a sulphur containing amino acid) and vitamin C offer some protection. Levels from smoking should be relatively very tiny compared to those from drinking.
Indeed : Sugars or their derivatives produce numerous substances upon heating. One of these isacetaldehyde, which enhances the addictiveness of nicotine when injected into experimental animals, probably by inhibiting monoamine oxidase (MAO) in the brain.Smokers have decreased levels of MAO in the brain. However, there is no proof that acetaldehyde in the smoke contributes significantly to blood levels of acetaldehyde. On the other hand, acetaldehyde generates in the smoke the compounds harman and norharman which may also inhibit MAO.
http://webcache.googleusercontent.c...moking+acetaldehyde+harman&cd=5&hl=en&ct=clnk
Hence the potential for e-liquids to employ MAO inhibitors without any need for acetaldehyde as a precursor (via the pyrolysis of sugars). Some MAOIs do exist, AFAIK, in the tobacco leaf, aside from extra formed via acetaldehyde.
Harman and norharman (beta-carbolines) are, however, are themselves often listed as toxins, being heterocyclic amines. Though only a handful of the 4000 toxins in tobacco smoke.
Further, I noticed that Valerian root is an allowed tobacco additive in Germany.
http://webcache.googleusercontent.c...moking+acetaldehyde+harman&cd=5&hl=en&ct=clnk
Also of note:
* Swedish Match has far lower TSNA levels than Copenhagan.
* Passiflora incarnata is a central nervous system depressant. Its flavonoid constituents have sedative properties and can induce sleep. Do not drive or operate potentially dangerous machinery when taking this herb.
Do not take Passiflora incarnata with other central nervous system depressants, such as benzodiazepines, barbiturates, narcotics, antidepressants or alcohol, because the combination can cause serious side effects.
The alkaloid components in Passiflora incarnata include the monoamine oxidase inhibitors (MAO-inhibitors) harmaline, harmine and harman. MAO-inhibitors are prescribed for the treatment of depression. Do not take Passiflora incarnata with other antidepressant MAO-inhibitors as it may enhance the effects of those drugs.
Do not take Passiflora incarnata if you are using two other classes of antidepressants, tricyclic antidepressants and serotonin reuptake inhibitors, because the combination may cause excessive sedation or low blood pressure.
Read more: http://www.livestrong.com/article/30610-side-effects-passiflora-incarnata/#ixzz0vOTb6uFV
Obviously, vaping a tiny amount presents much less risk than when using the herb orally but do take care to note any drowsiness. If on any medications, experimenting is best avoided.
Last edited:
Hi Kin,
I can finally post here. see bolded red in response to your comment about drinking.
I for one, am not a drinker at all. I enjoy it once in a while socially, but the after effects aren't worth it. I get hungover from only a few drinks, and my mood is depressed for days afterwards.
This is copy pasted from my posts in the 'new members' section, in addendum to the previous post.
"Some research, implies that the acetaldehyde is made into Harman when burned in the cigarette, (which the E-cig would not do), so some people have added the Harman Alkoloids to their E-Juice.
But this study injected the acetaldehyde directly into the bloodstream, indicating that maybe adding it to E-juice would be effective.
I'm one of those people that cannot be satisfied by nicotine alone. I find I vape like mad, sometimes the desire fades, but most often I just get driven to the point where I just need an analogue, and within a half a cigarette, I feel 'fine' again. Vaping has not cut back my tobacco consumption significantly, and higher nic does nothing but make me feel even MORE jittery, and needing a cigarette. I'm generally better off with very low, or NO nic E-juice.
another quote in the article is confirming of this synergistic effect of acetaldehyde with alcohol, again no 'burning' is required.
"Any substance that delivers low levels of acetaldehyde -- below about 30 or 40 [mu]g/kg of body weight -- should be reinforcing," his data indicate. Indeed, as the first product formed during the body's breakdown of alcohol, acetaldehyde may be responsible for the addictive properties leading to alcoholism, he says. DeNoble's report even raises the possibility that acetaldehyde may explain the often observed link between smoking and drinking, adds Herbert D. Kleber of the Center on Addiction and Substance Abuse at Columbia University. "People who try to give up smoking find it hardest when they're drinking," he notes.
This research was done by Phillip Morriss, and they did not want what they found released.
"We were permitted to give talks [outside the company] on nicotine but never on acetaldehyde," DeNoble testified.
By late 1983, he learned that even the lab's reports on nicotine's potential addictiveness proved a threat because of litigation facing Philip Morris. In April -- without warning -- supervisors gave DeNoble a day to shut down his program. Told that the company had no work for researchers of their stature, DeNoble's team were encouraged to find work elsewhere, which they did.
But confidentiality agreements that the researchers signed forbade them from ever discussing their studies at the Richmond lab. The subcommittee got a waiver from Philip Morris so that DeNoble and a coworker could testify."
the rest of the article is here
findarticles.com/p/articles/mi_m1200/is_n19_v145/ai_15264835/
I can finally post here. see bolded red in response to your comment about drinking.
I for one, am not a drinker at all. I enjoy it once in a while socially, but the after effects aren't worth it. I get hungover from only a few drinks, and my mood is depressed for days afterwards.
This is copy pasted from my posts in the 'new members' section, in addendum to the previous post.
"Some research, implies that the acetaldehyde is made into Harman when burned in the cigarette, (which the E-cig would not do), so some people have added the Harman Alkoloids to their E-Juice.
But this study injected the acetaldehyde directly into the bloodstream, indicating that maybe adding it to E-juice would be effective.
I'm one of those people that cannot be satisfied by nicotine alone. I find I vape like mad, sometimes the desire fades, but most often I just get driven to the point where I just need an analogue, and within a half a cigarette, I feel 'fine' again. Vaping has not cut back my tobacco consumption significantly, and higher nic does nothing but make me feel even MORE jittery, and needing a cigarette. I'm generally better off with very low, or NO nic E-juice.
another quote in the article is confirming of this synergistic effect of acetaldehyde with alcohol, again no 'burning' is required.
"Any substance that delivers low levels of acetaldehyde -- below about 30 or 40 [mu]g/kg of body weight -- should be reinforcing," his data indicate. Indeed, as the first product formed during the body's breakdown of alcohol, acetaldehyde may be responsible for the addictive properties leading to alcoholism, he says. DeNoble's report even raises the possibility that acetaldehyde may explain the often observed link between smoking and drinking, adds Herbert D. Kleber of the Center on Addiction and Substance Abuse at Columbia University. "People who try to give up smoking find it hardest when they're drinking," he notes.
This research was done by Phillip Morriss, and they did not want what they found released.
"We were permitted to give talks [outside the company] on nicotine but never on acetaldehyde," DeNoble testified.
By late 1983, he learned that even the lab's reports on nicotine's potential addictiveness proved a threat because of litigation facing Philip Morris. In April -- without warning -- supervisors gave DeNoble a day to shut down his program. Told that the company had no work for researchers of their stature, DeNoble's team were encouraged to find work elsewhere, which they did.
But confidentiality agreements that the researchers signed forbade them from ever discussing their studies at the Richmond lab. The subcommittee got a waiver from Philip Morris so that DeNoble and a coworker could testify."
the rest of the article is here
findarticles.com/p/articles/mi_m1200/is_n19_v145/ai_15264835/
From Wiki,
"Acetaldehyde is a probable carcinogen in humans.... "There is sufficient evidence for the carcinogenicity of acetaldehyde (the major metabolite of ethanol) in experimental animals."
but does not indicate at what dosages those effects were observed.
and as
"Acetaldehyde occurs naturally in coffee, bread, and ripe fruit, and is produced by plants as part of their normal metabolism"
and it is also produced by oxidation of ethanol, consumed copiously by so many around the world for centuries, the risks must be taken context.
The simplest adjunct might be to try cutting the juice with 200 proof alcohol, which I have not tried. Has anyone else noticed any difference in satiation from ethanol in their juice?
"Acetaldehyde is a probable carcinogen in humans.... "There is sufficient evidence for the carcinogenicity of acetaldehyde (the major metabolite of ethanol) in experimental animals."
but does not indicate at what dosages those effects were observed.
and as
"Acetaldehyde occurs naturally in coffee, bread, and ripe fruit, and is produced by plants as part of their normal metabolism"
and it is also produced by oxidation of ethanol, consumed copiously by so many around the world for centuries, the risks must be taken context.
The simplest adjunct might be to try cutting the juice with 200 proof alcohol, which I have not tried. Has anyone else noticed any difference in satiation from ethanol in their juice?
And Nicotine is really safe? lol
The difference between a medicine and a poison is of course dosage.
Thanks for those links, much fodder for the afternoon.
hi tceight,
i do feel uncomfortable talking about things which are not completely safe (as though there were such things) - but of course the point is to find a (much) safer alternative to smoking for those who would otherwise continue to smoke. And it is clear than a sizable proportion of people do not smoke for nicotine alone, or nicotine at all.
i do feel uncomfortable talking about things which are not completely safe (as though there were such things) - but of course the point is to find a (much) safer alternative to smoking for those who would otherwise continue to smoke. And it is clear than a sizable proportion of people do not smoke for nicotine alone, or nicotine at all.
Technically i believe acetaldehyde can exacerbate certain carcinogens rather than is one itself (?) - bad enough - but the amounts in smoking are small compared to drinking (that combo is known to be high risk for certain cancers).
The point is though that we don't need to think acetaldehyde, just think MAOIs themselves as the 'benefits' of acetaldehyde come from its conversion to beta carbolines.
Inerestingly, as a fairly regular drinker, I find alcohol can not substitute for the 'something missing'. Vaping and drinking over the same period doesn't 'work' (at least for me). Perhaps acetaldehyde itself is not the key, and useful only to the extent that it forms MAOIs before inhalation (or in the mouth/lung rather than digestive system). I havent tried PF with vaping yet (either in e-liquid or as a tea) but others report that that does work.
The acetaldehyde - alcohol addiction link might be overplayed; I suspect it is more to do with feeling a need to get sloshed to socialise / relax than a biochemically based addiction as such (if you see what i mean.
~~~
I nearly always drink decaf coffee these days and actually prefer it; still feel a feint 'addiction' to the stuff though, quite to what i'm not sure, perhaps just the taste (via association with perk-up maybe) or its flavonoids biochemically or potassium, or who knows. Anyway, I can understand your point about zero nic liquids.
Last edited:
Kin, I had started down the MAOI route first, but found it lacking in efficacy (for me anyway), which led me to the potential of the precursor aldehyde as possibly creating other metabolites than just harman.
along the WTA route,
as I see it, we are looking for a 'safe' process of getting all the alkaloids, and somehow separating them from all the sugars, and the fats, as well as other contaminants such as tannins, ending up with a vapable product in PG, PEG, or VG, and at no time concentrating the nicotine to levels above 50mg/ml.
Does that sum up the task at hand?
Solvent Predicted Solubility (M) of Nicotine in 'safe' solvents.
ethyl acetate 10.83
methanol 3.6
ethanol 3.58
so ethyl acetate seems great as a potential non polar for extracting nicotine.
Does anyone have the SMILES for any of the other alkaloids found in tobacco?
along the WTA route,
as I see it, we are looking for a 'safe' process of getting all the alkaloids, and somehow separating them from all the sugars, and the fats, as well as other contaminants such as tannins, ending up with a vapable product in PG, PEG, or VG, and at no time concentrating the nicotine to levels above 50mg/ml.
Does that sum up the task at hand?
Solvent Predicted Solubility (M) of Nicotine in 'safe' solvents.
ethyl acetate 10.83
methanol 3.6
ethanol 3.58
so ethyl acetate seems great as a potential non polar for extracting nicotine.
Does anyone have the SMILES for any of the other alkaloids found in tobacco?
Anxiety is a beast, and much of what we do consciously or not, is in attempt to slay it by whatever means. Self medicate with alcohol, tobacco, name your poison.
Very interesting. While I wouldn't go near methanol, the ethyl acetate looks promising. It's the solvent used in decaffination of coffee, though I don't know the details of how they get only the caffeine.
One might estimate that the other alkaloids might also dissolve better in ethyl acetate. Is this ester miscible with ethanol? I presume so. -- Yes, just checked.
As it has a low BP (77C), would be a good choice also as a way to concentrate the extract by preferential evaporation of the EA.
A good find !
Last edited:
While methanol is of course very 'toxic', it is found in beer and wine, as well as pot distilled liquors, gin of course being the most renowned. It's also a metabolite of aspartame. Rum and diet coke never sounded so dangerous! Again, it's all about context and concentration.
Intuitively, if EA dissolve all the alkaloids we need preferentially to the other soluble constituents,
then I see a 'simple extraction' consisting of.
1. grinding some tobacco with sodium carbonate to free the nicotine from its salts,
2. a short soak, or even just a 'drip through' with the EA, so it picks up the alkaloids, but not much of the other contaminants.
3. 'assume' a 50% yield of the total nicotine(likely far less, but to be safely conservative).
4. add the correct amount of PG or VG immediately to ensure a concentration of less than 50mg/ml
5. let the EA evaporate, or heat to speed it up.
one could let the EA evaporate first before adding the PG, but then you have concentrated nicotine and associated concerns.
of course, if the fats/sugars/tannins etc are equally soluble, there is no advantage to EA over ethanol or water, and further processing would be required.
so again, if anyone has the SMILES for the constituents of tobacco, then I can determine solubility for those components.
~~~~ Ethyl acetate can be hydrolyzed in acidic or basic conditions to regain acetic acid... so maybe the sodium carbonate is out. It may dissolve the malates and citrates anyway.
Intuitively, if EA dissolve all the alkaloids we need preferentially to the other soluble constituents,
then I see a 'simple extraction' consisting of.
1. grinding some tobacco with sodium carbonate to free the nicotine from its salts,
2. a short soak, or even just a 'drip through' with the EA, so it picks up the alkaloids, but not much of the other contaminants.
3. 'assume' a 50% yield of the total nicotine(likely far less, but to be safely conservative).
4. add the correct amount of PG or VG immediately to ensure a concentration of less than 50mg/ml
5. let the EA evaporate, or heat to speed it up.
one could let the EA evaporate first before adding the PG, but then you have concentrated nicotine and associated concerns.
of course, if the fats/sugars/tannins etc are equally soluble, there is no advantage to EA over ethanol or water, and further processing would be required.
so again, if anyone has the SMILES for the constituents of tobacco, then I can determine solubility for those components.
~~~~ Ethyl acetate can be hydrolyzed in acidic or basic conditions to regain acetic acid... so maybe the sodium carbonate is out. It may dissolve the malates and citrates anyway.
Last edited:
solubility for Harmine,
now this is interesting! it's 3 times as soluble in ethanol than nicotine.
This might help to explain why some people find the simple soaks so effective, when the expert opinion/measurements indicate low/no nicotine present.
ethyl acetate17.16
ethanol9.9
still looking good for ethyl acetate.
now this is interesting! it's 3 times as soluble in ethanol than nicotine.
This might help to explain why some people find the simple soaks so effective, when the expert opinion/measurements indicate low/no nicotine present.
ethyl acetate17.16
ethanol9.9
still looking good for ethyl acetate.
A good protocol.
Some research or trials would be required to know if there would be any benefit in a shorter soak.
I think the extraction could be higher than 50%, but as this is all alkaloids and not just nicotine, the end result might need much more dilution (and a lower nic %) than commonly used in nic-only e-liquids. At least that seems to have been found when doing an extraction using snuss; and might apply in the case of 'normal' tobacco. The effect trumps the figures of course; but we still want to know the figures.
Finings might be useful to remove unwanted tanins and proteins as discussed in a sister thread.
The salts should dissolve reasonably well anyway (?); and perhaps unlocked later.
~~~
Later : Even if not all tanins etc are removed and these burn up in the atomiser, this still avoids the bulk of the tobacco material, and the 'burning' is dehydration/sooting rather than combustion as such (sorry late so technical terms escaping me).
Yes, adding VG first would slow the evaporation but avoid high concentrations.
"of course, if the fats/sugars/tannins etc are equally soluble, there is no advantage to EA over ethanol or water, and further processing would be required."
Still the advantages of greater extraction and potential to easily concentrate.
Last edited:
I seemed to miss this post earlier.
Good to see those numbers - seems to confirm what the experience suggested. Although the actual solvents used were I believe mostly VG, the relative solubilities might be similar.
Distillation might be the best way to remove all the unwanteds. They would be left behind by gently heating the solution until approacjing dry and condensing the vapors; this is not tempertaure critical and involves no fractionalisation. It's a bit complicated to do at home, but not too difficult.
bad news, nicotine citrate does not dissolve.
good news, neither does sucrose
good news, isomers of nicotine citrate do dissolve
bad news, so do isomers of sugars.
I can't find the info for malates, and all this is just theoretical solubility predictions anyway.
Agreed, I believe that pyrolysis of various compounds is the greatest evil we are attempting to avoid.
those are advantages to some, I am more interested in efficacy and simplicity than efficiency. Even if the extraction comes out to only 10% yield, tobacco is cheap at twice the price.
If I can find the dipole moments for glycerol and propylene glycol, I will compare them to ethanol.
I've found information on distillation of nicotine to be very limited. It sounds like it should be simple, but there appears to be azeotrope issues (at least with water) and the nicotine oxidizes and decomposes quickly unless this is done in a hydrogen atmosphere.
"Nicotine is slowly volatilized at ordinary temperature, and can be distilled with the vapors of boiling water(steam distillation). Heated by itself, it boils, with decomposition, at about 240° C. (464° F.), but does not decompose in an atmosphere of hydrogen. It begins to distill at a much lower temperature (146° C., or 294.8° F.)"
some of the 'older' methods,
Archiv der Pharm., 1893
Nicotine may be obtained by adding to a concentrated tobacco extract, solution of caustic soda or lime, distilling with steam, extracting the distillate with ether, and carefully evaporating the solvent.
and
Fresenius' Zeitschrift f. Analyt. Chem., 1882
assays tobacco by agitating 20 grammes, in powder form, with alcoholic caustic soda, exhausting the mixture with ether, carefully distilling off the greater part of the solvent, adding diluted caustic soda to the residue, distilling off the nicotine with steam, and titrating each 100 Cc. of the distillate with volumetric sulphuric acid solution, using rosolic acid for indicator.
a simple distillation may get our other alkaloids, but the nicotine seems to be a devious molecule.
Last edited:
- Status
Similar threads
- Locked
- Locked
