Hey everyone,
I hope you'll forgive a small rant but this needs some introduction. I'm a scientist, my fields are in aerospace engineering specifically in space applications, but I also have a fascination with the life sciences. my mother was a doctor so I was exposed to it early, learned a lot about it and my study didn't stop just because I moved out of the nest.
but I made this profile to try to talk about something I've seen on these forums for a while, I would have posted on the relevant threads but I'm a new member so I cant
basically I've seen a lot of posts about the effectiveness of ecigs on the improvement of health. for now I wanted to share some of the research I did before getting my first ecig, a joye 510. I wasn't a smoker really before only did cigars maybe twice a month but I like the nicotine feeling, so I decided to try ecigs, but I did a lot of research before I did to make sure it wouldn't deteriorate my health.
the main problem with smoking is the inhibition of your natural cleansing mechanisms when they try to clear out all the stuff you just inhaled. the inhibition of the cilia being the most important in my view. since if the lungs could clear all the stuff out before it does long term damage it would take much more to get bad health effects.
now I see a lot of speculation on what exactly the cause of the paralysis is. and it is a valid question, since if it is nicotine that is the inhibitor, then ecigs would hardly be as good as we hope since the avioli would still get hardened by macrophages trying to digest things in the increased mucosa generation that would result. however if another substance is the culprit, than regardless of the toxicity of nicotine, in small doses, the body is fully equipped to deal with this stress.
from my research it is my opinion that nicotine is not the element which inhibits cilia motion, I believe it is the tar. but I didn't come here to add more speculation. I came here to offer some piece of mind with the reason I came to this conclusion.
apparently I can't upload files, so I will quote the relevant information here:
Study done and published in the journal of molecular medicine.
"Nicotine increases ciliary beat frequency by a direct effect on respiratory cilia"
H.-L. Hahn, D. Kleinschrot, and D. Hansen
Medizinische Poliklinik, Universit/it Wfirzburg
can be found in full form in the Clinical Investigator (1992) 70:244-251
Goal was to study "the direct effects of nicotine on the ciliary beat frequency (CBF) undisturbed by interference from mucus secretion by using epithelial strips from ferret tracheae which contain no goblet cells and, because the glands were left behind in the submucosa, no gland tissue either."
the introduction also states that previous articles listed in the references show that cigarette smoke decreased the CBF (ciliary beat frequency) dramatically and that, quote: "The discrepancy could be explained by differences between the effects of nicotine and of other components of cigarette smoke"
therefore this study was to test the direct effect of nicotine alone, without the other chemicals in analog smoke. which makes it the perfect baseline to get some solid conclusions.
the introduction follows with this goal statement: "The present study was performed with the aim of identifying the effects of "realistic" concentrations of nicotine on CBF. Direct rather than secondary effects were studied by applying nicotine to a preparation containing only cilia (no mucusse......g elements)"
a summary of the method is that they took trachea from ferrets and harvested a lining of cilia to place in an isolated chamber where it would be perfused by a series of compounds, the main ones being, benign fluids, M-199 (culture nutrients or 'medium'), and nicotine (pure).
the method of detection comes next but is not a big concern here, so if you're really interested you can read the full text.
the perfusion sequence was Baseline 1 > Baseline 2 > Treatment.
Treatment consisted of nicotine concentrations of: 0,e-5,e-4,e-3 M
the article notes that its concentrations of nicotine to the tissue are indeed comparable to in vivo situations, based on another study involving the concentration of nicotine in tissue from smoke itself, saying:
"Are the concentrations of nicotine used in our and the Swedish studies relevant to conditions in vivo? We believe that they are. In the experiments by Russell et al. [16], the concentrations of nicotine after smoking one cigarette were between 25 and 444 nmol/1, median 207 nmol/l=2 x 10 -7 M/1. Similar data were obtained by Armitage [1], who arrived at an absorption of 2-3 gg/kg per puff or of 20-30 gg/kg per cigarette. This works out at around 2 x 10 -7 M/1 (average) or approximately 5 x 10-7 M/1 (maximum). Assuming an even distribution of nicotine throughout the body and a specific gravity of 1 for tissue, we calculate that an average of 203 x 70 kg = 14 210 nmol (14.2 gmol) is present in a 70-kg man after one cigarette."
this is important because it means that the possibility that nicotine is so toxic, in the form we take it (regardless of ecigarette or analog), that it can inhibit ciliary motion is by itself much less likely, since if the study finds that the cilia are still in motion, at normal toxicity levels of nicotine, you cannot conclude that cigarette or ecig nicotine levels are high enough that they will paralyze the cilia.
most of the graphs and analysis you will have to read the whole article for, but the relevant conclusion is clear:
"Figure 4 shows a typical example of a series of 80 frequency spectra. This was displayed as a 3-dimensional graph of amplitude vs. frequency over time. In the example shown, during the initial 5 min of nicotine perfusion, CBF increased. The increase was maximum during the 2nd and 3rd minute of perfusion but decreased again during the last 2 min."
"We conclude that nicotine stimulates CBF, that the effect is rapid but transient, and that it probably occurs at realistic concentrations of nicotine. The effects are independent of mucus secretion. Thus, the cilioinhibitory effects of cigarette smoke in vitro [14] are due to alterations in mucus composition, to excessive, toxic concentrations of nicotine, or to components of cigarette smoke other than nicotine."
since nicotine does not chemically react or change the properties of the mucose, and since these tests were done at realistic nicotine levels, it is unlikely that the mucose would combine with nicotine to inhibit the cilia and also unlikely that the nicotine would be in any higher concentrations that would change the results of what was found here, therefore it was my conclusion that the last statement must be true. that the inhibition of ciliary motion comes from something other than nicotine.
I hope this helps dispel some of the questions surrounding the effects of analog vs. ecigs.
if the administrators like what they see here please allow me more attachment privileges so I can append this with the actual article. I know I always feel better when I see the real article or scientific paper in my hands.
I hope you'll forgive a small rant but this needs some introduction. I'm a scientist, my fields are in aerospace engineering specifically in space applications, but I also have a fascination with the life sciences. my mother was a doctor so I was exposed to it early, learned a lot about it and my study didn't stop just because I moved out of the nest.
but I made this profile to try to talk about something I've seen on these forums for a while, I would have posted on the relevant threads but I'm a new member so I cant
basically I've seen a lot of posts about the effectiveness of ecigs on the improvement of health. for now I wanted to share some of the research I did before getting my first ecig, a joye 510. I wasn't a smoker really before only did cigars maybe twice a month but I like the nicotine feeling, so I decided to try ecigs, but I did a lot of research before I did to make sure it wouldn't deteriorate my health.
the main problem with smoking is the inhibition of your natural cleansing mechanisms when they try to clear out all the stuff you just inhaled. the inhibition of the cilia being the most important in my view. since if the lungs could clear all the stuff out before it does long term damage it would take much more to get bad health effects.
now I see a lot of speculation on what exactly the cause of the paralysis is. and it is a valid question, since if it is nicotine that is the inhibitor, then ecigs would hardly be as good as we hope since the avioli would still get hardened by macrophages trying to digest things in the increased mucosa generation that would result. however if another substance is the culprit, than regardless of the toxicity of nicotine, in small doses, the body is fully equipped to deal with this stress.
from my research it is my opinion that nicotine is not the element which inhibits cilia motion, I believe it is the tar. but I didn't come here to add more speculation. I came here to offer some piece of mind with the reason I came to this conclusion.
apparently I can't upload files, so I will quote the relevant information here:
Study done and published in the journal of molecular medicine.
"Nicotine increases ciliary beat frequency by a direct effect on respiratory cilia"
H.-L. Hahn, D. Kleinschrot, and D. Hansen
Medizinische Poliklinik, Universit/it Wfirzburg
can be found in full form in the Clinical Investigator (1992) 70:244-251
Goal was to study "the direct effects of nicotine on the ciliary beat frequency (CBF) undisturbed by interference from mucus secretion by using epithelial strips from ferret tracheae which contain no goblet cells and, because the glands were left behind in the submucosa, no gland tissue either."
the introduction also states that previous articles listed in the references show that cigarette smoke decreased the CBF (ciliary beat frequency) dramatically and that, quote: "The discrepancy could be explained by differences between the effects of nicotine and of other components of cigarette smoke"
therefore this study was to test the direct effect of nicotine alone, without the other chemicals in analog smoke. which makes it the perfect baseline to get some solid conclusions.
the introduction follows with this goal statement: "The present study was performed with the aim of identifying the effects of "realistic" concentrations of nicotine on CBF. Direct rather than secondary effects were studied by applying nicotine to a preparation containing only cilia (no mucusse......g elements)"
a summary of the method is that they took trachea from ferrets and harvested a lining of cilia to place in an isolated chamber where it would be perfused by a series of compounds, the main ones being, benign fluids, M-199 (culture nutrients or 'medium'), and nicotine (pure).
the method of detection comes next but is not a big concern here, so if you're really interested you can read the full text.
the perfusion sequence was Baseline 1 > Baseline 2 > Treatment.
Treatment consisted of nicotine concentrations of: 0,e-5,e-4,e-3 M
the article notes that its concentrations of nicotine to the tissue are indeed comparable to in vivo situations, based on another study involving the concentration of nicotine in tissue from smoke itself, saying:
"Are the concentrations of nicotine used in our and the Swedish studies relevant to conditions in vivo? We believe that they are. In the experiments by Russell et al. [16], the concentrations of nicotine after smoking one cigarette were between 25 and 444 nmol/1, median 207 nmol/l=2 x 10 -7 M/1. Similar data were obtained by Armitage [1], who arrived at an absorption of 2-3 gg/kg per puff or of 20-30 gg/kg per cigarette. This works out at around 2 x 10 -7 M/1 (average) or approximately 5 x 10-7 M/1 (maximum). Assuming an even distribution of nicotine throughout the body and a specific gravity of 1 for tissue, we calculate that an average of 203 x 70 kg = 14 210 nmol (14.2 gmol) is present in a 70-kg man after one cigarette."
this is important because it means that the possibility that nicotine is so toxic, in the form we take it (regardless of ecigarette or analog), that it can inhibit ciliary motion is by itself much less likely, since if the study finds that the cilia are still in motion, at normal toxicity levels of nicotine, you cannot conclude that cigarette or ecig nicotine levels are high enough that they will paralyze the cilia.
most of the graphs and analysis you will have to read the whole article for, but the relevant conclusion is clear:
"Figure 4 shows a typical example of a series of 80 frequency spectra. This was displayed as a 3-dimensional graph of amplitude vs. frequency over time. In the example shown, during the initial 5 min of nicotine perfusion, CBF increased. The increase was maximum during the 2nd and 3rd minute of perfusion but decreased again during the last 2 min."
"We conclude that nicotine stimulates CBF, that the effect is rapid but transient, and that it probably occurs at realistic concentrations of nicotine. The effects are independent of mucus secretion. Thus, the cilioinhibitory effects of cigarette smoke in vitro [14] are due to alterations in mucus composition, to excessive, toxic concentrations of nicotine, or to components of cigarette smoke other than nicotine."
since nicotine does not chemically react or change the properties of the mucose, and since these tests were done at realistic nicotine levels, it is unlikely that the mucose would combine with nicotine to inhibit the cilia and also unlikely that the nicotine would be in any higher concentrations that would change the results of what was found here, therefore it was my conclusion that the last statement must be true. that the inhibition of ciliary motion comes from something other than nicotine.
I hope this helps dispel some of the questions surrounding the effects of analog vs. ecigs.
if the administrators like what they see here please allow me more attachment privileges so I can append this with the actual article. I know I always feel better when I see the real article or scientific paper in my hands.
