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Big Tobacco's Conspiracy To Hide Health Risks & Deceive, They Knew & Documents Show They Knew - Here
#21
Carol Thompson Wrote:I haven't replied to your insinuations that I am "a tobacco lobbyist or just a tobacco junkie," because they are personal smears.

I disagree. This is a question that should be answered openly and without reservation, simply because you are representing views that could, reasonably, be said to reflect those of big tobacco. It is certainly not a smear to ask this question. Nor have I heard the argument before that a straight-forward question is typified an "insinuation".

In the last analysis, a question as to your "bona fides" needs to be answered fully, fairly and honestly, or else other readers will assume that you are hiding connections that damage your argument. This is human nature.

I recommend you proceed accordingly.

Lastly, it isn't even remotely possible that big tobacco is the "poor cousin" in all this. It is not short of money. Not by any measure of extreme wealth.

The fact remains that the historic lawsuit brought against them was enfeebled - out of the pubic eye - by all sorts of appeals and other legal impediments since the judgement was handed down. Big tobacco has not paid a fraction of the hundreds of billions awarded to the plaintiffs. And it was overflowing with unimaginably vast pools of funds prior to that. Billions of people still smoke, primarily now in LDC's - which big tobacco targeted after the lawsuit, confident that non-Europeans, (Southern Hemisphere peoples) wouldn't have the ability to defend against the power and advertising of a largely unregulated strum und drang onslaught unleashed by big tobacco to garner a vast stream of largely untapped revenue in exchange for their carcinogenic laden product.
The shadow is a moral problem that challenges the whole ego-personality, for no one can become conscious of the shadow without considerable moral effort. To become conscious of it involves recognizing the dark aspects of the personality as present and real. This act is the essential condition for any kind of self-knowledge.
Carl Jung - Aion (1951). CW 9, Part II: P.14
Reply
#22
Charles Drago Wrote:Peter, et al,

Do these tactics put you in mind of anyone:

Complete disregard for the critical questions getting to identity and motive.

Flooding the thread with endless recitations of long-debunked disinformation.

Ending erudite if sophistic screeds with gutter language.

Most significantly, the all-important challenge to engage, engage, engage ... in other words, prolong the long-settled debate so as to dignify its myriad sophistries and outright lies.

This is the stock-in-trade of agents provocateurs such as those who have found save haven at and, in many instances, now rule the EF. The many entities who write under the "Colby" identity engage in these operations on a routine basis.

The emergence of "Thompson" in the immediate wake of the Bronstein hacking/hijacking of this forum, when coupled with "Thompson's" subject matter -- the tobacco holocaust in which the historic "Colby's" father played a Mengele/Goebbels hybrid role -- give away this provocation.

"Thompson's" masters are playing a win-win game: If "she" remains, the disinformation spreads as the bandwidth shrinks; if "she" is booted, "Colby," Burton, and their gang of thieves at EF will be shouting about yet another instance of this forum banning someone who does not spout the true owners' shared party line.

Ladies and gentlemen: I submit to you that, in my highly educated and Constitutionally-protected opinion, there is an overwhelming case to be made that "Carol Thompson" -- whether a real person, a cover identity, or both -- comes to the Deep Politics Forum as an agent provocateur.

"Complete disregard for the critical questions getting to identity and motive."

Evidently you believe that smearing people as holocaust deniers invalidates their scientific evidence.

"Flooding the thread with endless recitations of long-debunked disinformation."

Who debunked it and where? Certainly not in any Surgeon General report, which all evade this evidence by stonewalling.

"Ending erudite if sophistic screeds with gutter language."

Explain any so-called sophistry.

"Most significantly, the all-important challenge to engage, engage, engage ... in other words, prolong the long-settled debate so as to dignify its myriad sophistries and outright lies."

Cite examples of supposed "sophistries and outright lies." (Ha! The truth is that you don't have any. You are merely trying to pretend that disputing the say-so of authority is automatically a lie.) Furthermore, in REAL science, debates are not settled by censoring alternative hypotheses. In REAL science, debates are re-opened by new evidence, which is then freely discussed.

As for Colby, he's a perfect example of a strawman who works for the anti-smokers. All he does is snivel that he doesn't believe, while his fanatical inquisitors froth at the mouth with rage at a mere refusal to submit unquestioningly to their religious dogma. At no time do Colby or any of his ilk attack anti-smoker scientific fraud. Their only purpose is to serve as theater, to deceive the public that the pro-smoker side has no strong arguments to present.

And if someone appears who does have strong arguments, they get banned and censored.
Reply
#23
David Guyatt Wrote:I disagree. This is a question that should be answered openly and without reservation, simply because you are representing views that could, reasonably, be said to reflect those of big tobacco. It is certainly not a smear to ask this question. Nor have I heard the argument before that a straight-forward question is typified an "insinuation".

In the last analysis, a question as to your "bona fides" needs to be answered fully, fairly and honestly, or else other readers will assume that you are hiding connections that damage your argument. This is human nature.

I recommend you proceed accordingly.

Lastly, it isn't even remotely possible that big tobacco is the "poor cousin" in all this. It is not short of money. Not by any measure of extreme wealth.

The fact remains that the historic lawsuit brought against them was enfeebled - out of the pubic eye - by all sorts of appeals and other legal impediments since the judgement was handed down. Big tobacco has not paid a fraction of the hundreds of billions awarded to the plaintiffs. And it was overflowing with unimaginably vast pools of funds prior to that. Billions of people still smoke, primarily now in LDC's - which big tobacco targeted after the lawsuit, confident that non-Europeans, (Southern Hemisphere peoples) wouldn't have the ability to defend against the power and advertising of a largely unregulated strum und drang onslaught unleashed by big tobacco to garner a vast stream of largely untapped revenue in exchange for their carcinogenic laden product.

My views can NOT "reasonably, be said to reflect those of big tobacco," because Big Tobacco has never expressed these views, and particularly not where it would matter the most, namely in a court of law.

My views represent the interest that smokers and everyone else in the world has in legitimate, state-of-the-art science, rather than pseudo-science founded on lifestyle questionnaires, frozen in time to embrace only hypotheses involving chemicals and genes which were fashionable during the Third Reich, while ignoring the evidence implicating infection which has developed during the last 30 years.

Considering the tobacco companies' performance in the US, their moving into foreign markets is a sign that the anti-smokers are moving into those countries. And they'll perform their same fraudulent acts of theater there that they did here, so that the anti-smokers can win.

And, out of all the hundreds of billions of dollars that have been looted from smokers, not one cent has ever been used to protect smokers' rights, which have been grievously violated by the anti-smoker-controlled US government.
Reply
#24
Carol Thompson Wrote:My views can NOT "reasonably, be said to reflect those of big tobacco," because Big Tobacco has never expressed these views, and particularly not where it would matter the most, namely in a court of law.

My views represent the interest that smokers and everyone else in the world has in legitimate, state-of-the-art science, rather than pseudo-science founded on lifestyle questionnaires, frozen in time to embrace only hypotheses involving chemicals and genes which were fashionable during the Third Reich, while ignoring the evidence implicating infection which has developed during the last 30 years.

Considering the tobacco companies' performance in the US, their moving into foreign markets is a sign that the anti-smokers are moving into those countries. And they'll perform their same fraudulent acts of theater there that they did here, so that the anti-smokers can win.

And, out of all the hundreds of billions of dollars that have been looted from smokers, not one cent has ever been used to protect smokers' rights, which have been grievously violated by the anti-smoker-controlled US government.

:rofl: Let me see if I get this right. The USG is controlled by some anti-smoker 'gang'; and this explains everything - whether related to smoking or not. Now I get it.....the WTC towers came down due to smokers in the hallways. Anyone have the Colby letter handy [I have it, but for this parade, I'm not sure I want to hunt for it...maybe later] in which the inside Tobacco Scientists ADMIT to hiding data and building a false consensus. Carol [if that is your name], I think you should smoke if you want to...but I don't allow it in my house or even near me outside.....because it is a dangerous mix of toxins, radioactives and immune system inhibitors. I personally believe people should be allowed to smoke if they want; just as I do not think that suicide should be illegal....but murder should be and allowing smokers to pollute other's air, water, land, landfills, rivers, etc. is just slow murder. My guess is you know Len Colby or are Len Colby....but that is must my hunch.
"Let me issue and control a nation's money and I care not who writes the laws. - Mayer Rothschild
"Civil disobedience is not our problem. Our problem is civil obedience! People are obedient in the face of poverty, starvation, stupidity, war, and cruelty. Our problem is that grand thieves are running the country. That's our problem!" - Howard Zinn
"If there is no struggle there is no progress. Power concedes nothing without a demand. It never did and never will" - Frederick Douglass
Reply
#25
Peter Lemkin Wrote::rofl: Let me see if I get this right. The USG is controlled by some anti-smoker 'gang'; and this explains everything - whether related to smoking or not. Now I get it.....the WTC towers came down due to smokers in the hallways. Anyone have the Colby letter handy [I have it, but for this parade, I'm not sure I want to hunt for it...maybe later] in which the inside Tobacco Scientists ADMIT to hiding data and building a false consensus. Carol [if that is your name], I think you should smoke if you want to...but I don't allow it in my house or even near me outside.....because it is a dangerous mix of toxins, radioactives and immune system inhibitors. I personally believe people should be allowed to smoke if they want; just as I do not think that suicide should be illegal....but murder should be and allowing smokers to pollute other's air, water, land, landfills, rivers, etc. is just slow murder. My guess is you know Len Colby or are Len Colby....but that is must my hunch.

That's nothing but an imaginary army of straw men, capped with an ad hominem.
Reply
#26
Carol Thompson Wrote:That's nothing but an imaginary army of straw men, capped with an ad hominem.

Will post a few like this .....as I have time.....

http://www.sourcewatch.org/index.php?tit...acco_smoke

The following describes a 1974 Liggett & Myers internal memo titled Comments on Recent News Releases Concerning Lead - 210 and Polonium - 210 in Cigarette Smoke

In 1974, a scientist name Edward Martell published a study in the scientific journal Nature that showed cigarette smoke contains radioactive polonium-210 and lead-210. Martell postulated that the alpha radiation emitted by these substances concentrates in the lungs of smokers and may be a contributor to lung cancer. The article caused a stir both inside and outside the tobacco industry. This 1974 Liggett memo acknowledges what Martell found--that radioactive polonium-210 and lead-210 are indeed present in cigarette smoke--and shows Liggett scientists planned to "counterbalance" Martell's information with "opposing opinions of equally reputable scientists..."

In the memo, Vello Norman, then Liggett's Supervisor of Physical Chemistry, states,
[Page 1]: "Tobacco leaf, as do all plant tissues, contains small amounts of many inorganic constituents, among them some lead and polonium."
[Page 2]: "Some of the recent publications have made some very strong statements about the significance of these levels of radiation such as: E.A. Martell, Nature, 249, 217 (1974): 'Thus, is seems that alpha radiation from [Polonium-210] in insoluble smoke particles may be the primary agent of bronchial cancer in smoking."

Norman then writes,
"We will have to counterbalance this by opposing opinions of equally reputable scientists such as: B. Rajewski and W. Stahlhofen: (the calculated dose rate) 'would seem to show that carcinogenesis caused by inhalation of [Polonium-210] with the tobacco smoke is rather unlikely."

Norman discounts Martell's conclusions by saying Martell is after money or "laurels," and essentially admits that the company doesn't know just how damaging the radioactive polonium and lead in smoke are, that they still need to do research to find this out:

Researchers, particularly when in pursuit of research grant monies or some other laurels, have been known to occasionally overstate what is warranted by facts in order to enhance the merits of their own thing. As it stands, we shall have to delay objective judgment as to just how significant Po-210 [polonium-210] in smoke is until considerable additional research is completed.

Title Comments on Recent News Releases Concerning Lead-210 and Polonium-210 in cigarette smoke
Org. Author Liggett & Myers
Per. Author Vello Norman
Date 19740725
Type Memorandum, Scientific report
Bates 81151933/1935
Collection Lorillard
Pages 3
URL: http://legacy.library.ucsf.edu/tid/qzl41e00

Related tobacco industry documents

A confidential Philip Morris (PM) memo from 1980 written by Roger Comes (a Associate Senior Scientist in PM's Research and Development department in Richmond, Virginia) responds to news reports about a research article that was published at the time by Edward Martell that revealed that cigarette smoke contained low levels of the radioactive alpha particle-emitting constituent Polonium-210. The memo confirms that PM was aware at that time that smoke from their cigarettes contained radioactive lead and polonium, and that it was derived from the uranium contained in the calcium phosphate fertilizers that farmers regularly used on tobacco-growing soils. Comes states that

"210-Pb [radioactive lead] and 210-Po [radioactive polonium] are present in tobacco and smoke...."

He also suggested that switching to another fertilizer could probably help the situation:

"...using ammonium phosphate instead of calcium phosphate as fertilizer is probably a valid but expensive point..."


Title: "Newscript" Radioactive Cigarettes 800222
Organizational Author: Philip Morris
Per. Author: R.A. Comes
Date: 19800402 (April 2, 1980)
Type: Memorandum, bibliography, scientific report
Bates No. 2012611337/1338
Collection: Philip Morris
Pages: 2
URL: http://legacy.library.ucsf.edu/tid/syr46e00

Related Sourcewatch resources
Handwritten note from Philip_Morris scientist Jim Charles (1982 note from PM scientist acknowledging presence of Polonium-210 in smoke)
Cigarette Filters and Polonium-210 (Lorillard document discussing Polonium-210)
Brown & Williamson document titled "Environment" (Estimated 1976 document which muses about whether Po-210 in soil will be eliminated in the future through hydroponic agriculture)

External resources
Andy Rowell Tobacco firms kept quiet on polonium role in cigarettes U.K. Independent, Health News section, August 24, 2008
Monique E. Muggli, MPH, Jon O. Ebbert, MD, Channing Robertson, PhD and Richard D. Hurt, MD Waking a Sleeping Giant: The Tobacco Industry's Response to the Polonium-210 Issue, American Journal of Public Health, September 2008, Vol 98, No. 9, Pp. 1643-1650
Robert N. Proctor, Ph.D. Puffing on Polonium, New York Times opinion section, December 1, 2006.
"Let me issue and control a nation's money and I care not who writes the laws. - Mayer Rothschild
"Civil disobedience is not our problem. Our problem is civil obedience! People are obedient in the face of poverty, starvation, stupidity, war, and cruelty. Our problem is that grand thieves are running the country. That's our problem!" - Howard Zinn
"If there is no struggle there is no progress. Power concedes nothing without a demand. It never did and never will" - Frederick Douglass
Reply
#27
Carol Thompson Wrote:"Complete disregard for the critical questions getting to identity and motive."

Evidently you believe that smearing people as holocaust deniers invalidates their scientific evidence.

"Flooding the thread with endless recitations of long-debunked disinformation."

Who debunked it and where? Certainly not in any Surgeon General report, which all evade this evidence by stonewalling.

"Ending erudite if sophistic screeds with gutter language."

Explain any so-called sophistry.

"Most significantly, the all-important challenge to engage, engage, engage ... in other words, prolong the long-settled debate so as to dignify its myriad sophistries and outright lies."

Cite examples of supposed "sophistries and outright lies." (Ha! The truth is that you don't have any. You are merely trying to pretend that disputing the say-so of authority is automatically a lie.) Furthermore, in REAL science, debates are not settled by censoring alternative hypotheses. In REAL science, debates are re-opened by new evidence, which is then freely discussed.

As for Colby, he's a perfect example of a strawman who works for the anti-smokers. All he does is snivel that he doesn't believe, while his fanatical inquisitors froth at the mouth with rage at a mere refusal to submit unquestioningly to their religious dogma. At no time do Colby or any of his ilk attack anti-smoker scientific fraud. Their only purpose is to serve as theater, to deceive the public that the pro-smoker side has no strong arguments to present.

And if someone appears who does have strong arguments, they get banned and censored.

All,

This is a classic iteration -- laughable if it weren't so tragic -- of all that I referenced in the above-quoted section.

I'm convinced. "Thompson" is "Colby." Even the "cite examples" language is lifted verbatim from dozens upon dozens of "Colby" posts.

"Cite examples," to reiterate, is in service to the need to engage, engage, engage. All the enemy wants is to prolong the long-settled arguments. Such is the brief of "Colby" and "Thompson."

It is clear to me that one or more of the individuals posting as "Colby" is/are at it here. Let's let it go a bit longer so as to draw them out. Then let's enjoy their "The DPF doesn't allow dissent" posts on the Ef.

I guess that if you have all the material resources in the world, you can afford to employ idiots.

"Thompson," you are exposed.

Charles
Reply
#28
Everyone knows the Surgeon General's warning about cigarette smoking but what about cigarette eating? Nicotine poisoning is a very real concern anywhere that a pet may find cigarettes, cigarette butts, chewing tobacco, or even nicotine gum or patches. Dogs, particularly puppies, tend to chew things up first and ask questions later. Cats may find a cigarette butt to be a nicely sized pouncing toy worthy of chewing.

[One thing they failed to mention and I will, is that cigarette butts on the sidewalks and streets, especially in rain/snow will cause Nicotine to be absorbed into the pads on the bottom of dogs paws]

Luckily for pets and small children, tobacco tastes terrible. Even chewing tobacco must have flavorings added to make it something worthy of oral enjoyment. Still, cigarettes have plenty of nicotine and even a small cigarette butt can mean serious illness or even death for a small pet.

The toxic dose for nicotine in pets is 1/2 -1mg per pound of pet body weight while the lethal dose is 4mg per pound of pet body weight. A cigarette contains 9-30 mg of nicotine depending on the type of cigarette; while a cigarette butt contains about 25% of the nicotine of the original cigarette despite its deceptively small amount of tobacco. (Smoking seems to concentrate some of the nicotine in the tail end of the cigarette.) Cigars can contain up to 40 mg. Chewing tobacco carries 6-8 mg per gram while the gum is 2-4 mg per piece and patches 8.3-114 mg. Smoking a cigarette yields only 0.5-2 mg of nicotine but eating one is a different ballgame as all of the nicotine becomes available for absorption into the body. One way to rephrase this is that a 40lb dog would get very sick after eating one cigarette but would need 11 cigarettes to actually die from nicotine poisoning.

Some good news is that nicotine is not absorbed directly in the acid environment of the stomach; the nicotine must move past the stomach into the small intestine for absorption. One of the first things nicotine does in the body is stimulate the vomit center of the brain, thus inducing vomiting which may save the patient's life if there is more cigarette material in the stomach.

SYMPTOMS OF NICOTINE POISONING

Signs begin as quickly as one hour post-ingestion. Symptoms include:
Tremors

Constricted pupils

Drooling

Auditory and Visual Hallucinations

Excitement

Vomiting and Diarrhea

Twitching possibly progressing to Seizures

Racing heart rate but slow heart rate with small doses

High blood pressure but at higher doses there is a circulatory collapse

It is easy to confuse nicotine poisoning with other poisonings such as strychnine, chocolate, organophosphate insecticide, and certain molds. Hopefully, there will be cigarette materials in the vomit to give away the diagnosis.

TREATMENT

Washing out the stomach to get rid of any remaining cigarette materials is helpful but is likely to require sedation. Since most patients are agitated, this is often a good thing anyway. Seizures are treated with seizure suppressing
drugs. It is tempting to use antacids to protect the stomach but as it is the stomach acid that is inhibiting the nicotine absorption, it is best to avoid this therapy. If the pet survives the first 4 hours, prognosis is felt to be good. Nicotine is inactivated by a healthy liver and its metabolites are excreted in urine. After 16 hours, the nicotine ingested should be gone.
"Let me issue and control a nation's money and I care not who writes the laws. - Mayer Rothschild
"Civil disobedience is not our problem. Our problem is civil obedience! People are obedient in the face of poverty, starvation, stupidity, war, and cruelty. Our problem is that grand thieves are running the country. That's our problem!" - Howard Zinn
"If there is no struggle there is no progress. Power concedes nothing without a demand. It never did and never will" - Frederick Douglass
Reply
#29
Using Smokeless Tobacco is gambling with your health!

Smokeless "Spit" tobacco contains over 2,000 chemicals, many of which have been directly related to causing cancer. Here are a few photos of mouth problems caused by the reaction of tobacco in the mouth. Photos courtesy of A.Christen, Indiana University. Source of information: US Surgeon General Report, 1986

Carcinogensis Associated With Smokeless Tobacco Use

1. The scientific evidence is strong that the use of smokeless tobacco can cause cancer in humans. The association between smokeless tobacco use and cancer is strongest for cancers of the oral cavity.

2. Oral cancer has been shown to occur several times more frequently among snuff dippers than among nontobacco users, and the excess risk of cancers of the cheek and gum may reach nearly fifty-fold among long-term snuff users.

3. Some investigations suggest that the use of chewing tobacco also may increase the risk of oral cancer.

4. Evidence for an association between smokeless tobacco use and cancers outside of the oral cavity in humans is sparse. Some investigations suggest that smokeless tobacco users may face increased risks of tumors of the upper digestive tract, but results are currently inconclusive.

5. Experimental investigations have revealed potent carcinogens in snuff and chewing tobacco. These include nitrosamines, polycyclic aromatic hydrocarbons, and radiation-emitting polonium. The tobacco-specific nitrosamines N-nitrosonornicotine and 4-(methylnitrosamino)-1-(3-pyridyl -l-butanone have been detected in smokeless tobacco at levels 100 times higher than the regulated levels of other nitrosamines found in bacon, beer, and other foods. Animals exposed to these tobacco-specific nitrosamines, at levels approximating those thought to be accumulated during a human lifetime by daily smokeless tobacco users, have developed an excess of a variety of tumors. The nitrosamines can be metabolized by target tissues to compounds that can modify cellular genetic material.

6. Bioassays exposing animals to smokeless tobacco, however, have generally shown little or no increased tumor production, although some bioassays suggest that snuff may cause oral tumors when tested in animals that are infected With herpes simplex virus.

Noncancerous and Precancerous Oral Health Effects Associated With Smokeless Tobacco Use

1. Some snuff-induced oral leukoplakic lesions have been noted upon continued smokeless tobacco use to undergo transformation to a dysplastic state. A portion of these dysplastic lesions can further develop into carcinomas of either a verrcous or squamous cell variety.

2. Recent studies of the effects of smokeless tobacco use on gingival and periodontal tissues have resulted in equivocal findings. While gingival recession is a common outcome from use, gingivitis may or may not occur. Because longitudinal data are not available, the role of smokeless tobacco in the development and progression of gingivitis or periodontitis has not been confirmed.

3. The evidence concerning the effects of smokeless tobacco use on the salivary' glands is inconclusive.

Nicotine Exposure: Pharmacokinetics, Addiction, and Other Physiologic Effects

l. The use of smokeless tobacco products can lead to nicotine dependence or addiction.

2. An examination of the pharmacokietics of nicotine (i.e., nicotine absorption, distribution, and ellimination) resulting from smoking and smokeless tobacco use indicates that the magnitude of nicotine exposure is similar for both.

3. Despite the complexities of tobacco smoke self-administration, systematic analysis has confirmed that the resulting addiction is similar to that produced and maintained by other addictive drugs in both humans and animals. Animals can learn to discriminate nicotine from other substances because of its effects on the central nervous system. These effects are related to the dose and rate of administration, as is also the case with other drugs of abuse.

4. It has been shown that nicotine functions as a reinforcer under a variety of conditions. It has been confirmed that nicotine can function in all of the capacities that characterize a drug with a liability to widespread abuse. Additionally, as is the case with most other drugs of abuse, nicotine produces effects in the user that are considered desirable to the user. These effects are caused by the nicotine and not simply by the vehicle of delivery (tobacco or tobacco smoke).

5. Nicotine is similar in all critical measures to prototypic drugs of abuse such as morphine and cocaine. The methods and criteria used to establish these similarities are identical to those used for other drugs suspected of having the potential to produce abuse and physiologic dependence. Specifically, nicotine is psychoactive, producing transient dose-related changes in mood and feeling. It is a euphoriant that produces dose-related increases in scores on standard measures of euphoria. It is a reinforcer (or reward, in both human and animal intravenous self-administration paradigms, functioning as do other hags of abuse. Additionally, nicotine through smoking produces the same effects, and it causes neuroadaptation leading to tolerance and physiologic dependence. Taken together, these results confirm the hypothesis that the role of nicotine in the compulsive use of tobacco is the same as the role of morphine in the compulsive use of opium derivatives or of cocaine in the compulsive use of era derivatives.

6. The evidence that smokeless tobacco is addicting includes the pharmacologic role of nicotine dose in regulating tobacco intake; the commonalities between nicotine and other prototypic dependence-producing substances; the abuse liability and dependence potential of nicotine; and the direct, albeit limited at present, evidence that orally delivered nicotine retains the characteristics of an addictive drug.

7. Several other characteristics of tobacco products in general, including smokeless tobacco, may function to enhance further the number of persons who are afflicted by nicotine dependence: nicotine-delivering products are widely available and relatively inexpensive; and the self-administration of such products is legal, relatively well tolerated by society, and produces minimal disruption to cognitive and behavioral performance. Nicotine produces a variety of individual-specific therapeutic actions such as mood and performance enhancement; and the brief effects of nicotine ensure that conditioning occurs, because the behavior is associated with numerous concomitant environmental stimuli.

8. All commonly marketed and consumed smokeless tobacco products contain substantial quantities of nicotine. The nicotine is delivered to the central nervous system in addicting quantities when used in the fashion that each form is commonly used (or as recommended in smokeless tobacco marketing campaigns).

9. Since the exposure to nicotine from smokeless tobacco is similar in magnitude to nicotine exposure from cigarette smoking, the health consequences of smoking that are caused by nicotine also would be expected to be hazards of smokeless tobacco use. Areas of particular concern in which nicotine may play a contributory or supportive role in the pathogenesis of disease include coronary artery and peripheral vascular disease, hypertension, peptic ulcer disease, and fetal mortality and morbidity.



Smokeless Tobacco Is Less Risky Than Smoking, though still dangerous. Some other effects are:

TOOTH ABRASION - Grit and sand in smokeless tobacco products scratches teeth and wears away the hard surface or enamel. Premature loss of tooth enamel can cause added sensitivity and may require corrective treatment.

GUM RECESSION - Constant irritation to the spot in the mouth where a small wad of chewing tobacco is placed can result in permanent damage to periodontal tissue. It also can damage the supporting bone structure. The injured gums pull away from the teeth, exposing root surfaces and leaving teeth sensitive to heat and cold. Erosion of critical bone support leads to loosened teeth that can be permanently lost.

INCREASED TOOTH DECAY - Sugar is added to smokeless tobacco during the curing and processing to improve its taste. The sugar reacts with bacteria found naturally in the mouth, causing an acid reaction, which leads to decay.

TOOTH DISCOLORATION AND BAD BREATH - Common traits of long-term smokeless tobacco users are stained teeth and bad breath. Moreover, the habit of continually spitting can be both unsightly and offensive.

NICOTINE DEPENDENCE - Nicotine blood levels achieved by smokeless tobacco use are similar to those from cigarette smoking. Nicotine addiction can lead to an artificially increased heart rate and blood pressure. In addition, it can constrict the blood vessels that are necessary to carry oxygen-rich blood throughout the body. Athletic performance and endurance levels are decreased by this reaction.

UNHEALTHY EATING HABITS - Chewing tobacco lessens a person's sense of taste and ability to smell. As a result, users tend to eat more salty and sweet foods, both of which are harmful if consumed in excess.

ORAL CANCER - With the practice of "chewing" and "dipping," tobacco and its irritating juices are left in contact with gums, cheeks and/or lips for prolonged periods of time. This can result in a condition called leukoplakia. Leukoplakia appears either as a smooth, white patch or as leathery-looking wrinkled skin. It results in cancer in 3 percent to 5 percent of all cases.

OTHER CANCERS - All forms of smokeless tobacco contain high concentrations of cancer-causing agents. These substances subject users to increased cancer risk not only of the oral cavity, but also the pharynx, larynx and esophagus.

DANGER SIGNS - If you use smokeless tobacco, or have in the past, you should be on the lookout for some of these early signs of oral cancer:

* A sore that does not heal
* A lump or white patch
* A prolonged sore throat
* Difficulty in chewing
* Restricted movement of the tongue or jaws
* A feeling of something in the throat

Pain is rarely an early symptom. For this reason, all tobacco users need regular dental check-ups. http://www.quittobacco.com/facts/effects.htm
"Let me issue and control a nation's money and I care not who writes the laws. - Mayer Rothschild
"Civil disobedience is not our problem. Our problem is civil obedience! People are obedient in the face of poverty, starvation, stupidity, war, and cruelty. Our problem is that grand thieves are running the country. That's our problem!" - Howard Zinn
"If there is no struggle there is no progress. Power concedes nothing without a demand. It never did and never will" - Frederick Douglass
Reply
#30
Nicotine
From Wikipedia, the free encyclopedia
This article is about the chemical compound. For other uses, see Nicotine (disambiguation).
Nicotine

Systematic (IUPAC) name
3-[(2S)-1-methylpyrrolidin-2-yl]pyridine
Identifiers
CAS number 54-11-5
ATC code N07BA01 QP53AX13
PubChem CID 942
DrugBank DB00184
ChemSpider 80863
UNII 6M3C89ZY6R
Chemical data
Formula C10H14N2
Mol. mass 162.26 g/mol
SMILES eMolecules & PubChem
InChI[show]
Physical data
Density 1.01 g/cm³
Melt. point -79 °C (-110 °F)
Boiling point 247 °C (477 °F)
Pharmacokinetic data
Bioavailability 20 to 45% (oral)
Metabolism hepatic
Half-life 2 hours
Therapeutic considerations
Pregnancy cat. D(US)
Legal status Unscheduled (AU) ? (UK) ? (US)
Dependence liability Medium to high
Routes smoked (as smoking tobacco, mapacho, etc.), insufflated (as tobacco snuff or nicotine nasal spray), chewed (as nicotine gum, tobacco gum or chewing tobacco), transdermal (as nicotine patch, nicogel or topical tobacco paste), intrabuccal (as dipping tobacco, snuffs, dissolvable tobacco or creamy snuff), vaporized (as electronic cigarette, etc.), directly inhaled (as nicotine inhaler), oral (as nicotini), buccal (as snus)
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Nicotine is an alkaloid found in the nightshade family of plants (Solanaceae) that constitutes approximately 0.63.0% of the dry weight of tobacco,[1][2] with biosynthesis taking place in the roots and accumulation occurring in the leaves. It functions as an antiherbivore chemical with particular specificity to insects; therefore nicotine was widely used as an insecticide in the past,[3][4] and currently nicotine analogs such as imidacloprid continue to be widely used. Nicotine is also found in several other members of the Solanaceae family, with small amounts being present in species such as the Eggplant and Tomato.

In low concentrations (an average cigarette yields about 1 mg of absorbed nicotine), the substance acts as a stimulant in mammals and is the main factor responsible for the dependence-forming properties of tobacco smoking. According to the American Heart Association, nicotine addiction has historically been one of the hardest addictions to break, while the pharmacological and behavioral characteristics that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine.[5] Nicotine content in cigarettes has slowly increased over the years, and one study found that there was an average increase of 1.6% per year between the years of 1998 and 2005. This was found for all major market categories of cigarettes.[6]Contents [hide]
1 History and name
2 Chemistry
3 Optical activity
4 Pharmacology
4.1 Pharmacokinetics
4.2 Detection of use
4.3 Pharmacodynamics
4.3.1 In CNS
4.3.2 In SNS
4.3.3 In adrenal medulla
5 Psychoactive effects
6 Dependence and withdrawal
6.1 Immunology prevention
7 Toxicology
8 Link to circulatory disease
9 Therapeutic uses
10 Research as a potential basis for an antipsychotic agent
11 See also
12 References
13 Further reading
14 External links

[edit]
History and name

Nicotine is named after the tobacco plant Nicotiana tabacum, which in turn is named after Jean Nicot de Villemain, French ambassador in Portugal, who sent tobacco and seeds from Brazil to Paris in 1560 and promoted their medicinal use. Nicotine was first isolated from the tobacco plant in 1828 by German chemists Posselt & Reimann, who considered it a poison.[7] Its chemical empirical formula was described by Melsens in 1843,[8] its structure was discovered by Adolf Pinner and Richard Wolffenstein in 1893, and it was first synthesized by A. Pictet and Crepieux in 1904.[9]
[edit]
Chemistry

Nicotine is a hygroscopic, oily liquid that is miscible with water in its base form. As a nitrogenous base, nicotine forms salts with acids that are usually solid and water soluble. Nicotine easily penetrates the skin. As shown by the physical data, free base nicotine will burn at a temperature below its boiling point, and its vapors will combust at 308 K (35 °C; 95 °F) in air despite a low vapor pressure. Because of this, most of the nicotine is burned when a cigarette is smoked; however, enough is inhaled to cause pharmacological effects.
[edit]
Optical activity

Nicotine is optically active, having two enantiomeric forms. The naturally occurring form of nicotine is levorotatory, with [α]D = 166.4°. The dextrorotatory form, (+)-nicotine, has only one-half the physiological activity of ()-nicotine. It is therefore weaker in the sense that a higher dose is required to attain the same effects.[10] The salts of (+)-nicotine are usually dextrorotatory.
[edit]
Pharmacology
[edit]
Pharmacokinetics

Side effects of nicotine.[11]

As nicotine enters the body, it is distributed quickly through the bloodstream and can cross the blood-brain barrier. On average it takes about seven seconds for the substance to reach the brain when inhaled.[citation needed] The half life of nicotine in the body is around two hours.[12]

The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. For chewing tobacco, dipping tobacco, snus and snuff, which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco. Nicotine is metabolized in the liver by cytochrome P450 enzymes (mostly CYP2A6, and also by CYP2B6). A major metabolite is cotinine.

Other primary metabolites include nicotine N'-oxide, nornicotine, nicotine isomethonium ion, 2-hydroxynicotine and nicotine glucuronide.[13]

Glucuronidation and oxidative metabolism of nicotine to cotinine are both inhibited by menthol, an additive to mentholated cigarettes, thus increasing the half-life of nicotine in vivo.[14]
[edit]
Detection of use

Nicotine can be quantified in blood, plasma, or urine to confirm a diagnosis of poisoning or to facilitate a medicolegal death investigation. Urinary or salivary cotinine concentrations are frequently measured for the purposes of pre-employment and health insurance medical screening programs. Careful interpretation of results is important, since passive exposure to cigarette smoke can result in significant accumulation of nicotine, followed by the appearance of its metabolites in various body fluids.[15][16] Nicotine use is not regulated in competitive sports programs, yet the drug has been shown to have a significant beneficial effect on athletic performance.[17]
[edit]
Pharmacodynamics

Nicotine acts on the nicotinic acetylcholine receptors, specifically the ganglion type nicotinic receptor and one CNS nicotinic receptor. The former is present in the adrenal medulla and elsewhere, while the latter is present in the central nervous system (CNS). In small concentrations, nicotine increases the activity of these receptors. Nicotine also has effects on a variety of other neurotransmitters through less direct mechanisms.
[edit]
In CNS

Effect of nicotine on dopaminergic neurons

By binding to nicotinic acetylcholine receptors, nicotine increases the levels of several neurotransmitters - acting as a sort of "volume control". It is thought that increased levels of dopamine in the reward circuits of the brain are responsible for the euphoria and relaxation and eventual addiction caused by nicotine consumption. Nicotine has a higher affinity for acetylcholine receptors in the brain than those in skeletal muscle, though at toxic doses it can induce contractions and respiratory paralysis.[18] Nicotine's selectivity is thought to be due to a particular amino acid difference on these receptor subtypes.[19]

Tobacco smoke contains the monoamine oxidase inhibitors harman, norharman,[20] anabasine, anatabine, and nornicotine. These compounds significantly decrease MAO activity in smokers.[20][21] MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin.

Chronic nicotine exposure via tobacco smoking up-regulates alpha4beta2* nAChR in cerebellum and brainstem regions[22][23] but not habenulopeduncular structures.[24] Alpha4beta2 and alpha6beta2 receptors, present in the ventral tegmental area, play a crucial role in mediating the reinforcement effects of nicotine.[25]
[edit]
In SNS

Nicotine also activates the sympathetic nervous system,[26] acting via splanchnic nerves to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the bloodstream. Nicotine also has an affinity for melanin-containing tissues due to its precursor function in melanin synthesis or its irreversible binding of melanin and nicotine. This has been suggested to underlie the increased nicotine dependence and lower smoking cessation rates in darker pigmented individuals.[27]

Effect of nicotine on chromaffin cells
[edit]
In adrenal medulla

By binding to ganglion type nicotinic receptors in the adrenal medulla nicotine increases flow of adrenaline (epinephrine), a stimulating hormone and neurotransmitter. By binding to the receptors, it causes cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and thus the release of epinephrine (and norepinephrine) into the bloodstream. The release of epinephrine (adrenaline) causes an increase in heart rate, blood pressure and respiration, as well as higher blood glucose levels.[28]

Nicotine is the natural product of tobacco, having a half-life of 1 to 2 hours. Cotinine is an active metabolite of nicotine that remains in the blood for 18 to 20 hours, making it easier to analyze due to its longer half-life.[29]
[edit]
Psychoactive effects

Nicotine's mood-altering effects are different by report: in particular it is both a stimulant and a relaxant.[30] First causing a release of glucose from the liver and epinephrine (adrenaline) from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, sharpness, calmness, and alertness.[31] Like any stimulant, it may very rarely cause the often catastrophically uncomfortable neuropsychiatric effect of akathisia. By reducing the appetite and raising the metabolism, some smokers may lose weight as a consequence.[32][33]

When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates the release of many chemical messengers including acetylcholine, norepinephrine, epinephrine, vasopressin, arginine, dopamine, autocrine agents, and beta-endorphin.[34] This release of neurotransmitters and hormones is responsible for most of nicotine's effects. Nicotine appears to enhance concentration[35] and memory due to the increase of acetylcholine. It also appears to enhance alertness due to the increases of acetylcholine and norepinephrine. Arousal is increased by the increase of norepinephrine. Pain is reduced by the increases of acetylcholine and beta-endorphin. Anxiety is reduced by the increase of beta-endorphin. Nicotine also extends the duration of positive effects of dopamine[36] and increases sensitivity in brain reward systems.[37] Most cigarettes (in the smoke inhaled) contain 1 to 3 milligrams of nicotine.[38]

Research suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine.[39] This stimulates nerve transmission. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, nicotine potently enhances the actions of norepinephrine and dopamine in the brain, causing a drug effect typical of those of psychostimulants. At higher doses, nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain-killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use.

Technically, nicotine is not significantly addictive, as nicotine administered alone does not produce significant reinforcing properties.[40] However, only after coadministration with an MAOI, such as those found in tobacco, nicotine produces significant behavioral sensitization, a measure of addiction potential. This is similar in effect to amphetamine.[41]

Nicotine gum, usually in 2-mg or 4-mg doses, and nicotine patches are available, as well as smokeless tobacco and electronic cigarettes which do not have all the other ingredients in smoked tobacco.[citation needed]

A 21 mg patch applied to the left arm. The Cochrane Collaboration finds that NRT increases a quitter's chance of success by 50 to 70%.[42] But in 1990, researchers found that 93% of users returned to smoking within six months.[43]
[edit]
Dependence and withdrawal
See also: Smoking cessation

Modern research shows that nicotine acts on the brain to produce a number of effects. Specifically, its addictive nature has been found to show that nicotine activates reward pathwaysthe circuitry within the brain that regulates feelings of pleasure and euphoria.[44]

Dopamine is one of the key neurotransmitters actively involved in the brain. Research shows that by increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has been shown to be more addictive than cocaine and heroin.[citation needed] Like other physically addictive drugs, nicotine withdrawal causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. As dopamine regulates the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. An example is the increase in norepinephrine, one of the successors to dopamine, which inhibit reuptake of the glutamate receptors,[45] in charge of memory and cognition. The net effect is an increase in reward pathway sensitivity, opposite of other drugs of abuse such as cocaine and heroin, which reduce reward pathway sensitivity.[37] This neuronal brain alteration persists for months after administration ceases. Nicotine also has the potential to cause dependence in many animals other than humans, assuming they were to consume it.[citation needed]

A study found that nicotine exposure in adolescent mice retards the growth of the dopamine system, thus increasing the risk of substance abuse during adolescence.[46]
[edit]
Immunology prevention

Because of the severe addictions and the harmful effects of smoking, vaccination protocols have been developed. The principle is under the premise that if an antibody is attached to a nicotine molecule, it will be prevented from diffusing through the capillaries, thus making it less likely that it ever affects the brain by binding to nicotinic acetylcholine receptors.

These include attaching the nicotine molecule to a hapten such as Keyhole limpet hemocyanin or a safe modified bacterial toxin to elicit an active immune response. Often it is added with bovine serum albumin.

Additionally, because of concerns with the unique immune systems of individuals being liable to produce antibodies against endogenous hormones and over the counter drugs, monoclonal antibodies have been developed for short term passive immune protection. They have half-lives varying from hours to weeks. Their half-lives depend on their ability to resist degradation from pinocytosis by epithelial cells.[47]
[edit]
Toxicology
See also: Nicotine poisoning

The LD50 of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 4060 mg (0.5-1.0 mg/kg) can be a lethal dosage for adult humans.[48][49] Nicotine therefore has a high toxicity in comparison to many other alkaloids such as cocaine, which has an LD50 of 95.1 mg/kg when administered to mice. It is unlikely that a person would overdose on nicotine through smoking alone, although intoxication can occur through the excessive use of nicotine patches, gum, nasal sprays or oral inhalers intended as smoking cessation aids.[50][51] Spilling a high concentration of nicotine onto the skin can cause intoxication or even death, since nicotine readily passes into the bloodstream following dermal contact.[52]

The carcinogenic properties of nicotine in standalone form, separate from tobacco smoke, have not been evaluated by the IARC, and it has not been assigned to an official carcinogen group. The currently available literature indicates that nicotine, on its own, does not promote the development of cancer in healthy tissue and has no mutagenic properties. However, nicotine and the increased cholinergic activity it causes have been shown to impede apoptosis, which is one of the methods by which the body destroys unwanted cells (programmed cell death). Since apoptosis helps to remove mutated or damaged cells that may eventually become cancerous, the inhibitory actions of nicotine may create a more favourable environment for cancer to develop, though this also remains to be proven.[53]

Though the teratogenic properties of nicotine may or may not yet have been adequately researched, women who use nicotine gum and patches during the early stages of pregnancy face an increased risk of having babies with birth defects, according to a study of around 77,000 pregnant women in Denmark. The study found that women who use nicotine-replacement therapy in the first 12 weeks of pregnancy have a 60 percent greater risk of having babies with birth defects, compared to women who are non-smokers, the Daily Mail reported. The findings were published in the journal Obstetrics and Gynaecology.

Effective April 1, 1990, the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency added nicotine to the list of chemicals known to the state to cause developmental toxicity, for the purposes of Proposition 65.[54]
[edit]
Link to circulatory disease This section needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (November 2009)


Nicotine has very powerful effects on arteries throughout the body. Nicotine is a stimulant, it raises blood pressure, and is a vasoconstrictor, making it harder for the heart to pump through the constricted arteries. It causes the body to release its stores of fat and cholesterol into the blood.[55]

It has been speculated[who?] that nicotine increases the risk of blood clots by increasing plasminogen activator inhibitor-1, though this has not been proven. Plasma fibrinogen levels are elevated in smokers and are further elevated during acute COPD exacerbation. Also Factor XIII, which stabilizes fibrin clots, is increased in smokers. But neither of these two effects has been shown to be caused by nicotine [56] as of 2009.

Peripheral circulation in arteries going to the extremities is also highly susceptible to the vasoconstrictor effects of nicotine and the increased risk of clots and clogging.[citation needed]
[edit]
Therapeutic uses

The primary therapeutic use of nicotine is in treating nicotine dependence in order to eliminate smoking with the damage it does to health. Controlled levels of nicotine are given to patients through gums, dermal patches, lozenges, electronic/substitute cigarettes or nasal sprays in an effort to wean them off their dependence.

However, in a few situations, smoking has been observed to apparently be of therapeutic value. These are often referred to as "Smoker's Paradoxes".[57] Although in most cases the actual mechanism is understood only poorly or not at all, it is generally believed that the principal beneficial action is due to the nicotine administered, and that administration of nicotine without smoking may be as beneficial as smoking, without the higher risk to health due to tar and other ingredients found in tobacco.

For instance, recent studies suggest that smokers require less frequent repeated revascularization after percutaneous coronary intervention (PCI).[57] Risk of ulcerative colitis has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking.[58][59] Smoking also appears to interfere with development of Kaposi's sarcoma in patients with HIV,[1].[60]

Nicotine reduces the chance of Breast cancer among women carrying the very high risk BRCA gene,[61] preeclampsia,[62] and atopic disorders such as allergic asthma.[63] A plausible mechanism of action in these cases may be nicotine acting as an anti-inflammatory agent, and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects.[64]

Tobacco smoke has been shown to contain compounds capable of inhibiting MAO. Monoamine oxidase is responsible for the degradation of dopamine in the human brain. When dopamine is broken down by MAO-B, neurotoxic by-products are formed, possibly contributing to Parkinson's and Alzheimers disease.[65] Many such papers regarding Alzheimer's disease[66] and Parkinson's Disease[67] have been published. Recent studies find no beneficial link between smoking and Alzheimer's disease and in some cases, suggest it may actually result in an earlier onset of the disease.[68][69][70][71] However, nicotine has been shown to delay the onset of Parkinson's disease in studies involving monkeys and humans.[72][73][74]

Recent studies have indicated that nicotine can be used to help adults suffering from autosomal dominant nocturnal frontal lobe epilepsy. The same areas that cause seizures in that form of epilepsy are responsible for processing nicotine in the brain.[75]

Studies suggest a correlation between smoking and schizophrenia, with estimates near 75% for the proportion of schizophrenic patients who smoke. Although the nature of this association remains unclear, it was recently argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine.[76][77] More recent research has found that mildly dependent users got some benefit from nicotine, but not those who were highly dependent.[78] All of these studies are based only on observation, and no interventional (randomized) studies have been done. Research on nicotine as administered through a patch or gum is ongoing.

Nicotine appears to improve ADHD symptoms. Some studies are focusing on benefits of nicotine therapy in adults with ADHD.[79]

Nicotine (in the form of chewing gum or a transdermal patch) is being explored as an experimental treatment for OCD. Small studies show some success, even in otherwise treatment-refractory cases.[80][81][82]
[edit]
Research as a potential basis for an antipsychotic agent

When the metabolites of nicotine were isolated and their effect on first the animal brain and then the human brain in people with schizophrenia were studied, it was shown that the effects helped with cognitive and negative symptoms of schizophrenia. Therefore, the nicotinergic agents, as antipsychotics which do not contain nicotine but act on the same receptors in the brain are showing promise as adjunct antipsychotics in early stages of FDA studies on schizophrenia. The prepulse inhibition (PPI) is a phenomenon in which a weak prepulse attenuates the response to a subsequent startling stimulus. Therefore, PPI is believed to have face, construct, and predictive validity for the PPI disruption in schizophrenia, and it is widely used as a model to study the neurobiology of this disorder and for screening antipsychotics.[83] Additionally, studies have shown that there are genes predisposing people with schizophrenia to nicotine use.[84]

Therefore with these factors taken together the heavy usage of cigarettes and other nicotine related products among people with schizophrenia may be explained and novel antipsychotic agents developed that have these effects in a manner that is not harmful and controlled and is a promising arena of research for schizophrenia.
[edit]
See also
Nicotiana
Nicotiana rustica
Mapacho
Nicotiana tabacum
Tobacco
Tobacco products
Nicotinic acid (Niacin)
Drug addiction
Tobacco cessation
Chantix
Zyban
Nicogel
Nicotini
NicVAX
Nicotine gum
Nicotine patch
Nicotine inhaler
Nicotine nasal spray
Snus
Electronic Cigarette
Psychoactive drug
Drug Discovery and Development: Nicotinic Acetylcholine Receptor Agonists
Nicotinic receptor
[edit]
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[edit]
Further reading
Bilkei-Gorzo A, Rácz I, Michel K, Darvas M, Rafael Maldonado López, Zimmer A. (2008). "A common genetic predisposition to stress sensitivity and stress-induced nicotine craving". Biol. Psychiatry 63 (2): 16471. doi:10.1016/j.biopsych.2007.02.010. PMID 17570348.
Willoughby JO, Pope KJ, Eaton V (Sep 2003). "Nicotine as an antiepileptic agent in ADNFLE: an N-of-one study". Epilepsia 44 (9): 123840. doi:10.1046/j.1528-1157.2003.11903.x. PMID 12919397.
Minna JD (Jan 2003). "Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer". J Clin Invest. 111 (1): 313. doi:10.1172/JCI17492. PMID 12511585.
Fallon JH, Keator DB, Mbogori J, Taylor D, Potkin SG (Mar 2005). "Gender: a major determinant of brain response to nicotine". Int J Neuropsychopharmacol. 8 (1): 1726. doi:10.1017/S1461145704004730. PMID 15579215.
West KA, Brognard J, Clark AS, et al. (Jan 2003). "Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells". J Clin Invest. 111 (1): 8190. doi:10.1172/JCI16147. PMID 12511591.
National Institute on Drug Abuse
Erowid information on tobacco
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"Civil disobedience is not our problem. Our problem is civil obedience! People are obedient in the face of poverty, starvation, stupidity, war, and cruelty. Our problem is that grand thieves are running the country. That's our problem!" - Howard Zinn
"If there is no struggle there is no progress. Power concedes nothing without a demand. It never did and never will" - Frederick Douglass
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