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The Wiz!Nic absorption with snus
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The Wiz!
Seems like we just lost and loster.....the report doesn't say how long the portions were left in. I assume it was based on 30 minutes/portion usage, but I leave a 02 in for at least an hour, normally 2.
As do I. By keeping the portion in for well over an hour I know I've gotten whatever it has to offer.
Waste not, want not. That's wha......Hey, you're s'posed to be washing the dog....
Big post warning !
That's the sort of thing I'm trying to get a handle on too.
Interesting that GetSnus say you get all the nicotine in 1/2 an hour,
presumably meaning 'all the nicotine that is going to be adsorbed, happens in 1/2 hour' ?.
Browsed through their site, can't see that specific quote, can you remember the link?
Anyway, your calculations are justified as far as I can see, I guess the comparison with ciggies
depends on how many snus per day are taken, presumably even hardcore snus-ers (is that a word?)
don't put a fresh on in every half hour.
Are you hardcore OTD & TV ?
From the Swedish match link:
i.e. for snus: of the total available 0.85/100*16000 = 136 mg nicotine, only 25 mg was taken up,
(that's only 18%, not 37% so there's already a discrepancy, but maybe it's a greater %age for stronger snus ?),
& for ciggies: of the total 18 to 36 mg nic available, say 27 mg so most (90%+) of it must have been taken up.
The SwedishMatch document shows a graph of nic. in blood for a snus users (vs 2mg gum users), over a 12 hour period,
it reaches a peak of 30ng/ml equaling only 0.135 mg nic. in your whole 4.5 litres of blood (at that instant in time).
Which begs the question where is the rest of the nicotine holding up, in the gum tissue ?
(or lung tissue for ciggies).
You're right TV, it doesn't say how often snus is popped,
but assuming it was the same as the the quoted paragraph above &
combining a similar graph comparing plasma nic levels in ciggies vs 2mg gum users
(Plasma nicotine levels after cigarette smoking and chewing nicotine gum.)
gives the following graph:
The 2mg gum lines (pink & light-blue) are sort of similar (i.e. results may be comparable),
but the snus & ciggy lines (dark-blue & yellow) are more similar to each other than seems reasonable.
If say you used was one snus (of the 12mg per portion strength) every hour, then input rate is
4.5 mg per hour, delivered (mostly) over the first 30 minutes.
I think Mister found a link suggesting that practically all the nicotine from ciggie smoke is taken up,
we both felt that sounded a bit odd, especially since you blow out a lot of the smoke.
But say smoking was 50% efficient on the 1 to 2 mg nicotine you get per ciggie once an hour
(i.e. 80 to 90% of the 10 mg of nic. in a ciggie is apparently combusted, according to typical sources),
so say half of 1.5 mg nic. per hour, but delivered in 3 minutes.
So if it's a only question of simple maths, how does that compare given the 2 hour half life ?,
Could be as below :
Ciggies input = 1.5mg in/hr in a 3min spike
Snus input = 4.5mg/hr in a slower spike over 1/2 hr,
both with 2 hours half life (?)
Equation of half-life (exponential decay) is :
Intact nicotine at time t = nicotine at 'time zero' x 0.5 to the power ( t / t-half ).
i.e. for a single nic. spike at time zero :
nic. at t hours = Initial nic. x 0.5 to power ( t / 2 )
Combining these input and removal rates you could make a graph....
I'm trying this & although an Excel sheet is easy to knock up, the maths shows that
2 hours is vastly too long a halflife to stop significant continuous nic. accumulation,
especially with the snus.
hmmmm, gonna have to think about this a bit more to get a handle on it...
Maybe it's a gross over simplification to say 'half life in the body', perhaps it's one decay
rate in blood plasma, another rate in gum or lung tissue and another rate for 'use by brain receptors'.
And there's the 'reserviour' of nicotine in the tissue(s) itself to consider.
Certainly it's got to be used up at a quicker rate than "50% over 2 hours",
else you'd be swimming in nicotine after 16 hours with snus, less so for ciggies.
e.g. over 16 hours with different 'half-lifes' (120, 60 and 30 mins),
'mg nicotine in the body somewhere' :
Whichever way you look at that the steady-state nicotine level 'in the body somewhere'
for snus should be higher than for ciggies !
Maybe an explanation is that half life in gum tissue is significantly lower than in plasma.
.
.
That's the sort of thing I'm trying to get a handle on too.
Interesting that GetSnus say you get all the nicotine in 1/2 an hour,
presumably meaning 'all the nicotine that is going to be adsorbed, happens in 1/2 hour' ?.
Browsed through their site, can't see that specific quote, can you remember the link?
Anyway, your calculations are justified as far as I can see, I guess the comparison with ciggies
depends on how many snus per day are taken, presumably even hardcore snus-ers (is that a word?)
don't put a fresh on in every half hour.
Are you hardcore OTD & TV ?
From the Swedish match link:
i.e. for snus: of the total available 0.85/100*16000 = 136 mg nicotine, only 25 mg was taken up,
(that's only 18%, not 37% so there's already a discrepancy, but maybe it's a greater %age for stronger snus ?),
& for ciggies: of the total 18 to 36 mg nic available, say 27 mg so most (90%+) of it must have been taken up.
The SwedishMatch document shows a graph of nic. in blood for a snus users (vs 2mg gum users), over a 12 hour period,
it reaches a peak of 30ng/ml equaling only 0.135 mg nic. in your whole 4.5 litres of blood (at that instant in time).
Which begs the question where is the rest of the nicotine holding up, in the gum tissue ?
(or lung tissue for ciggies).
You're right TV, it doesn't say how often snus is popped,
but assuming it was the same as the the quoted paragraph above &
combining a similar graph comparing plasma nic levels in ciggies vs 2mg gum users
(Plasma nicotine levels after cigarette smoking and chewing nicotine gum.)
gives the following graph:
The 2mg gum lines (pink & light-blue) are sort of similar (i.e. results may be comparable),
but the snus & ciggy lines (dark-blue & yellow) are more similar to each other than seems reasonable.
If say you used was one snus (of the 12mg per portion strength) every hour, then input rate is
4.5 mg per hour, delivered (mostly) over the first 30 minutes.
I think Mister found a link suggesting that practically all the nicotine from ciggie smoke is taken up,
we both felt that sounded a bit odd, especially since you blow out a lot of the smoke.
But say smoking was 50% efficient on the 1 to 2 mg nicotine you get per ciggie once an hour
(i.e. 80 to 90% of the 10 mg of nic. in a ciggie is apparently combusted, according to typical sources),
so say half of 1.5 mg nic. per hour, but delivered in 3 minutes.
So if it's a only question of simple maths, how does that compare given the 2 hour half life ?,
Could be as below :
Ciggies input = 1.5mg in/hr in a 3min spike
Snus input = 4.5mg/hr in a slower spike over 1/2 hr,
both with 2 hours half life (?)
Equation of half-life (exponential decay) is :
Intact nicotine at time t = nicotine at 'time zero' x 0.5 to the power ( t / t-half ).
i.e. for a single nic. spike at time zero :
nic. at t hours = Initial nic. x 0.5 to power ( t / 2 )
Combining these input and removal rates you could make a graph....
I'm trying this & although an Excel sheet is easy to knock up, the maths shows that
2 hours is vastly too long a halflife to stop significant continuous nic. accumulation,
especially with the snus.
hmmmm, gonna have to think about this a bit more to get a handle on it...
Maybe it's a gross over simplification to say 'half life in the body', perhaps it's one decay
rate in blood plasma, another rate in gum or lung tissue and another rate for 'use by brain receptors'.
And there's the 'reserviour' of nicotine in the tissue(s) itself to consider.
Certainly it's got to be used up at a quicker rate than "50% over 2 hours",
else you'd be swimming in nicotine after 16 hours with snus, less so for ciggies.
e.g. over 16 hours with different 'half-lifes' (120, 60 and 30 mins),
'mg nicotine in the body somewhere' :
Whichever way you look at that the steady-state nicotine level 'in the body somewhere'
for snus should be higher than for ciggies !
Maybe an explanation is that half life in gum tissue is significantly lower than in plasma.
.
.
I read those same reports and studies exo.
I count on you and DVap and Vaporer and Madame to make sense of them as they usually leave me scratchin' the bald spot and wondering what did I just read!
The frequency of a fresh snus portion would seem to have been made clear in that report. As for me, I don't think I would qualify as a "hardcore" snuser.
I still generally use 4 to 6 portions in a day. Regardless of strength I usually keep them in for 1 to 1.5 hours.
Usually 8mg portions. 4mg mini's occasionally, stronger ones at 9mg or 11mg perhaps once a day if at all.
But this time I just made it worse
Now that makes a lot more sense, 4 in 16 hours rather than 1 an hour,
your personal graph then (with 37% absorption of 8 mg portions) & 2 hour half-life is :
Much closer to 1 per hour ciggies...
.
After reading exogenesis post I agree with you TV. Just as soon as I think I understand it, I discover a whole lot of info to the contrary.
exogenesis
Here is what I read:
Here is the link. How to Snus - GetSnus.com
I may have taken their remark out of context but that is how I interpreted it. I do agree with TV and OTD in that from now on I will wait at least one hour between portions.
Where's our nicotine wikipedia when we need it. There is tons of data out there. Someone needs to compile and come up with a condenced acurate version of "Everything you ever wanted to know about tobacco".
I'll address this to you both. I have had a couple of times that a General White Wintergreen has developed a tear in the portion bag. I haven't had this with the others. That's one reason why I don't leave them in that long and abuse them by constantly kneeding them. What say you?
Yup, I found this link: ScienceDirect - Toxicology Letters : Respiratory retention of nicotine and urinary excretion of nicotine and its five major metabolites in adult male smokers. It says that 98% of nicotine was absorbed. It is a subscription site and I didn't pay to read the article details. I found a few more pages saying 98% but they were unsubstantiated.
98% seems surprisingly high but I don't think we can immediately dismiss it. The cigarette companies have been improving the cigarette for a long time.
But I subsequently realized that this number is not especially important to our understanding as vapers. What we'd most like to know is:
1) How much nicotine does a smoker absorb from A cigarettes of type B?
2) How much nicotine does a vaper absorb from C units of strength D liquid?
There may be other factors affecting (2) but I think that you (exogenesis) have eliminated the most likely ones, i.e. atomizer temperature and base liquid type (PG vs. VG.)
We'll also be curious about where the rest of the nicotine gets lost along the way when vaping. But I think that where the rest of the nicotine gets lost for smokers is of little direct interest.
To understand how much nicotine is absorbed by a smoker we either need studies which measure this directly or we need studies which show how much nicotine is lost during smoking. Both figures turn out to be almost impossible to get.
A lot of nicotine is destroyed in the process of burning a cigarette. A bit under 90% according to various figures.
But cigarettes are not labelled according to how much nicotine they contain. They are labelled according to a standardized ISO test which appears to be intended to measure the amount of nicotine the cigarette delivers to the smoker.
I learned at one point that the ISO measurement is pretty much crap. (Copy of that post inserted at the end of this post.)
The post at The influence of cigarette consumption and smoking... [J Oral Pathol Med. 1997] - PubMed result was the most useful to me in trying to understand the relationship between the ISO measurement and the actual nicotine absorbed by smokers. The summary at that link doesn't explicitly show the arithmetic required to support its conclusions (e.g. "These results indicate that the actual uptake of nicotine by smokers could not be estimated from the smoking machine yields") but it does include enough specific data for us to do the arithmetic.
For example, the referenced first study's group 2 smoked an average of 17.9 cigarettes per day at an average ISO nicotine rating of 1.05, for a total of 17.9 * 1.05 = 18.8 mg of nicotine supposedly delivered per day. But the amount of nicotine metabolites excreted was 24.4mg per day! So this particular group was absorbing 130% of the delivered nicotine. Yeah, right. Other groups also come out to plainly wrong numbers. It is clear that the ISO numbers, which are the only thing available to us about a particular cigarette's nicotine content, are wrong.
Although we end up not knowing what percentage of nicotine is absorbed by cigarette smokers we do end up knowing that:
1) That's probably not a very important thing to know in itself.
2) In general we expect that a smoker can absorb more nicotine from a cigarette than is stated as the nicotine content on the cigarette's package.
3) We don't have a good correlation across brands as to what multiplier to use against the cigarette packaging to determine amount of nicotine which can be absorbed. So we're left guessing a bit in any case.
Here's a copy of the note I originally posted about this:
I've never had one tear open. So far the 02's and Thunder seem to have pretty hardy material.
I can't say for OTD, but I haven't done anything or anyone loose in years
.
Nope to the los a2d. Never have, probably never will
I have read of others complaining specifically about the Gen. Wintergreen tearing. I've been fortunate I guess. Given the amount if time I keep a portion in along with how much I move it around while in use, touch wood, haven't had one tear yet.
EDIT: Morning Twisted!
[FONT="][/FONT][quote="TWISTED VICTOR, post: 949574"]
I can't say for OTD, but I haven't done anything or anyone loose in years.[/quote]
OK...two big posts to follow with my (utterly, totally layman's) hypothesis on how this nic absorption from snus might:
(1) have a longer half-life and
(2) not require the same nicotine intake as you'd need from smoking tobacco.
I ain't qualified for any of this (one look at my organic chem scores and you'll know why I didn't go to medical or pharmacy school), and DVap made a very good point about not simplifying complex systems, but I will use the excuse of youthful recklessness...
I can't say for OTD, but I haven't done anything or anyone loose in years
.[/quote]OK...two big posts to follow with my (utterly, totally layman's) hypothesis on how this nic absorption from snus might:
(1) have a longer half-life and
(2) not require the same nicotine intake as you'd need from smoking tobacco.
I ain't qualified for any of this (one look at my organic chem scores and you'll know why I didn't go to medical or pharmacy school), and DVap made a very good point about not simplifying complex systems, but I will use the excuse of youthful recklessness...
(I hope my Q&A style in this post isn't too cutesy. It's my way of challenging myself to explain and understand things in clearer terms. I welcome feedback.)
Just a note to segue into my hypothesis:
Half-life isn't a function of ‘break-down’ in blood plasma -- drugs don't decay in the body like radioactive elements.
A drug's half-life is a function of metabolism of the drug, usually through the liver.
(Some drugs are metabolized elsewhere, such as ibuprofen through the kidneys; there's also metabolism in the lungs and other organs to a much lesser extent -- I don't understand those systems much at all though.)
So half-life is an expression of how long serum levels of a drug are maintained, while your blood's constantly being filtered by the liver. (Uptake into the blood could be slower with snus, it appears. But the idea of a "tissue reservoir" is not one I'm qualified to evaluate.)
But once it's in the bloodstream, that's when the clock starts ticking.
As that nic-laced blood starts pumping through the liver, nicotine is mostly chewed into its metabolites by the cytochrome P450 enzymes*, largely by the CYP2A6 enzyme (but a few others are responsible as well).
(Only 2-35% of nicotine goes unchanged into the urine. The extent of "renal clearance", as it's delicately called, depends on pH and systemic factors that are beyond my understanding.)
Why are you bringing an obscure enzyme name into this?
Because CYP2A6 has the biggest influence on the half-life of nicotine in your bloodstream. (Think of it as the nicotine-fitted blade in the garbage disposal of your liver.) And because a ton of stuff affects CYP2A6 activity: medications, genetics**, even some foods...and certain tobacco constituents.
So some other things in tobacco affect nicotine metabolism? Mmmm, whole alkaloids...
Yeeeeeesssss. This is the kicker: Other alkaloids in tobacco inhibit CYP2A6, according to this study. (I have the ungated full text PDF if anyone wants it.) Anatabine specifically is a stronger inhibitor of 2A6 than nicotine itself (yes, nicotine slows down its own metabolism).
(Caveats as always apply: This is one study, in vitro -- not even a rat study.)
Translation: Other alkaloids, especially anatabine, may work to keep the nicotine in your body for longer by 'slowing' nicotine metabolism. In other words, it leaves you with higher blood levels of nicotine for longer periods of time.
How is this relevant to snus? Get to the point, Madame! My portion is losing flavor!
It looks like smokeless tobacco users get more of certain alkaloids by not burning them (pyrolysis). Including...anatabine.
(That's my interpretation of this abstract.)
The charts that I posted here seem to corroborate this idea: smokeless tobacco (chewing tobacco and snuff) users excreted a higher ratio of anatabine and anabasine relative to nicotine intake.
*Fun fact: nicotine induces CYP1A2, another cytochrome P450 enzyme that metabolizes caffeine. So, chronic nicotine users will metabolize/eliminate caffeine more quickly, and maintain lower blood levels, than non-users. Drink a lot of coffee?
** Really interesting bit: Individuals can vary a lot in how fast they can metabolize nicotine. CYP2A6 metabolism can vary by a factor of 100 or more, and it may be responsible for varying predispositions to smoking.
Nice Excel work, Exo! Really interesting ideas...
Just a note to segue into my hypothesis:
Half-life isn't a function of ‘break-down’ in blood plasma -- drugs don't decay in the body like radioactive elements.
A drug's half-life is a function of metabolism of the drug, usually through the liver.
(Some drugs are metabolized elsewhere, such as ibuprofen through the kidneys; there's also metabolism in the lungs and other organs to a much lesser extent -- I don't understand those systems much at all though.)
So half-life is an expression of how long serum levels of a drug are maintained, while your blood's constantly being filtered by the liver. (Uptake into the blood could be slower with snus, it appears. But the idea of a "tissue reservoir" is not one I'm qualified to evaluate.)
But once it's in the bloodstream, that's when the clock starts ticking.
As that nic-laced blood starts pumping through the liver, nicotine is mostly chewed into its metabolites by the cytochrome P450 enzymes*, largely by the CYP2A6 enzyme (but a few others are responsible as well).
(Only 2-35% of nicotine goes unchanged into the urine. The extent of "renal clearance", as it's delicately called, depends on pH and systemic factors that are beyond my understanding.)
Why are you bringing an obscure enzyme name into this?
Because CYP2A6 has the biggest influence on the half-life of nicotine in your bloodstream. (Think of it as the nicotine-fitted blade in the garbage disposal of your liver.) And because a ton of stuff affects CYP2A6 activity: medications, genetics**, even some foods...and certain tobacco constituents.
So some other things in tobacco affect nicotine metabolism? Mmmm, whole alkaloids...
Yeeeeeesssss. This is the kicker: Other alkaloids in tobacco inhibit CYP2A6, according to this study. (I have the ungated full text PDF if anyone wants it.) Anatabine specifically is a stronger inhibitor of 2A6 than nicotine itself (yes, nicotine slows down its own metabolism).
(Caveats as always apply: This is one study, in vitro -- not even a rat study.)
Translation: Other alkaloids, especially anatabine, may work to keep the nicotine in your body for longer by 'slowing' nicotine metabolism. In other words, it leaves you with higher blood levels of nicotine for longer periods of time.
How is this relevant to snus? Get to the point, Madame! My portion is losing flavor!
It looks like smokeless tobacco users get more of certain alkaloids by not burning them (pyrolysis). Including...anatabine.
(That's my interpretation of this abstract.)
(Note: this does not cover snus. I do not know how alkaloid content might change given snus processing.)
The charts that I posted here seem to corroborate this idea: smokeless tobacco (chewing tobacco and snuff) users excreted a higher ratio of anatabine and anabasine relative to nicotine intake.
*Fun fact: nicotine induces CYP1A2, another cytochrome P450 enzyme that metabolizes caffeine. So, chronic nicotine users will metabolize/eliminate caffeine more quickly, and maintain lower blood levels, than non-users. Drink a lot of coffee?
** Really interesting bit: Individuals can vary a lot in how fast they can metabolize nicotine. CYP2A6 metabolism can vary by a factor of 100 or more, and it may be responsible for varying predispositions to smoking.
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OK...two big posts to follow with my (utterly, totally layman's) hypothesis on how this nic absorption from snus might:
(1) have a longer half-life and
(2) not require the same nicotine intake as you'd need from smoking tobacco.
I ain't qualified for any of this (one look at my organic chem scores and you'll know why I didn't go to medical or pharmacy school), and DVap made a very good point about not simplifying complex systems, but I will use the excuse of youthful recklessness...
Well, at least I can honestly say I understand what you just said.....and, boy, what a relief........can somebody open a window
?
The upshot:
Supposing this is all true...
A smokeless tobacco user consumes less nicotine but takes in relatively more anatabine.
Anatabine slows down the metabolism of nicotine (not with the first dose – it takes time for enzyme inhibition to build up).
This leads to a longer half-life in the bloodstream, longer “satisfaction”, slower elimination of nic.
Concluding thoughts:
(1) Nicotine obtained from snuff and (possibly) snus might have a longer half-life in the blood than nicotine obtained from smoking because of certain metabolic alterations by other alkaloids.
(2) This is just one hypothesis of how a change in nicotine half-life could be observable when you switch from cigarettes to smokeless tobacco.
(3) This s*** is really, really complicated.
(4) Following #3, if anyone thinks they can replicate tobacco’s effect without some kind of tobacco, I am not buying it.
(5) Did I mention this is complicated?
I need a beer.
Supposing this is all true...
A smokeless tobacco user consumes less nicotine but takes in relatively more anatabine.
Anatabine slows down the metabolism of nicotine (not with the first dose – it takes time for enzyme inhibition to build up).
This leads to a longer half-life in the bloodstream, longer “satisfaction”, slower elimination of nic.
Concluding thoughts:
(1) Nicotine obtained from snuff and (possibly) snus might have a longer half-life in the blood than nicotine obtained from smoking because of certain metabolic alterations by other alkaloids.
(2) This is just one hypothesis of how a change in nicotine half-life could be observable when you switch from cigarettes to smokeless tobacco.
(3) This s*** is really, really complicated.
(4) Following #3, if anyone thinks they can replicate tobacco’s effect without some kind of tobacco, I am not buying it.
(5) Did I mention this is complicated?
I need a beer.
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And you've earned it!
Thanks for putting it into simpler terms for TV. Oh, and me as well
I thought this statement for the report was interesting:
"Inhibition of the CYP2A6 enzyme to slow nicotine metabolism is a promising approach to increase nicotine availability and potentially reduce harm from tobacco smoking."
So, apparently, we've got this going on, also. Yeah, "(3) This s*** is really, really complicated." You said it, Madame
.
"Inhibition of the CYP2A6 enzyme to slow nicotine metabolism is a promising approach to increase nicotine availability and potentially reduce harm from tobacco smoking."
So, apparently, we've got this going on, also. Yeah, "(3) This s*** is really, really complicated." You said it, Madame
.- Status
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