Facts You Should Know About Smokeless (Spit) Tobacco

Joined: 19 Dec 2008, 00:03

16 Aug 2006, 19:49 #21

Thank you for the education. Yuk!

Amanda x

Joined: 18 Dec 2008, 23:57

24 Apr 2007, 04:07 #22

There is also a thing out there called "hard snuff" which basically looks like lozenges in a blister pack. They are sold here in TX in convenience stores. I've never purchased any (I don't do nicotine, thank you) so I don't know their physical properties exactly.

To me though, in their ads they look suspiciously similar to the NRT lozenges designed to help you "quit smoking."

It would be interesting to know if hard snuff and NRT losenges are different at all.

Don't be fooled!


Lee (aka Beavis)

Joined: 11 Nov 2008, 19:22

08 Apr 2011, 12:31 #23

Imagine the insanity of a chemical addiction that makes the heart beat 12 beats per minute faster while constricting all blood vessels supplying much needed oxygen to it.  That's like trying to run while holding your breath.  Give it a try sometime.   Want out?   There was always only one rule ... no nicotine today.

Breathe deep, hug hard, live long,

John (Gold x11)       

Acute effects of tobacco chewing on the systemic, pulmonary and coronary circulation

Am J Cardiovasc Drugs. 2011;11(2):109-14. doi: 10.2165/11586750-000000000-00000.

Ramakrishnan S, Thangjam R, Roy A, Singh S, Ramakrishnan L, Seth S, Narang R, Bhargava B.


Background: Tobacco use is highly prevalent in India, with almost half of adult men consuming tobacco in either smoke or smokeless forms (particularly chewing). Although cigarette smoking is known to produce acute hemodynamic effects, there is a lack of data concerning such effects of chewing tobacco.

Objective: The aim of this study was to determine the acute hemodynamic and coronary vasomotor effects of chewing tobacco. Methods: Twelve habitual tobacco chewers (mean ± SD age 51.3 ± 6.9 years) undergoing elective coronary angiography were included in the study. Following coronary angiography, a 7F thermodilution Swan Ganz continuous cardiac output pulmonary artery catheter was used to continuously measure the right heart pressures and cardiac output. Having obtained baseline hemodynamic data, 1g of tobacco was given to be chewed. Subsequently, hemodynamic data were obtained periodically over a period of 60 minutes. A repeat left coronary injection was performed, 10 minutes after giving the tobacco, in the right anterior oblique view to estimate the diameter of the left anterior descending (LAD) artery by quantitative coronary angiography.

Results: Chewing tobacco led to a significant acute increase in heart rate (from 68.3 ± 12.4 beats/min to 80.6 ± 14.6 beats/min, peaking at 10 minutes) and cardiac output (from 3.8 ± 0.45 L/min to 4.7 ± 0.64 L/min, peaking at 15 minutes). There were no significant changes in the right atrial, pulmonary artery, or wedge pressures and hence no change in the pulmonary vascular resistance. More importantly, chewing tobacco was associated with coronary vasoconstriction (proximal LAD diameter change from 3.17 ± 0.43 mm to 2.79 ± 0.37 mm; p-value 0.02; mid LAD diameter change from 2.75 ± 0.36 mm to 2.40 ± 0.22 mm; p-value 0.03).

Conclusion: Chewing smokeless tobacco leads to coronary vasoconstriction and also produces significant hemodynamic alterations. These changes may have a bearing on excess vascular disease.

http://adisonline.com/cardiovascular/pa ... e=abstract

Joined: 11 Nov 2008, 19:22

11 Apr 2011, 01:51 #24

Glen,  it's my impression that the evidence as to which is easier to stop using, cigarettes or oral tobacco,  is mixed.   It had been my belief that since oral users generally had higher overall blood serum nicotine levels, while smokers reached higher peak levels and far far quicker, that it was probably a toss up.  This was reinforced by knowing that nicotine's blood serum half-life is identical for both, roughly two hours, and we'd seen no studies suggesting that re-sensitization or receptor count down-regulation was different for either group.   

Recent focus has been on one major difference between smoke and all forms of oral nicotine delivery.  We know that aside from nicotine stimulating dopamine pathway acetylcholine receptors, that some other still vague chemical in smoke somehow inhibits MAO A and MAO B (known as killjoy enzymes)  whose function it is to clean-up dopamine (either break it down or return it) once released.  This means that dopamine released by nicotine is allowed to linger longer for smokers than oral users.   Does this help explain why oral users generally have higher blood serum nicotine levels than smokers, that oral users are battling higher levels of MAO A and MAO B?  We don't know.

Your mention of none being remaining in the morning brought back memories of some medical records I was reviewing for a disability claim that included a sleep study.  With the entire world watching, this guy awoke in the middle of the night, put a plug in his mouth and went back to bed.  I must say, as a three pack a day smoker,  although I always smoked heavily on both sides of sleep I can't ever recall getting up because I needed more nicotine.  I found it fascinating that this guy did and wondered how common that was.

As for photos, I've been sent some horrible, horrible mouth cancer images from a cancer doctor in India but I've been reluctant to share them.  I recall a couple of participants in smoking seminars saying afterwards that the few lung cancer images I shared were too much for them to handle and they were tame by comparison.  Those images are out there and available but we certainly don't want to be chasing folks off.  We're just trying to strike some balance.

Thanks for the firsthand input, Glen.  As you know, regardless of how nicotine enters the bloodstream there's just one guiding principle that if followed provides a 100% guarantee to all of us ... no nicotine today!

Breathe deep, hug hard, live long,

John (Gold x11)