Latest Health NZ study published

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Kate51

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I have no questions for Dr. Laugeson. He is not the one who has drawn the unsupported conclusion we've been discussing, you are.
Did you look at all at Table 3 Pharmacokinetic properties
It is there, supported, published in black and white, pertinent numbers are in bold print, and done by Dr Laugeson and others, all you have to do is read it like everyone else can.

If you have further questions, please ask someone else, you have disrupted the thread, tried my patience for no reason other than severe myopathy, and I am moving on.
 

paladinx

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Who cares? Maybe its 10, maybe there are more variables. Nothing is totally conclusive. Its just an idea. Some people seem to get more nicotine than others. For me personally, it always felt weaker than cigarettes. yet there are others who get nicotine overdose symptoms go figure.

Again if its really 10 percent, than to me thats not a great thing.
 

rothenbj

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Who cares? Maybe its 10, maybe there are more variables. Nothing is totally conclusive. Its just an idea. Some people seem to get more nicotine than others. For me personally, it always felt weaker than cigarettes. yet there are others who get nicotine overdose symptoms go figure.

Again if its really 10 percent, than to me thats not a great thing.

My thoughts precisely. After finally getting off cigarettes for the last two months after spending seven vaping and intermittently smoking, I was frustrated as heck at not being able to quit where so many before me had no problem. Then I got deeper into this site and found snus and 2 to 4 portions of that a day but me over the top.

I've come to the conclusion that there are three aspects to smoking that make it extremely difficult to quit and I'm not sure now "addictive" the nicotine is, at least in my case. The hand to mouth habit is major and the e cig takes care of that, even as I continue to lower the nic level in what I am vaping. Of course the nic has it's affect, but to me it seems similar to caffeine. Then there are the alkaloids in tobacco which I've had the most trouble avoiding, thus the success of snus in addressing that aspect.

A few portions of snus a day and vaping at this point less than 10mg nic and I'm good to go. I don't need to vape constantly, more if I'm in a place where people are smoking or if I'm having a drink, but certainly not to the number of puffs I took on 2 to 3 packs a day. It's certainly not the center of my universe anymore. Science is science and common sense...... does that exist anymore?
 

Dillinger

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Mister, my sympathies. Don't despair, I hear you. I think your point is simply going over people's heads.

I totally agree with yvilla. Mister's posts make absolute sense.

*This in no way implies that there is an error in the report, just that data is being misinterpreted.*
 

Mister

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... those who read reports and understand them.
They do NOT understand them in this regard. Two numbers have been plucked from the test data, one divided by the other, and the resulting 10% pronounced to support the idea that 10% of the nicotine we vape gets absorbed. But doing arithmetic on those two numbers does not have that meaning.

For those who don't understand the math I presented earlier (which I'm assuming includes all the people insisting I'm wrong, since none of them has argued the math) try looking at this another way: Knowing how much nicotine we absorb is a big deal to a lot of people. It gets asked a lot on the forums. Many people are curious about it for various reasons. If a conclusion about how much of the liquid's nicontine gets absorbed could be made from the study's results, don't you think the authors would have stated that conclusion in the study?
 
How utterly condescending and insulting to the intelligence of those who read reports and understand them. Posters here do not expect that kind of undeserved, ugly slap from you, Yvilla. You are most often above it.

Yolanda can certainly speak for herself, but I didn't read her comment in a condescending manner. I think she meant simply that she understood the point Mister was making while the people who were arguing with him did not. That point being that this study does not provide enough quantitative data to extrapolate a 1/10th nicotine absorption rate based on the unknown quantity consumed.

On the other hand, (not only do we have different fingers) we also have the fact that the study DOES show approximately 10x higher nicotine plasma measurements in test subjects who smoked a cigarette compared to one who used a 16mg/ml e-cig for a similar amount of time. While Mister's point that this does not serve as "proof" for the nicotine absorption rate of e-cigs, I think it is reasonable to say that these data are what we would expect under the 10% absorption hypothesis.
 

Kate51

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Another voice from our past, with huge respect for continued research:
This is from a post by Kate of UK, respectfully inserted here for reason of continuity, as follows:
I've been in touch with:

Thomas Eissenberg, Ph.D.
Professor of Psychology
Institute for Drug and Alcohol Studies
Virginia Commonwealth University

Dr Eissenberg sent me a message today after his return from a conference in Ireland. As he is conducting research on blood nicotine levels with vaping I had asked him for some results. He doesn't have any himself yet but said Ruyan's team came up with this:

"... Bullen, Glover, Laugesen, Lin, McRobbie, and Thornley report that after 9 participants used the Ruyan device (16 mg cartridge) for 5 minutes, peak plasma nicotine concentration was 1.3 ng/ml (95% confidence interval = 0.0 to 2.6). In contrast, for those same participants, a cigarette produced a peak plasma nicotine concentration of 13.4 ng/ml (95% CI = 6.5-20)."

Then he went on to say:

"These data, if they are valid and can be replicated, provide little support to the manufacturers' claim that the devices can do what they are marketed to do: deliver a physiologically active nicotine dose to the lung."

I am glad that we now have the first statistics on actual absorption of nicotine from vaping. This result is surprising to me though, it appears that 16mg nicotine eliquid gives a tenth of the nicotine to the bloodstream after five minutes vaping as a cigarette.
Then to follow: from the Lizinator:Human monoamine oxidase is inhibited by tobacco smoke:
beta-carboline alkaloids act as potent and reversible inhibitors
by
Herraiz T, Chaparro C.
Spanish Council for Scientific Research, CSIC,
Instituto de Fermentaciones Industriales,
Juan de la Cierva, 3,
28006, Madrid, Spain.
Biochem Biophys Res Commun. 2005 Jan 14;326(2):378-86

ABSTRACT

Monoamine oxidase (MAO) is a mitochondrial outer-membrane flavoenzyme involved in brain and peripheral oxidative catabolism of neurotransmitters and xenobiotic amines, including neurotoxic amines, and a well-known target for antidepressant and neuroprotective drugs. Recently, positron emission tomography imaging has shown that smokers have a much lower activity of peripheral and brain MAO-A (30%) and -B (40%) isozymes compared to non-smokers. This MAO inhibition results from a pharmacological effect of smoke, but little is known about its mechanism. Working with mainstream smoke collected from commercial cigarettes we confirmed that cigarette smoke is a potent inhibitor of human MAO-A and -B isozymes. MAO inhibition was partly reversible, competitive for MAO-A, and a mixed-type inhibition for MAO-B. Two beta-carboline alkaloids, norharman (beta-carboline) and harman (1-methyl-beta-carboline), were identified by GC-MS, quantified, and isolated from the mainstream smoke by solid phase extraction and HPLC. Kinetics analysis revealed that beta-carbolines from cigarette smoke were competitive, reversible, and potent inhibitors of MAO enzymes. Norharman was an inhibitor of MAO-A (K(i)=1.2+/-0.18muM) and MAO-B (K(i)=1.12+/-0.19muM), and harman of MAO-A (K(i)=55.54+/-5.3nM). beta-Carboline alkaloids are psychopharmacologically active compounds that may occur endogenously in human tissues, including the brain. These results suggest that beta-carboline alkaloids from cigarette smoke acting as potent reversible inhibitors of MAO enzymes may contribute to the MAO-reduced activity produced by tobacco smoke in smokers. The presence of MAO inhibitors in smoke like beta-carbolines and others may help us to understand some of the purported neuropharmacological effects associated with smoking.
And add from a source from Smokey Joe:
 
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yvilla

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How utterly condescending and insulting to the intelligence of those who read reports and understand them. Posters here do not expect that kind of undeserved, ugly slap from you, Yvilla. You are most often above it.

No T. Bob, my post was not a slap at others at all, but rather support for Mister. He was continually being told to read the report, well after having made it perfectly clear he had read it, and understood it thoroughly. His posts were also repeatedly being characterized as "asking" for information about what the report contained, when it was obvious that he was trying to provide information (about the limits on what could properly be extrapolated from the study).

It was painfully clear that his point was simply not being understood, and I felt his frustration. So, as I have always found Mister's posts to be sound, positive, and extremely helpful, I wanted to let him know that he was in fact being heard, by someone at least.
 

Kate51

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My only complaint, yvilla, is that in the interest of keeping the Thread respectful, especially in consideration of the fact the OP did us well again! Mister may have found a more diplomatic way to express his view; I was under the impression he wanted me somehow to verify his formula, which of course meant that with the Study as posted I could not winnow out information that was not there, so Mister was plying me repeatedly for information I could not personally supply to him and he then accused me of misinterpretation. The information is, however, in prior studies involving vapor and smoke collection and photospectrometry testing. Which is reflected in the chart I posted. Yes, we need more testing, specifically regarding the use of nicotine in this format, absolutely we do. But all data so far seems to point to my own well thought out conclusions. It has to be gleaned out of a published medically-based study, it's not going to be standing out on it's own, like a prescription. If that is wrong, then I have based an entire year or more in the wrong light. But my own body tells me that is not the case, and I know I am not alone in that regard.

I really do long for the old days on ECF where a person wasn't skewered with a red hot post every time someone interjects disagreement with the subject matter. It just makes good conversation into discourse rather than a more creative inclusive course for both sides of an issue. Yes, I felt slighted, however not the first or the last time. I'll probably get over it.
 
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Mister

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Kate, I have no problem with you expressing your views or beliefs. What I have a problem with is you saying that a study supports your views or beliefs when it does not. That kind of posting gives readers misinformation which they come to believe as fact instead of as opinion. As I and Thulium have said, the study does not disagree with your belief. Neither does a study which shows how many calories are in a cupcake. But when you assert a conclusion that the study supports your belief, and there is no such conclusion in the study (there are just some numbers you have taken to have this meaning), it is upon you to substantiate that those numbers have that meaning. I assert that they do not. Prove me wrong if you can and I'll take it. Merely yell at me and I won't take it.

Edit: Trying to be as clear as I can be, I have not asked you any questions for more information. I have only asked you to show why the information you have given out regarding this study is correct, vs. my stated reasons for saying it is not correct information.
 
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Kate51

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by Mister:
As I and Thulium have said, the study does not disagree with your belief.
A bit outside your theory that I have misrepresented something.
Let me show you my 'theory', and develop it out for you.
Usual cigarette (n¼9) 14.3 (8.8 to 19.9) 13.4 (6.5 to 20.3)
16 mg ENDD (n¼8) 19.6 (4.9 to 34.2) 1.3 (0.0 to 2.6)
This from the chart as posted in previous post and in the OP: approx 10% absorption showed from a 16mg/ml cartidge as a Usual cigarette.
This from my last saliva test, April 2010 A pack of cigarettes smoked would yield approx 1000ng/l+ cotinine. That is established by Nymox Corp. The test shows my cotinine level at low Level 3 (indicated by the show of color below Level 3), which is 100-200ng/l Again, about 1/10th that of 20 cigarettes.
Nymox saliva 04 09.jpg
In my theory, I am absorbing/metabolizing 1/10th nicotine using 12mg.ml X 2ml per day, or 24mg/ml nicotine, or approximately the nicotine metabolized from 2 cigarettes.
How is that not shown to be indicated by the Published data. Without more substantial personal data, I would say this comes at least approximately extremely close to the data, when represented in ng/l. This is what I believe.
If this is wrong, again I invite you to challenge my theory and submit your own data. I simply applied the data to my own circumstance, and it does coincide very nicely.
I took exception to your accusation that I was misrepresenting the data. I was not 'yelling', as you insinuated.
 
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Mister

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Let me show you my 'theory', and develop it out for you.

This from the chart as posted in previous post: approx 10% absorption showed.
16 mg ENDD (n¼8) 19.6 (4.9 to 34.2) 1.3 (0.0 to 2.6)
Ok I think I see where you're getting your number now. Since you bolded two numbers above, am I right to think that you have divided 1.3 by 16 to get your answer?

If so then that's where you've gone wrong.
Problem #1: The 16mg in that line means 16mg/ml juice. Dividing by that 16 means that you think the test subject consumed an entire ml. But we don't actually know how much the subjects used at all. Certainly not a full 16mg by vaping an entire ml in five minutes!
Problem #2: The 1.3 number in that line means that 1.3 nanograms of nicotine was measured in the subject's blood, per ml. To know how much nicotine was in their body you'd have to multiply that by the number of ml's of blood in their body, and account for a bunch of other variables. No need to detail them.

Even if those numbers could be divided by one another, your answer would not be 10%, it would be .000008% (.0000000013 / .016 to correctly convert between mg and ng). Giving an answer of pretty darn near zero absorption. But you just can't do arithmetic on those two numbers, they don't have any direct relationship. You might just as well divide the number of hairs on a dog by its number of legs to calculate its age.

This from my last saliva test ...
I'm aware of the thread where you've posted your own tests, and of a fair number of other self-test results posted on the forums. I read as many such posts as I can find, hoping there will eventually be enough data to draw some conclusions. The problem is that the various self-test results posted are so highly inconsistent that we can't work out an absorption guess from them.
 
How is that not shown to be indicated by the Published data. Without more substantial personal data, I would say this comes at least approximately extremely close to the data, when represented in ng/l. This is what I believe.
If this is wrong, again I invite you to challenge my theory and submit your own data. I took exception to your accusation that I was misrepresenting the data. I was not 'yelling', as you insinuated.

Except the data is represented in ng/ml.
 

Kate51

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I think I have explained all that you bring back. 1) Usual cigarette (n¼9) 14.3 (8.8 to 19.9) 13.4 (6.5 to 20.3) The 16mg/ml cart was only absorbed at 1.3ng/ml, will recheck the measurement used (it is ng/ml). The readings were based on Timed absorption, for all three devices, not total of mg of nicotine content for each. Fair enough? The sample sizes are given and preservation of samples as well. Read the data that contexts the chart. 2) The Nymox people wouldn't like what you said about their test strips! They are shown to be accurate down to minuscule sampling (1PPM).
Nicotine & Tobacco Research (2003) 5, 349–355
You would have to copy and paste that for a Google search. And Thulium, 3) I believe I did specify ng/l reflecting test measurement.
Sorry guys.
My Theory with my nicotine consumption stands as presented in the Study. And also as presented on the Published Clinical test. I simply applied the data to cotinine testing as a personal benchmark (acceptable as personal proof of degree of use of nicotine).
 
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