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• Dope smokers get addicted to cigs: study 

Cannabis use is to blame for higher rates of cigarette addiction in alternative lifestyle communities, Australian research shows.

A study of young men living on the NSW north coast suggests that high rates of dope smoking are responsible for high rates of tobacco use, and not vice-versa as was previously thought.

In what researchers have dubbed the "reverse gateway" process, it is claimed many young men become dependent on tobacco because they mix it with cannabis.

"Subsequently, long-term cannabis users find it difficult to quit smoking tobacco because of the reinforcing influence of their cannabis use," said Eric van Beurden, of the North Coast Area Health Service.

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Nicotine addiction among physicians in Greece 

Of those who reported smoking as “just a habit”, 30,7 % (23 of 75) scored > 6 on the FTND subscale. Scores FTND>6 indicate “Nicotine Dependance”. There were significant differences on demographic subscales between those presenting with or without nicotine addiction (i.e age, years of smoking and family conditions).

Conclusions

An extrapolation of our results to encompass all physicians in Greece would be reasonable, since physicians are a rather homogeneous group in this country. Our results are especially alarming because anti-smoking campaigns are usually more successful in doctors than in the general population. References

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NIDA Researchers Identify Genetic Variant Linked to Nicotine Addiction and Lung Cancer 

Scientists have identified a genetic variant that not only makes smokers more susceptible to nicotine addiction but also increases their risk of developing two smoking-related diseases, lung cancer and peripheral arterial disease. The research was supported by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health (NIH).

The study, published in the April 3 issue of the journal Nature, "highlights the advances that are being made in genetics research, which can now identify gene variants that increase the risk of complex bio-behavioral disorders," says NIH Director Dr. Elias Zerhouni. "This finding will help us in our efforts to further reduce the scope and devastating consequences of cigarette smoking."

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Genetic variations raise lung cancer risk for smokers and ex-smokers 

Two common inherited genetic variations are associated with increased risk of lung cancer for smokers and former smokers, a research team led by scientists at The University of Texas M. D. Anderson Cancer Center reports April 2 in the online edition of Nature Genetics.

"This is the first study to identify a common genetic variant that influences the risk for developing lung cancer," said lead author Chris Amos, Ph.D., professor in M. D. Anderson's Department of Epidemiology. The variants are present in about half of the Caucasian population studied.

The paper is one of three published by Nature this week from three unique teams that have identified the same genetic locus as associated with increased lung cancer risk. The findings are a major step forward in identifying those at high risk for non-small cell lung cancer and for understanding how smoking and genetic factors interact to cause the disease.

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SMOKERS AND THAT "DOUBLE-WHAMMY" GENE. 

"What this finding means is that some individuals --- who are unfortunately at higher risk for getting lung cancer if they carry the genetic factor --- also may find it more difficult to quit."

The gene variations in these new studies could help explain some of the anomalies we all know about: 90-year-old smokers who don't get cancer, for example ... and why some people get hooked on nicotine and some don't.

All of these new studies link the variations on Chromosome 15 to lung cancer, says CBS News Medical Correspondent Dr. Emily Senay ... but they disagree as to how it works.

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Masked smoking-related images modulate brain activity in smokers. 

The questions of whether and how indiscriminate drug-related stimuli could influence drug-users are important to our understanding of addictive behavior, but the answers are still inconclusive. In the present preliminary functional magnetic resonance imaging study using a backward masking paradigm, the effect of indiscriminate smoking-related stimuli on 10 smokers and 10 nonsmokers was examined. The BOLD response showed a significant reduction (P = 0.001) in the right amygdala of smokers when they viewed but did not perceive masked smoking-related stimuli, while no significant differences were found in the nonsmoker group. . . .

The BOLD response in drug-users indicates the amygdala responds to drug-related stimuli that are below the perceptual threshold. The functional connectivity data suggest a functional interaction between the amygdala and the anterior cingulate cortex when drug users view 33ms back-masked drug-related stimuli. This observation suggests that the amygdala plays an important role in the indiscriminate drug-related cue process.

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Neurobiology of nicotine addiction: implications for smoking cessation treatment. 

Molecular biology studies suggest that the alpha(4)beta(2) nicotinic acetylcholine receptor subtype is the main receptor mediating nicotine dependence. Nicotine acts on these brain nicotinic cholinergic receptors to facilitate neurotransmitter release (dopamine and others), producing pleasure, stimulation, and mood modulation. Neuroadaptation develops with repeated exposure to nicotine, resulting in tolerance to many of the effects of nicotine. When a smoker stops smoking, a nicotine withdrawal syndrome ensues, characterized by irritability, anxiety, increased eating, dysphoria, and hedonic dysregulation, among other symptoms. . . .

Pharmacotherapies to aid smoking cessation should ideally reduce nicotine withdrawal symptoms and block the reinforcing effects of nicotine obtained from smoking without causing excessive adverse effects. Further, given the important role of sensory effects of smoking and psychoactive effects of nicotine, counseling and behavioral therapies are important adjuncts to and substantially augment the benefits of pharmacotherapy.

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Higher-risk workers need not apply?  

Attorney Susan Lessack said litigation is increasingly being brought against companies for "lifestyle" regulations, which target smokers, overweight individuals -- even extreme sports enthusiasts.

"Employers are paying attention to high risk activities because it affects health insurance claims and costs," Lessack said. "While bans on smoking and other activities are becoming a trend, they are usually violating state privacy statutes."

The Americans with Disabilities Act protects employees from discrimination for physical impairments, which some have argued can include obesity and addiction to nicotine.

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"Double Whammy" Gene Could Help Reduce Smoking // But Three Studies Emphasize It's Much Better Not to Start 

"These studies provide even stronger proof that nicotine is a drug which causes physiological addiction in the same way as heroin or cocaine, and that the addiction can be even stronger than with these and other illegal drugs.

The fact that some 60% of the population has at least one copy of this double whammy gene is consistent with the view that nicotine in addictive to over 60% of the population, but not to everyone," says Professor John Banzhaf of ASH.

These studies may one day open the door to more effective smoking cessation programs, which today have an abysmal success rate.

On the other hand, since quitting involves overcoming both a physiological addiction to nicotine and a psychological habituation to using cigarettes in many every-day stressful-and-otherwise situations, even major improvements in the addictive component will have only a limited impact, says Banzhaf, noting that smokers who are given nicotine replacement therapy in the form of gums and pills still have major problems giving up smoking.

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Nicotine-Linked Gene Change Raises Risk of Cancer (Update2) 

Genetic changes may determine which smokers get hooked, smoke more than others and are most likely to develop lung cancer, scientists said today.

The variations in genes that control the body's response to nicotine, an addictive chemical in tobacco, raise the risk of lung cancer and blood-vessel disease, according to three studies published today by the journals Nature and Nature Genetics.

Researchers from DeCode Genetics Inc. and laboratories around the world found the risk-linked changes in a stretch of DNA containing genetic instructions for making proteins, called receptors, that respond to nicotine. Determining how the cancer- associated variant differs from lower-risk versions will throw much-needed light on prevention, said Norman Edelman, chief medical officer of the American Lung Association.

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Genetics Linked to Lung Cancer  

A trio of papers published Wednesday identifies for the first time a specific genetic variation linked to increased risk of lung cancer, but the studies disagree about whether the risk is elevated because the gene variant increases smoking behavior or addiction to nicotine.

The studies, conducted by three independent research groups and published in the journals Nature and Nature Genetics, all found that increased lung-cancer risk was associated with a gene variant on chromosome 15. The variant increased the risk by as much as 80% among smokers who had two copies of the variation and by about 30% if they had one copy. However, smoking far outweighs a genetic predisposition in developing lung cancer, say the researchers.

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Scientists smoke out genes behind lung cancer 

Scientists have found important genetic differences between people that may help explain why some smokers get lung cancer and others do not.

Three teams from France, Iceland and the United States said on Wednesday they had pinpointed a region of the genome containing genes that can put smokers at even greater risk of contracting the killer disease.

In all three studies, nicotine appears a major culprit.

The findings could eventually lead to better ways to prevent and treat lung cancer, the biggest cause of cancer-related death globally in men and the second most common in women.

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• A Smoking Gene: deCODE Shows How a Single Variant in the Sequence of the Genome Confers Nicotine Dependence and Risk of Lung Cancer and Other Disease 

Today scientists from deCODE genetics and their colleagues from several universities report in the journal Nature a clear link between a single-letter variant in the sequence of the human genome (SNP) and susceptibility to nicotine dependence. Moreover, in part because of this impact on smoking behavior, each copy of the risk variant of this SNP confers an approximately 30% increase in risk of lung cancer and a 20% increase in risk of peripheral arterial disease (PAD) . . .

The SNP, rs1051730, is located on chromosome 15q24 in a nicotine acetylcholine receptor called CHRNA3. The paper, 'A variant associated with nicotine dependence, lung cancer and peripheral arterial disease,' is published today in the online edition of Nature, at www.nature.com.

"These findings provide an example of the power of human genetics for shedding light on the most complex health challenges. . . .

The deCODE team began this study with a smoking history questionnaire distributed to some 50,000 Icelanders

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• Genetic link for lung cancer identified  

Amongst smokers, genetics may raise the risk of lung cancer by 80%.

Three independent genetic studies have found some of the strongest evidence yet that your genes influence your risk of developing lung cancer.

Lung cancer, the most common killer cancer in the world, is largely caused by smoking. Tobacco is thought to be responsible for about 5 million premature deaths every year and smoking is still clearly the largest risk factor. But the new results suggest that, amongst smokers, some people may be as much as 80% more at risk than others thanks to their genes.

People who have never smoked might also have a slightly increased risk of developing lung cancer and similar problems, although the three studies disagree on whether this is actually the case. It is not clear whether the genetic effect occurs independently of smoking, or whether the genes raise the risk of cancer by exacerbating nicotine addiction. . . .

A third study3, involving almost 6,000 cancer cases and led by Christopher Amos of the University of Texas M. D. Anderson Cancer Center in Houston, also found that the gene variants raise cancer risk independently of smoking behaviour.

Stefansson, in contrast, believes that the genes promote cancer by making people more vulnerable to nicotine addiction. This view is supported by the fact that the genes for the brain's nicotine receptors are found in the same region of chromosome 15 as the genetic mutations.

People in Stefansson's study group tended to be more heavily addicted to smoking if they had more copies, or 'alleles' of the gene variants. "In our study, we found if you have one allele you smoke about one more cigarette per day; if you have 2 alleles you average two more cigarettes per day," he says.

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• Genetic link tied to smoking addiction 

WASHINGTON - Scientists say they have pinpointed a genetic link that makes people more likely to get hooked on tobacco, causing them to smoke more cigarettes, making it harder to quit, and leading more often to deadly lung cancer.

The discovery by three separate teams of scientists makes the strongest case so far for the biological underpinnings of the addiction of smoking and sheds light on how genetics and cigarettes join forces to cause cancer, experts said. The findings also lay the groundwork for more tailored quit-smoking treatments.

"This is kind of a double whammy gene," said Christopher Amos, a professor of epidemiology at the M.D. Anderson Cancer Center in Houston and author of one of the studies. "It also makes you more likely to be dependent on smoking and less likely to quit smoking." . . .

For Stefansson, the research hits home. His father, a smoker, died of lung cancer. And Stefansson, who doesn't smoke, frequently lectures his 23-year-old daughter "who smokes like a chimney." She acts like she is immortal and smoking can't kill her, Stefansson said. But his own research shows that her genes are probably stacked against her.

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