Nicotine appears to be a “gateway” drug that primes the brain to be susceptible to cocaine, according to a new study in mice.  The researchers say if further studies show the findings apply to humans, a decrease in smoking rates in young people would be expected to lead to a decrease in cocaine addiction, the Los Angeles Times reports.

The study found mice exposed to nicotine in drinking water for at least seven days showed an increased response to cocaine. The researchers also looked at data on cocaine use among a group of high school students, and found 81 percent of those who started using cocaine did so in a month when they were smoking tobacco.

The findings appear in the journal Science Translational Medicine.
Previous studies have shown that most illegal drug users report using tobacco products or alcohol before they started illicit drug use, according to a news release by the National Institute on Drug Abuse, which funded the study. Until now, studies have not shown a biological mechanism through which exposure to nicotine increases vulnerability to illegal drug use, the release notes.

“Now that we have a mouse model of the actions of nicotine as a gateway drug this will allow us to explore the molecular mechanisms by which alcohol and marijuana might act as gateway drugs,” lead author Eric Kandel, MD, of Columbia University Medical Center, said in the release. “In particular, we would be interested in knowing if there is a single, common mechanism for all gateway drugs or if each drug utilizes a distinct mechanism.”

Source:   www.drugfree.org.  4th Nov.

Removing branding and wrapping cigarettes in plain packaging helps remove the appeal of smoking according to new a Cancer Research UK-funded study published in Tobacco Control.
The researchers found that more women than men smoked less and found smoking less enjoyable when using the plain packs.
Some smokers also claimed that they would be more likely to attempt quitting if all cigarettes came in the dark brown unbranded packs used in this study.
In the first study of its kind nearly 50 young adult smokers used non branded cigarette packets in normal everyday situations for two weeks. The researchers then compared the reaction to this packaging to the reactions of using regular packs for two weeks.
The plain brown packs were given a fictional name with standard branding and the health warning “Smoking Kills”. Twice weekly questionnaires were followed up with face to face interviews for more in depth analysis of reaction.
Plainly wrapped cigarettes were rated negatively against the original packs. Taking out the cigarettes less often, handing out cigarettes less frequently and hiding the pack more were all reported as a result of the plain packaging.
Dr Crawford Moodie, the study’s lead author based at the University of Stirling, said: “Despite the small size of this study it adds an important real world dimension to the research on the way smokers respond to plain packaging. The study confirms the lack of appeal of plain packs, with the enjoyment and consumption of cigarettes being reduced. We’re now looking to build on this research to understand more about the impact of packaging on smokers.”
The UK government is expected to begin a public consultation on the future of tobacco packaging later this year.
Australia should be the first country in the world to wrap cigarettes in plain packaging. The Australian government has announced that all tobacco must be sold in plain packaging from July 1, 2012. Picture health warnings will also cover 75 per cent of the front and 90 per cent of the back of packs.
Jean King, Cancer Research UK’s director of tobacco control, said: “While a small study, this research provides important insights into the power of cigarette packaging. Colourful and slickly designed packs are one of the last remaining avenues for tobacco companies to market their deadly product, so it’s interesting to see what might happen if and when this is removed. It’s important to remember that smoking remains the single biggest preventable cause of death in the UK, so preventing more people from starting and helping smokers to quit is vital. We look forward to the possibility of removing the silent salesman of cigarette packets.”

Source: http://www.cancerresearchuk.org/ 8tj Sept. 2011

Smoking is an important risk factor in brain shrinkage and a decline in brain function in later years, a new study suggests. The study found smoking, along with high blood pressure, diabetes and excess weight, all contributed to potentially dangerous changes in the brain that could lead to a decline in mental functioning as soon as 10 years later. The study appears in the journal Neurology.
HealthDay reports the study included 1,352 people without dementia whose average age was 54. Each person was weighed, measured, given blood pressure, cholesterol and diabetes tests and underwent brain MRI scans over 10 years. The researchers found smokers lost brain volume overall and in the hippocampus—the part of the brain which converts short-term memory into long-term memory—at a faster rate than nonsmokers. They were also more likely to have a rapid increase in small areas of damage to the brain’s blood vessels.
Study author Charles DeCarli, M.D., of the University of California at Davis Alzheimer’s Disease Center, said in a journal news release, “Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it’s too late.”

Source: ThePartnership @drugfree.org. Aug.2011

Electronic cigarettes, or “e-cigarettes,” are crude drug delivery systems for refined nicotine that pose unknown risks, two experts write in this week’s New England Journal of Medicine. Researchers from the American Legacy Foundation’s Steven A. Schroeder National Institute for Tobacco Research and Policy Studies write that e-cigarettes have more in common with asthma inhalers than with cigarettes, according to Science Daily.
E-cigarettes are designed to deliver nicotine in the form of a vapor, which is inhaled by the user. They usually have a rechargeable, battery-operated heating element, a replaceable cartridge with nicotine or other chemicals and a device called an atomizer that converts the contents of the cartridge into a vapor when heated. E-cigarettes often are made to look like regular cigarettes.
The Food and Drug Administration (FDA) announced in April that it would regulate e-cigarettes as tobacco products, not as drug-delivery devices.
Last year, the FDA lost a court case after it tried to treat e-cigarettes as drug-delivery devices, which must satisfy stricter requirements than tobacco products, including clinical trials to prove they are safe and effective. FDA tests found that the liquid in some e-cigarettes contained toxins besides nicotine, as well as cancer-causing substances found in tobacco. Some public health experts say the level of the cancer-causing agents is similar to those found in nicotine replacement therapy, which contains nicotine extracted from tobacco.
The authors list several safety concerns about e-cigarettes. They note that the devices do not reliably deliver nicotine, and have not been sufficiently studied in the same way the FDA requires other smoking-cessation drugs and devices to be evaluated. Therefore, smokers who try to use e-cigarettes to help them quit smoking are likely to find them ineffective because of their variable nicotine content and unreliable delivery, they say.
They also note that smokers may use e-cigarettes in places where traditional tobacco smoking is not allowed, thus encouraging them to keep smoking instead of quitting. E-cigarettes also may become a smoking “starter” product for young people. E-cigarette cartridges can be bought over the Internet with flavors such as chocolate and grape, they write.

Source: DrugFreee.org 21st July 2011

Women who smoke while pregnant should be aware that they are increasing the chance their baby will be born malformed, say experts.
The risk for having a baby with missing or deformed limbs or a cleft lip is over 25% higher for smokers, data show. Along with higher risks of miscarriage and low birth weight, it is another good reason to encourage women to quit, say University College London doctors.
In England and Wales 17% of women smoke during pregnancy. And among under 20s the figure is 45%. Although most will go on to have a healthy baby, smoking can cause considerable damage to the unborn child.
Missing limbs
Researchers now estimate that each year in England and Wales several hundred babies are born with a physical defect directly caused by their mother’s smoking. Every year in England and Wales around 3,700 babies in total are born with such a condition. The experts base their calculations on 172 research papers published over the last 50 years, which looked at maternal smoking and birth defects.
The findings, from 174,000 cases of malformation and 11.7 million healthy births, revealed that smoking increased the risk of many abnormalities. The chance of a baby being born with missing or deformed limbs is 26% higher, and cleft lip or palate is 28% more likely.
Similarly, the risk of clubfoot 28% greater, and gastrointestinal defects 27% more. Skull defects are 33% more likely, and eye defects 25% more common. The greatest increase in risk – of 50% – was for a condition called gastroschisis, where parts of the stomach or intestines protrude through the skin. Professor Allan Hackshaw, who led the research, suspects many women who smoke while pregnant do not know about these risks.
“There’s still this idea among some women that if you smoke the baby will be small and that will make it easier when it comes to the delivery. “But what is not appreciated is that smoking during pregnancy increases the risk of defects in the child that are life-long.”
Women should quit smoking before becoming pregnant, or very early on, to reduce the risks
He said very few public health educational policies mention birth defects when referring to smoking and those that do are not very specific – this is largely because of past uncertainty over which ones are directly linked. “Now we have this evidence, advice should be more explicit about the kinds of serious defects such as deformed limbs, and facial and gastrointestinal malformations that babies of mothers who smoke during pregnancy could suffer from,” he said.
Of the 700,000 babies born each year in England and Wales, around 120,000 babies are born to mums who smoke. Amanda Sandford of Action on Smoking and Health said: “This study shows some of the worst outcomes of smoking during pregnancy. Pregnant smokers will be shocked to learn that their nicotine habit could cause eye or limb deformities in their baby.
“There is clearly a need to raise awareness of these risks among girls and to ensure pregnant women are given all the support they need to help them quit smoking and to stay stopped after the birth.” Basky Thilaganathan of the Royal College of Obstetricians and Gynaecologists said women who struggled to quit should at least cut down on how much they smoke.
Professor Hackshaw said the risk was likely dose-related – meaning the more a woman smokes, the bigger the risk to her unborn child.

Source: www.bbc.co.uk 12th July 2011

This study sets out to broaden the evidence base by running a trial, based in UK general practice, where only brief support was available for participants while they compared nicotine nasal spray to placebo. It was based in 27 general practices and there was a total of 761 heavy smokers (at least 15 cigs/day for at least 3 years) who received brief support and 12 weeks of treatment with either nicotine nasal spray or placebo. The primary outcome was biochemically-verified complete abstinence from smoking throughout weeks 3-12.

The results showed that nicotine nasal spray more than doubled the number who successfully stopped smoking (15.4% vs 6.7%) from weeks 3-12 giving an odds ratio of 2.6 (95% CI 1.5-4.4). Although many reported minor irritant adverse effects it was noted to be particularly effective amongst those who were highly dependent on nicotine.

SMMGP comment: Tobacco harm reduction strategies is a neglected area although we know
that replacing smoking with a smokeless delivery system for the primary drug, nicotine, can reduce risks by about 99%, about the same as abstinence. Because smoking is so popular, the total health benefits from tobacco harm reduction dwarf those from any other area of HR.
There is an increasing array of nicotine replacement therapy options and this study shows one effective way of delivery. One interesting facet was the tiny number (0.2%) that went on to achieve abstinence if they were still smoking at one week. This infers that it may be worth prescribing a single week of nicotine nasal spray and reassessing abstinence. It?s a relatively small, inexpensive punt and it can double the chance of abstinence for that individual – even without the more comprehensive smoking cessation services which some prescribing is based around.

Source: Stapleton JA, Sutherland G. Addiction 2011;106:824-832

A single 15-minute exposure to nicotine caused a long-term increase in the excitability of neurons involved in reward, according to a study published in The Journal of Neuroscience. The results suggest that nicotine and cocaine hijack similar mechanisms of memory on first contact to create long-lasting changes in a person’s brain.
“Of course, for smoking it’s a very long-term behavioral change, but everything starts from the first exposure,” said Danyan Mao, PhD, postdoctoral researcher at the University of Chicago Medical Center. “That’s what we’re trying to tackle here: when a person first is exposed to a cigarette, what happens in the brain that might lead to a second cigarette?”
Learning and memory are thought to be encoded in the brain via synaptic plasticity, the long-term strengthening and weakening of connections between neurons. When two neurons are repeatedly activated together, a stronger bond forms between them, increasing the ability of one to excite the other.
Previous research in the laboratory of Daniel McGehee, PhD, neuroscientist and associate professor in the Department of Anesthesia & Critical Care at the Medical Center, discovered that nicotine could promote plasticity in a region of the brain called the ventral tegmental area (VTA). Neurons that originate in the VTA release the neurotransmitter dopamine, known to play a central role in the effects of addictive drugs and natural rewards such as food and sex.
“We know that a single exposure to physiologically relevant concentrations of nicotine can lead to changes in the synaptic drive in the circuitry that lasts for several days,” said McGehee, senior author of this study. “That idea is very important in how addiction forms in humans and animals.”
In the new experiments, Mao monitored the electrical activity of VTA dopamine neurons in slices of brain dissected from adult rats. Each slice was bathed for 15 minutes in a concentration of nicotine similar to the amount that would reach the brain after smoking a single cigarette. After 3-5 hours, Mao conducted electrophysiology experiments to detect the presence of synaptic plasticity and determine which neurotransmitter receptors were involved in its development.
Mao discovered that nicotine-induced synaptic plasticity in the VTA is dependent upon one of the drug’s usual targets, a receptor for the neurotransmitter acetylcholine located on the dopamine neurons. But another element found necessary for nicotine’s synaptic effects was a surprise: the D5 dopamine receptor, a component previously implicated in the action of cocaine. Blocking either of these receptors during nicotine exposure eliminated the drug’s ability to cause persistent changes in excitability.
“We found that nicotine and cocaine employ similar mechanisms to induce synaptic plasticity in dopamine neurons in VTA,” Mao said.
While the subjective effects of nicotine and cocaine are very different in humans, the overlapping effects of the two drugs on the reward system of the brain may explain why both are highly addictive substances, the researchers said.
“We know without question that there are big differences in the way these drugs affect people,” McGehee said. “But the idea that nicotine is working on the same circuitry as cocaine does point to why so many people have a hard time quitting tobacco, and why so many who experiment with the drug end up becoming addicted.”
The overlap between nicotine and cocaine effects at the D5 receptor may also offer a novel strategy for preventing or treating addiction. However, currently-known blockers of the receptor also block another dopamine receptor, D1, that is important for normal, healthy motivation and movement.
“This dopamine receptor is attractive as a potential target,” McGehee said. “The real challenge is to tweak the addictive effect of drugs like nicotine or other psychostimulants without totally crushing the person’s desire to pursue healthy behavior.”
Future research will also focus on whether repeated exposure to nicotine, as would occur in a regular smoker, changes the drug’s effects on synaptic plasticity in the VTA. In the meantime, the current study builds evidence that addictive drugs appropriate the neurobiological tools of learning and memory to create long-term changes in brain reward pathways.
“It’s all fitting with the overriding idea that changes in synaptic strength are part of the way these drugs motivate behavior in a persistent way,” McGehee said.
The study, “Nicotine Potentiation of Excitatory Inputs to Ventral Tegmental Dopamine Neurons,” will be published May 4, 2011 by The Journal of Neuroscience. In addition to Mao and McGehee, Keith Gallagher of the University of Chicago is a co-author.
The research was supported by grants from the Women’s Council of the Brain Research Foundation and the National Institutes of Health.

Source: University of Chicago Medical Center (2011, May 4). Nicotine and cocaine leave similar mark on brain after first contact. ScienceDaily. Retrieved May 8, 2011, from http://www.sciencedaily.com¬ /releases/2011/05/110503171745.htm

Exposure to second hand smoke has a direct, measurable impact on the brain—and the effect is similar to what happens in the brain of the person doing the smoking. In fact, exposure to this secondhand smoke evokes cravings among smokers, according to a study funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.

The study, published in Archives of General Psychiatry, used positron emission tomography to demonstrate that one hour of secondhand smoke in an enclosed space results in enough nicotine reaching the brain to bind receptors that are normally targeted by direct exposure to tobacco smoke. This happens in the brain of both smokers and non-smokers.

Previous research has shown that exposure to secondhand smoke increases the likelihood that children will become teenage smokers and makes it more difficult for adult smokers to quit. Such associations suggest that secondhand smoke acts on the brain to promote smoking behavior.

“This study gives concrete evidence to support policies that ban smoking in public places, particularly enclosed spaces and around children,” said Arthur Brody, M.D., of the University of California at Los Angeles Department of Psychiatry and Biobehavioral Sciences and corresponding author for the article

Source: www.cadca.org 5th May 2011

A public-smoking ban in Australia has led more parents to smoke at home, raising health risks for kids, researchers say.
The research from the Australian National University’s Research School of Social Sciences concluded that “bans in recreational public places can perversely increase tobacco exposure of nonsmokers … Children seem to be particularly affected. The level of cotinine (a nicotine by product measurable in saliva) in children considerably increases as a result of bans in public places.”
Public smoking bans tend to “displace smokers to private places where they contaminate nonsmokers,” said authors Jerome Adda, Ph.D., and Francesca Cornaglia, Ph.D., visiting scholars from University College London.

Source: Medical Post April 4 2006

Abstract

Objective To examine the association between smoking and risk of invasive breast cancer using quantitative measures of lifetime passive and active smoking exposure among postmenopausal women.

Design Prospective cohort study. Setting 40 clinical centres in the United States. Participants 79?990 women aged 50–79 enrolled in the Women’s Health Initiative Observational Study during 1993–8. Main outcome measures Self reported active and passive smoking, pathologically confirmed invasive breast cancer.

Results In total, 3520 incident cases of invasive breast cancer were identified during an average of 10.3 years of follow-up. Compared with women who had never smoked, breast cancer risk was elevated by 9% among former smokers (hazard ratio 1.09 (95% CI 1.02 to 1.17)) and by 16% among current smokers (hazard ratio 1.16 (1.00 to 1.34)). Significantly higher breast cancer risk was observed in active smokers with high intensity and duration of smoking, as well as with initiation of smoking in the teenage years. The highest breast cancer risk was found among women who had smoked for =50 years or more (hazard ratio 1.35 (1.03 to1.77) compared with all lifetime non-smokers, hazard ratio 1.45 (1.06 to 1.98) compared with lifetime non-smokers with no exposure to passive smoking). An increased risk of breast cancer persisted for up to 20 years after smoking cessation. Among women who had never smoked, after adjustment for potential confounders, those with the most extensive exposure to passive smoking (=10 years’ exposure in childhood, =20 years’ exposure as an adult at home, and =10 years’ exposure as an adult at work) had a 32% excess risk of breast cancer compared with those who had never been exposed to passive smoking (hazard ratio 1.32 (1.04 to 1.67)). However, there was no significant association in the other groups with lower exposure and no clear dose response to cumulative passive smoking exposure.

Conclusions Active smoking was associated with an increase in breast cancer risk among postmenopausal women. There was also a suggestion of an association between passive smoking and increased risk of breast cancer.

Source: BMJ 2011; 342:d1016

Admiral Regina M. Benjamin, released a new report that shows that tobacco smoke, even occasional smoking or secondhand smoke, damages the human body and leads to disease and death.

The 700-page report, “A Report of the Surgeon General: How Tobacco Smoke Causes Disease-The Biology and Behavioral Basis for Smoking,” finds that cellular damage and tissue inflammation from tobacco smoke are immediate, and that repeated exposure weakens the body’s ability to heal the damage.

Even brief exposure to secondhand smoke can cause cardiovascular disease and could trigger acute cardiac events, such as heart attack. The report describes how chemicals from tobacco smoke quickly damage blood vessels and make blood more likely to clot. The evidence in this report shows how smoking causes cardiovascular disease and increases risks for heart attack, stroke, and aortic aneurysm.

The report also explains why it is so difficult to quit smoking. According to the research, cigarettes are designed for addiction. The design and contents of current tobacco products make them more attractive and addictive than ever before. Today’s cigarettes deliver nicotine more quickly and efficiently than cigarettes of many years ago.

You can read the full report at www.surgeongeneral.gov. Last week, CADCA hosted a webinar on tobacco cessation and smoking prevention. A recording of this session, as well as the PowerPoint presentations used during the session, can be accessed online.

Source: www.cadca.org Dec. 2010

Teens may smoke to “self-medicate” against depression, but researchers in Canada say smoking may increase depressive symptoms in some adolescents.

Lead author Michael Chaiton of the Ontario Tobacco Research Unit of the University of Toronto and co-author Jennifer O’Loughlin of the University of Montreal Hospital Research Centre say the study involved 662 high-school teenagers who completed as many as 20 questionnaires from grades 7-11 about their use of cigarettes to affect mood.

Study participants were divided into groups of: teens who never smoked; smokers who did not use cigarettes to self-medicate, improve mood or physical state; and smokers who used cigarettes to self-medicate. Study participants were asked to rate on a rating scale depressive symptoms such as: felt too tired to do things; had trouble going to sleep or staying asleep; felt unhappy, sad, or depressed; felt hopeless about the future; felt nervous or tense; and worried too much about things.

Smokers who used cigarettes as mood enhancers had higher risks of elevated depressive symptoms than teens who had never smoked, researchers concluded.

Source: Journal of Addictive Behaviors.Sept 2010

A new study from the David Geffen School of Medicine at UCLA suggests that increasing cigarette taxes could be an effective way to reduce smoking among individuals with alcohol, drug or mental disorders.

The study, published online in the American Journal of Public Health, found that a 10 percent increase in cigarette pricing resulted in an 18.2 percent decline in smoking among people in these groups.

The findings demonstrate that increasing cigarette taxes could be a way to curb smoking, which is still the leading preventable cause of death in the United States, according to the study’s lead author, Dr. Michael Ong, an assistant professor of medicine in the division of general internal medicine and health services research at the Geffen School of Medicine.
“Whatever we can do to reduce smoking is critical to the health of the U.S.,” said Ong, who is also a researcher at UCLA’s Jonsson Cancer Center. “Cigarette taxes are used as a key policy instrument to get people to quit smoking, so understanding whether people will really quit is important.

Individuals with alcohol, drug or mental disorders comprise 40 percent of remaining smokers, and there is little literature on how to help these people quit smoking.”

Prior research on the effect of cigarette pricing on smoking, which had been conducted using information from 1991, suggested that individuals with mental illness were less likely than other individuals to quit due to price increases. Unlike that research, however, the current study expanded the research to include people with alcohol and drug disorders.

The researchers based their work on data from 7,530 individuals from the 2000-01 Healthcare for Communities Household Survey. Of those, 2,106 people, or 23 percent, had alcohol, drug or mental disorders during the previous year. Of that group, 43.8 percent were smokers — a much higher proportion than among rest of the population.

Though the researchers found that people with alcohol dependence did not cut down on cigarettes when prices rose, people with binge-drinking problems, substance-use disorders and mental disorders were significantly more likely to quit smoking if prices rose, as would occur with a cigarette tax increase.

While the study does suggest that increasing cigarette prices through taxation could reduce smoking among individuals with alcohol, drug or mental disorders, the authors note that further study is needed to determine if recent cigarette price increases have reduced smoking among individuals with such disorders, and whether the identified association is causal.

Source: http://www.sciencedaily.com/releases June 3, 2010

It is well-known that maternal smoking during pregnancy can have long-term effects on the physical health of the child, including increased risk for respiratory disease, ear infections and asthma. New research shows that prenatal smoking also can lead to psychiatric problems and increase the need for psychotropic medications in childhood and young adulthood.

Finnish researchers found that adolescents who had been exposed to prenatal smoking were at increased risk for use of all psychiatric drugs especially those uses to treat depression, attention-deficit/hyperactivity disorder (ADHD) and addiction compared to non-exposed youths. The study was presented Tuesday, May 4 at the Pediatric Academic Societies (PAS) annual meeting in Vancouver, British Columbia, Canada.

“Recent studies show that maternal smoking during pregnancy may interfere with brain development of the growing fetus,” said Mikael Ekblad, lead author of the study and a pediatric researcher at Turku University Hospital in Finland. “By avoiding smoking during pregnancy, all the later psychiatric problems caused by smoking exposure could be prevented.”

Ekblad and his colleagues collected information from the Finnish Medical Birth Register on maternal smoking, gestational age, birthweight and 5-minute Apgar scores for all children born in Finland from 1987 through 1989. They also analyzed records on mothers’ psychiatric inpatient care from 1969-1989 and children’s use of psychiatric drugs.

Results showed that 12.3 percent of the young adults had used psychiatric drugs, and of these, 19.2 percent had been exposed to prenatal smoking.

The rate of psychotropic medication use was highest in young adults whose mothers smoked more than 10 cigarettes a day while pregnant (16.9 percent), followed by youths whose mothers smoked fewer than 10 cigarettes a day (14.7 percent) and unexposed youths (11.7 percent).

The risk for medication use was similar in males and females, and remained after adjusting for risk factors at birth, such as Apgar scores and birthweight, and the mother’s previous inpatient care for mental disorders.

Smoking exposure increased the risk for use of all psychotropic drugs, especially stimulants used to treat ADHD (unexposed: 0.2 percent; less than 10 cigarettes/day: 0.4 percent; and more than 10 cigarettes/day: 0.6 percent) and drugs for addiction. An increased risk for use of drugs to treat depression also was seen (unexposed: 6 percent; less than 10 cigarettes/day: 8.6 percent; and more than 10 cigarettes/day: 10.3 percent).

“Smoking during pregnancy is still quite common even though the knowledge of its harmful effects has risen in recent years,” Ekblad concluded. “Recent studies have shown that smoking during pregnancy has negative long-term effects on the health of the child. Therefore, women should avoid smoking during their pregnancy.”

Source: MediLexicon International Ltd 6th May 2010
American Academy of Pediatrics

The brain’s nucleus accumbens (NAC) is a core region of the mesocorticolimbic dopaminergic system and is interconnected with the ventral tegmental area (VTA) and the prefrontal cortex. The mesocorticolimbic system is thought to be central to the reinforcing effects of many drugs and plays an important role in addiction. A new study has found that alcohol abuse elevated the expression of a distinct set of genes in the NAC and VTA, while nicotine blunted this effect in the VTA.

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“In spite of their differences in pharmacology, alcohol and tobacco consumption are often intimately linked,” said Traute Flatscher-Bader, a postdoctoral research fellow at The University of Queensland and corresponding author for the study. “Nonetheless, the molecular mechanisms that underlie alcohol and nicotine abuse, and particularly their co-abuse, are still incompletely understood.”

“One thing that researchers have encountered is that it is often difficult to find ‘pure’ alcoholics, that is, alcoholics that only abuse alcohol and nothing else,” agreed Simon Worrall, director of postgraduate coursework programs in molecular biology at The University of Queensland. “Many alcoholics are poly-drug abusers, with the most common other drug being nicotine. Thus, many studies which have studied the effects of alcohol on the brain and other organs have been compromised because they have not taken account of the effects of nicotine addiction which is often superimposed on the effects of alcohol addiction.”

In the first part of the current study, Flatscher-Bader and her colleagues used DNA microarray technique to study the expression of many thousands of genes in the brains of non-smoking and smoking alcoholics and non-drinking smokers.

“We examined the impact of alcoholism and smoking on gene expression in the NAC in 20 chronic alcohol abusers and controls with and without recent smoking history,” said Flatscher-Bader. “The results revealed that in this brain region, the abuse of alcohol and nicotine had distinct effects on the expression of genes. In addition, altered expression of a number of genes was associated with both alcohol and nicotine abuse. Within the latter group was a set of genes which play a crucial role in a molecular pathway regulating cell structure.”

The researchers then went on to investigate in more detail the altered expression of six selected genes within the pathway regulating cell structure in two brain regions, using 30 cases comprised again of smoking and non-smoking controls and alcohol abusers. For this part of the study they used the method called “real time polymerase chain reaction.”

“This expanded investigation revealed that one of the genes, called RHOA, was elevated by alcohol abuse and its highest expression was evident in the smoking alcoholics in both brain regions,” said Flatscher-Bader. “The RHOA gene had previously been implicated in the initiation of tobacco smoking. In the NAC, the expression of a further four of the six selected genes was increased by alcohol abuse. Interestingly, the highest expression for each of the genes in the NAC was in the smoking alcoholics. In the other brain region called the VTA, alcohol abuse had a similar effect and elevated the expression of all six selected genes. In contrast to the NAC, however, concurrent smoking dampened the induction of five of these alcohol-sensitive genes in the VTA.”

“Many studies have analyzed the changes in gene expression in this brain system to try to untangle the molecular pathology of alcohol addiction,” said Worrall, “but this is amongst the first to take into account the effect of co-administration of nicotine with alcohol.

Flatscher-Bader stressed that there are several cell types in the brain and there are several steps between gene expression and impact on cell structure and function. “It has to be emphasized that our study is important as a first step in identifying molecular pathways underlying the effects of alcohol abuse and smoking and their co-joint abuse on the human NAC and VTA, “she said. “It now needs to be tested if our findings are, indeed, associated with changes to neuronal structure and function.”

“A better understanding of the molecular basis of withdrawal may help in the development of new treatments to ameliorate the symptoms,” added Dr Worrall. “Not many previous studies took into account the potential effects of nicotine addiction that may be superimposed on top of those from alcohol, so these results may help clinicians better use present therapy/drugs to treat patients abusing both alcohol and/or nicotine and may also lead to the development of new drugs.”

Source: www.medicalnewstoday.com 5.5.2010

The brain’s nucleus accumbens (NAC) is a core region of the mesocorticolimbic dopaminergic system and is interconnected with the ventral tegmental area (VTA) and the prefrontal cortex. The mesocorticolimbic system is thought to be central to the reinforcing effects of many drugs and plays an important role in addiction. A new study has found that alcohol abuse elevated the expression of a distinct set of genes in the NAC and VTA, while nicotine blunted this effect in the VTA.

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“In spite of their differences in pharmacology, alcohol and tobacco consumption are often intimately linked,” said Traute Flatscher-Bader, a postdoctoral research fellow at The University of Queensland and corresponding author for the study. “Nonetheless, the molecular mechanisms that underlie alcohol and nicotine abuse, and particularly their co-abuse, are still incompletely understood.”

“One thing that researchers have encountered is that it is often difficult to find ‘pure’ alcoholics, that is, alcoholics that only abuse alcohol and nothing else,” agreed Simon Worrall, director of postgraduate coursework programs in molecular biology at The University of Queensland. “Many alcoholics are poly-drug abusers, with the most common other drug being nicotine. Thus, many studies which have studied the effects of alcohol on the brain and other organs have been compromised because they have not taken account of the effects of nicotine addiction which is often superimposed on the effects of alcohol addiction.”

In the first part of the current study, Flatscher-Bader and her colleagues used DNA microarray technique to study the expression of many thousands of genes in the brains of non-smoking and smoking alcoholics and non-drinking smokers.

“We examined the impact of alcoholism and smoking on gene expression in the NAC in 20 chronic alcohol abusers and controls with and without recent smoking history,” said Flatscher-Bader. “The results revealed that in this brain region, the abuse of alcohol and nicotine had distinct effects on the expression of genes. In addition, altered expression of a number of genes was associated with both alcohol and nicotine abuse. Within the latter group was a set of genes which play a crucial role in a molecular pathway regulating cell structure.”

The researchers then went on to investigate in more detail the altered expression of six selected genes within the pathway regulating cell structure in two brain regions, using 30 cases comprised again of smoking and non-smoking controls and alcohol abusers. For this part of the study they used the method called “real time polymerase chain reaction.”

“This expanded investigation revealed that one of the genes, called RHOA, was elevated by alcohol abuse and its highest expression was evident in the smoking alcoholics in both brain regions,” said Flatscher-Bader. “The RHOA gene had previously been implicated in the initiation of tobacco smoking. In the NAC, the expression of a further four of the six selected genes was increased by alcohol abuse. Interestingly, the highest expression for each of the genes in the NAC was in the smoking alcoholics. In the other brain region called the VTA, alcohol abuse had a similar effect and elevated the expression of all six selected genes. In contrast to the NAC, however, concurrent smoking dampened the induction of five of these alcohol-sensitive genes in the VTA.”

“Many studies have analyzed the changes in gene expression in this brain system to try to untangle the molecular pathology of alcohol addiction,” said Worrall, “but this is amongst the first to take into account the effect of co-administration of nicotine with alcohol.

Flatscher-Bader stressed that there are several cell types in the brain and there are several steps between gene expression and impact on cell structure and function. “It has to be emphasized that our study is important as a first step in identifying molecular pathways underlying the effects of alcohol abuse and smoking and their co-joint abuse on the human NAC and VTA, “she said. “It now needs to be tested if our findings are, indeed, associated with changes to neuronal structure and function.”

“A better understanding of the molecular basis of withdrawal may help in the development of new treatments to ameliorate the symptoms,” added Dr Worrall. “Not many previous studies took into account the potential effects of nicotine addiction that may be superimposed on top of those from alcohol, so these results may help clinicians better use present therapy/drugs to treat patients abusing both alcohol and/or nicotine and may also lead to the development of new drugs.”

Source: www.medicalnewstoday.com 5.5.2010

A Canadian-led international study finds that the causes of a heart attack are the same for people throughout the world, with cigarette smoking one of the main risk factors, the “There hasn’t been a study like this ever in the world,” said lead investigator Dr. Salim Yusuf, head of the Population Health Research Institute at McMaster University in Hamilton. “The risk factors that we’ve been able to measure account for 90 percent or more of heart disease. The impact of these risk factors in developing heart disease is global. It’s there in every ethnic group, in men, in women, in every region of the world, in young and old. It means we should be able to prevent the majority of premature heart attacks in the world.”

The research concluded that cigarette smoking and a poor ratio of bad to good cholesterol contribute to two-thirds of all heart attacks worldwide.

The five-year study involved 30,000 people in 52 countries. About half of the participants had suffered a heart attack. They were compared to an equal number of people with no heart disease, matched for age, sex, and city of residence.

“So now we’ll say: What causes the risk factor, not what causes the disease. And from a public-health point of view, there should be no more wallowing about that we need more information. We’ve got it,” said Dr. Sonia Anand, a specialist in vascular medicine and a member of the McMaster research team.

The latest figures show that 15 million people died from heart attacks worldwide in 1998. “The important issue is that the risk factors outlined in this study, the vast majority of them are modifiable,” said Toronto cardiologist Anthony Graham, a spokesman for the Heart and Stroke Foundation of Canada. “And what it suggests is that tobacco control is going to be as important in the developing world as it is in the western world.”

The study’s findings are published in issue of the British medical journal
Source: The Lancet. Sept. 11 2004

New research suggests that people who smoke and drink heavily are more at risk for oral cancer, the Researchers from King’s College in London, England, found an increase in oral cancer among men and women in their 20s and 30s who smoke and binge drink.

The researchers said that when tobacco smoke combines with alcohol, it produces dangerous levels of cancer-causing chemicals that attack the lining of the mouth.

“Our data show that smoking, drinking and poor diet are major risk factors, and that the younger people start smoking and drinking, the higher the risk,” said Newell Johnson, a professor of oral pathology at King’s College

Source: Daily Telegraph, London reported Nov. 9.2004

SMOKERS who suffer damage to a particular part of their brains appear to be able to quit their nicotine habit easily – a discovery that might open new avenues of addiction research.
A study of smokers who had suffered brain damage of various kinds after a stroke showed that those with injuries to a part of the brain called the insula were in many cases able to quit smoking quickly and easily – saying they had lost the urge to smoke altogether.
The insula receives information from the body and translates it into subjective feelings such as hunger, pain and craving, including craving for drugs.
However, the insula has not attracted much attention in studies on drug addiction, according to the research in the latest edition of the journal Science.
Deliberately damaging people’s insulas is not considered a realistic treatment option, because the risks are too great and the insula also has a role in many essential functions, such as the desire to eat.
But in the long term, the authors said, drugs might be developed to target the insula.
Other techniques for affecting the insula might in future also include electrical stimulation, already used in patients with depression. However, current techniques cannot penetrate the brain deeply enough to reach the insula.
The study was inspired by the experience of a man who had smoked 40 cigarettes a day before his insula was damaged in a stroke. He quit smoking immediately after, telling researchers his body “forgot the urge to smoke”.
Additional reporting: The Times

Source: news.com.au January 27th 2007

Fact sheet September 2006

Overall Mortality
• Tobacco use is the leading preventable cause of death in the United States.1 Cigarette smoking causes an estimated 438,000 deaths, or about 1 of every 5 deaths, each year.2,3 This estimate includes approximately 38,000 deaths from secondhand smoke exposure.2

• Cigarette smoking kills an estimated 259,500 men and 178,000 women in the United States each year.2

• More deaths are caused each year by tobacco use than by all deaths from human immunodeficiency virus (HIV), illegal drug use, alcohol use, motor vehicle injuries, suicides, and murders combined.2,4

• On average, adults who smoke cigarettes die 14 years earlier than nonsmokers.5

• Based on current cigarette smoking patterns, an estimated 25 million Americans who are alive today will die prematurely from smoking-related illnesses, including 5 million people younger than 18.6
Mortality from Specific Diseases
• Lung cancer (124,000), heart disease (108,000), and the chronic lung diseases of emphysema, bronchitis, and chronic airways obstruction (90,000) are responsible for the largest number of smoking-related deaths.2

• The risk of dying from lung cancer is more than 22 times higher among men who smoke cigarettes and about 12 times higher among women who smoke cigarettes compared with never smokers.7

• Since 1950, lung cancer deaths among women have increased by more than 600%.1 Since 1987, lung cancer has been the leading cause of cancer-related deaths in women.1

• Cigarette smoking results in a two- to three-fold increased risk of dying from coronary heart disease.7

• Cigarette smoking is associated with a ten-fold increased risk of dying from chronic obstructive lung disease.6 About 90% of all deaths from chronic obstructive lung diseases are attributable to cigarette smoking.1,7

• Pipe smoking and cigar smoking increase the risk of dying from cancers of the lung, esophagus, larynx, and oral cavity.8 Smokeless tobacco use increases the risk for developing oral cancer.8,9
References
1. U.S. Department of Health and Human Services. Women and Smoking: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2001. Available at: http://http://www.cdc.gov/tobacco/sgr/sgr_forwomen/index.htm. Accessed December 2006.

2. CDC. Annual Smoking–Attributable Mortality, Years of Potential Life Lost, and Productivity Losses — United States, 1997–2001. MMWR 2005: 54(25) 625-628. Available at http://0-www.cdc.gov.mill1.sjlibrary.org:80/mmwr/preview/mmwrhtml/mm5425a1.htm. Accessed: September 2006.

3. CDC. Health United States, 2005 With Chartbook on Trends in the Health of Americans. ( PDF–119KB) Hyattsville, MD: U.S. Department of Health and Human Services, CDC, National Center for Health Statistics; 2006. Accessed September 2006.

4. McGinnis J, Foege WH. Actual causes of death in United States. Journal of American Medical Association 1993;270:2207–2212.

5. CDC. Annual smoking-attributable mortality, years of potential life lost, and economic costs—United States, 1995–1999. MMWR 2002; 51(14):300–303. Accessed September 2006.

6. CDC. Perspectives in disease prevention and health promotion, smoking-attributable mortality and years of potential life lost—United States, 1984. MMWR 1997;46:444–451. Available at: http://0-www.cdc.gov.mill1.sjlibrary.org:80/mmwr/preview/mmwrhtml/00047690.htm. Accessed February 2004.

7. Novotny TE, Giovino GA. Tobacco use. In: Brownson RC, Remington PL, Davis JR (eds). Chronic Disease Epidemiology and Control. Washington, DC: American Public Health Association; 1998;117–148.

8. U.S. Department of Health and Human Services. Reducing the Health Consequences of Smoking—25 Years of Progress: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, CDC; 1989. DHHS Pub. No. (CDC) 89–8411. Available at: http://profiles.nlm.nih.gov/NN/B/B/X/S/. Accessed September 2006.

9. U.S. Department of Health and Human Services. The Health Consequences of Using Smokeless Tobacco: A Report of the Advisory Committee to the Surgeon General, 1986. Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service. NIH Pub. No. 86–2874. Accessed September 2006.
Note: More recent information may be available at the CDC’S Office on Smoking and Health Web site: http://0-www.cdc.gov.mill1.sjlibrary.org:80/tobacco.

Source: Centers for Disease Control and Prevention
National Center for Chronic Disease Prevention and Health Promotion
Office on Smoking and Health. tobaccoinfo@cdc.gov Sept.2006

Summary

DURHAM, N.C. — Within the mind of every smoker trying to quit rages a battle between the higher-order functions of the brain wanting to break the habit and the lower-order functions screaming for another cigarette, say researchers at Duke University Medical Center. More often than not, that cigarette gets lit.
Brain scans of smokers studied by the researchers revealed three specific regions deep within the brain that appear to control dependence on nicotine and craving for cigarettes. These regions play important roles in some of the key motivations for smoking: to calm down when stressed, to achieve pleasure and to help concentration.
“If you can’t calm down, can’t derive pleasure and can’t control yourself or concentrate, then it will be extremely difficult for you to break the habit,” said lead study investigator Jed E. Rose, Ph.D., director of the Duke Center for Nicotine and Smoking Cessation Research. “These brain regions may explain why most people try to quit several times before they are successful.”
Understanding how the brain responds to cigarette cravings can help doctors change nicotine cessation treatments to address all three of these components of withdrawal, Rose said. Drugs or therapies that target these regions may help smokers stave off the cravings that often spoil their attempts to quit.
The team’s findings are now online in the journal Neuropsychopharmacology. The research was funded by Phillip Morris USA.
Approximately one in five Americans smokes. Even though 70 percent of smokers report that they would like to quit, only 5 percent do so successfully.
In this study, the researchers manipulated the levels of nicotine dependence and cigarette craving among 15 smokers and then scanned their brains using positron emission tomography, or PET scans, to see which areas of the brain were most active.
Three specific regions of the brain demonstrated changes in activity when the smokers craved cigarettes versus when they did not.
One region that lights up, called the thalamus, is considered to be the key relay point for sensory information flowing into the brain. Some of the symptoms of withdrawal among people trying to quit stem from the inability to focus thoughts and the feeling of being overwhelmed, and could thus be explained by changes in this region, according to the researchers. The researchers found that changes in this region were most dramatic among those who said they smoked to calm down when under stress.
Another region that lights up is a part of the pleasure system of the brain. Changes in this region, called the striatum, were most notable in people who smoked to satisfy craving and for pleasurable relaxation, the researchers said.
A third region that lights up, called the anterior cingulate cortex, is vital to cognitive functions such as conflict, self regulation, decision making and emotion. People whose brain scans showed the most differences in this region also reported that they smoked to manage their weight.
“This knowledge gives us new clues about brain mechanisms underlying addiction to cigarettes and could allow us design better methods to help smokers quit,” Rose said.
Rose and his colleagues are now planning to perform brain scans on smokers undergoing nicotine replacement therapy, such as the nicotine patch, to determine how these treatments affect the same regions of the brain.
Other researchers participating in the study were Frederique M. Behm, Alfred N. Salley, James E. Bates, R. Edward Coleman, Thomas C. Hawk and Timothy G. Turkington.

Source: www.dukemednews March 2007

* Popular and clinical lore support the strong connection between smoking and alcohol consumption.

* Adolescent smokers appear to have a greater vulnerability to developing alcohol-use disorders.

* Results indicate that smoking “primes” the brain for subsequent addiction to alcohol and possibly other drugs.

Both academic studies and casual observation support the view that smokers tend to drink, and drinkers tend to smoke. New research using nationally representative data from the U.S. finds that smokers – particularly adolescent smokers – clearly have a greater vulnerability to alcohol-use disorders (AUDs) than do non-smokers.

Results are published in the December issue of Alcoholism: Clinical & Experimental Research.

“Smoking and alcohol – separately, or together – account for more than 20 percent of deaths in the United States,” said Richard A. Grucza, an epidemiologist at Washington University School of Medicine and corresponding author for the study. “Cigarettes and alcohol are also known to be ‘gateway’ drugs, that is, the overwhelming majority of illegal drug users begin their use with one or both of these legal drugs.”

“We have known about the link between cigarette smoking and alcohol use for a while, but we have not really asked the question, as the authors here asked, whether use of one could increase the vulnerability of becoming addicted to the other,” said Kevin W Chen, associate professor at the University of Maryland School of Medicine.

“Ours was the first,” added Grucza, “to examine quantity of drinking in relationship to smoking and AUDs. Our central questions were: Can this association be explained by the fact that smokers are heavier drinkers, or is there something else going on? In other words, do smokers appear to be more sensitive to the effects of alcohol?” The short answer appears to be yes.

Researchers examined data from an aggregate of 2002 through 2004 U.S. National Surveys on Drug Use and Health. Randomly selected, household-dwelling adolescents and young adults (n=74,836) were selected from the non-institutionalized and civilian American population and queried about their drinking and smoking practices.

Results indicate that smokers – particularly adolescent smokers -have a greater vulnerability to AUDs than do non-smokers.

“In general, smokers were at more than a 50 percent higher risk, although the differences were larger in younger adolescents and among light drinkers,” said Grucza. “For example, among 15- to 17-year-olds who drank fewer than eight drinks in the month before the survey, more than 20 percent reported an AUD, compared with about five percent among the non-smoking group with the same level of drinking. We conclude that, although smokers do drink higher rates of alcohol, this alone does not explain their higher vulnerability to AUDs.”

Grucza said that these findings go beyond the popular view that bad behaviors like smoking and drinking to excess simply tend to “go together,” especially during adolescence. “It seems that smoking makes the adolescent brain more vulnerable to other addictions,” he said. “Addictive drugs all act on a part of the brain that is described as the ‘central reward circuitry.’” Once this system is exposed to one drug, the brain may become more sensitive to the effects of other drugs, as demonstrated by a number of rodent studies.

“Studies like this will set up an alert – for those who consider adolescent smoking tolerable – to rethink the issue, or perceive the problem differently,” noted Chen. “Although we do not know the exact causal relation between the two, the damage to our health is so severe that we need to create a more objective image to reject both smoking and drinking among adolescents.”

“Ours is the first study to – establish a correlation between adolescent smoking and AUDs that cannot be explained by heavier drinking,” said Grucza. “Now we, and hopefully others, need to investigate whether or not smoking actually causes adolescents to be more susceptible to AUDs. Our results are in line with an emerging literature that shows adolescence may be a unique window of vulnerability for addictions development. If it is proven that nicotine directly impacts vulnerability to alcoholism and other addictions, then that is a new, strong message to add to the health-education arsenal. However, even if this correlation is completely non-causal, these results can help to identify kids who are at risk for AUDs.”

Source:Alcoholism: Clinical & Experimental Research. (ACER) Article Date: 30 Nov 2006 – 13:00 PDT

Research in Archives of Dermatology observed the effect by looking at the upper part of the inner arm in smokers and non-smokers.

Previous studies have focused on the face, where skin can also be damaged by exposure to the sun.

But the University of Michigan, Ann Arbour, team say this study shows smoking alone makes the skin age, which may help persuade some to quit.

The researchers photographed 82 people’s upper inner right arms.

Participants were aged 22 to 91. Such a wide age range was used in order to record the natural state of old and young skin.
There is strong evidence suggesting cigarette smoke has a negative effect on the appearance of skin
Indy Rihal, British Skin Foundation

Half of those studied had a history of smoking and had smoked, on average, for 24 years.

The number of packs of cigarettes they smoked ranged from a quarter of a packet to four packs per day.

The team created a nine-point scale to measure damage to skin which is not exposed to the light.

In those aged over 65, there was almost a two-point difference between smokers and non-smokers.

In the over-45s, the difference was around a point.

Writing in Archives of Dermatology, the researchers led by Dr Yolanda Helfrich, said: “We found that the number of packs of cigarettes smoked per day, total years of smoking and pack-years of smoking [an average of packs per day over the number of years of smoking] were correlated with the degree of skin aging.

“After controlling for age and other variables, we found that only packs of cigarettes smoked per day was a major predictor of the degree of photo-protected skin ageing.”

Evidence ‘mounting up’

Dr Helfrich said: “Previous studies have shown that smokers have a greater degree of skin ageing, but those have looked at facial skin.

“There are some sceptics who said the sun was having some of the effect.

“We have demonstrated that there was a significant degree of damage just from smoking.”

She added: “The evidence is certainly mounting up that smoking is not good for you. This just adds to all of that.”

She said more research was needed to show exactly how smoking damaged the skin.

Indy Rihal, of the British Skin Foundation, said: “In addition to UV light from the sun and sun beds, cigarette smoke is a main environmental factor that causes changes in the skin often associated with ‘looking old’ such as coarse wrinkling and a sallow, leathery texture.

“There is strong evidence suggesting cigarette smoke has a negative effect on the appearance of skin.

“Smoking enhances an enzyme in the skin, matrix metalloproteinase-1, resulting in increased collagen breakdown and diminished collagen production. The overall effect causes wrinkling and inelasticity.

“In addition the constriction of tiny blood vessels in the skin caused by smoking reduces the oxygen supply to the skin negatively affecting skin health and appearance in general.”

Amanda Sandford, of Action on Smoking and Health (ASH) said: “This study provides further evidence of the detrimental effects that smoking can have on the skin.

“No amount of anti-ageing cream will remove the wrinkles caused by cigarettes so the best way for smokers to avoid the wrinkled prune look is to stop smoking.”

Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/1/hi/health/6466041.stm

Published: 2007/03/21 00:03:21 GMT

© BBC MMVII

Research Summary
A pair of new studies find that smokers take many more sick days annually than nonsmokers and perform worse when they are on the job, Bloomberg News reported March 29.
A Swedish study by Petter Lundborg and colleagues from Free University of Amsterdam found that smokers took an average of 34 sick days per year, compared to 20 per year for people who never smoked and 25 per year among former smokers.
Sweden has one of the highest rates of sickness absence in the industrialized world; in the U.S., the average worker takes off nine days annually for illness. “The results suggest that policies that reduce and/or prevent smoking may also reduce the number of days of sick leave,” wrote Lundborg.
In a study of women in the U.S. Navy, San Diego State University researcher Terry Conway and colleagues found that smokers were more likely to be discharged for medical reasons, bad behavior, misconduct, drug misuse and personality disorders. Smokers also were more apt to resign from the Navy before serving their full terms, and were paid less.
However, noted Conway, “Cigarette smoking might simply be a marker for other underlying factors such as nonconformity and high risk-taking, that contribute to poorer performance.”
The research was published in the journal Tobacco Control.

Source: Bloomberg News March 29 2007

Research Summary

Smoking among young adults has plummeted since California implemented a groundbreaking tobacco-control plan 12 years ago, according to new research from the University of California at San Diego.

The California Tobacco Control Program, established in 1989, has been credited with reducing smoking among all adult smokers, but the decline among young adults has been especially striking, researchers said. Notably, cessation rates among young Californians were higher than among young adults in New York and New Jersey, which have similarly high tobacco prices but lack comprehensive stop-smoking campaigns, as well as compared to young adults in tobacco-growing states (TGS).

“We were surprised to find that, since the advent of the California campaign, young people have increased their rate of quitting by 50 percent, far more than their older counterparts,” said study author Karen Messer, Ph.D. “It used to be that smokers over age 50 were the ones quitting because they understood the health consequences of smoking …
“These young adults have grown up in a tobacco-controlled climate, where smoking isn’t the norm and isn’t socially supported. We may be seeing the first generation who believe it’s not cool to smoke, which could pay huge dividends in their future health.”

Another UCLA study focused on tobacco consumption trends. “We found that there is a national trend of declining cigarette consumption for all age groups, but the most significant by far was observed in California smokers over age 35,” noted researcher Wael K. Al-Delaimy, M.D., Ph.D.
“The data suggest that — compared with states with no tobacco control initiatives (TGS) or states with an increased cigarette price as the principal tobacco control measure (NY/NJ) – California’s comprehensive tobacco control program is more effective in decreasing cigarette consumption for those over age 35.”

Source: journal Tobacco Control April 2007

A prescription-only pill with a high success rate in helping people to quit smoking is to become available on the NHS after a decision yesterday by the government’s drugs watchdog.
The National Institute for Clinical Excellence gave draft approval for the health service to provide varenicline, which is manufactured by Pfizer under the brand name Champix. Trials showed the twice-daily pill provided relief from cravings and withdrawal symptoms experienced by smokers in the weeks after quitting.

The manufacturers said it also reduced the satisfaction smokers would get from cigarettes in the event of a relapse.
During the trials, 44% of smokers had quit by the end of a 12-week course. This compared with a 30% success rate for the anti-smoking drug Zyban and 18% for smokers who were given a placebo.
The recommended 12-week course of treatment costs about £163.80.
Giving draft approval allows NHS trusts or professional bodies to register objections before a decision in July. NHS trusts would then have three months to make funding available. A spokeswoman for Nice said: “Having looked at all the evidence, our independent committee has concluded that varenicline appears to be a good way to help people who want to quit smoking.”
Robert West, professor of health psychology at University College London, said: “This guidance gives smokers who are serious about stopping another choice from a good range of clinically proven treatments. Smokers who combine treatments with the right support…could significantly increase their odds of successfully quitting for life.”

Source Thursday May 31, 2007 The Guardian

Nicotine reaches the brain as quickly as 10 seconds after inhalation, triggering feelings of pleasure, increasing heart rate and raising blood pressure.
But alongside the nicotine, smokers breathe in a deadly cocktail of chemicals including arsenic, formaldehyde and polonium.
“Cigarette smoke contains at least 69 different cancer-causing chemicals and thousands of other poisons which can increase the risk of several different types of cancer,” said Ed Yong of Cancer Research.
“Nicotine itself doesn’t cause cancer, it just keeps the smokers hooked,” he added.
Tobacco is so addictive that doctors writing in the Lancet medical journal this year said it should be classified as an illegal drug, on a par with amphetamines and barbiturates.
The government says 70 per cent of smokers want to give up but are held back by the power nicotine has over them.
Only one in five who try quitting manage to abstain for a year, while just three per cent succeed in breaking the habit by willpower alone, according to statistics compiled by health charity Action on Smoking and Health (ASH).
One in six smokers say they light up within five minutes of waking up, with half having their first cigarette inside the first 30 minutes of the day.
The government says 106,000 people die a year in Britain from smoking-related illnesses.
From July 1 smoking is banned in enclosed public spaces across all of the United Kingdom when England introduces its own prohibition to match those already in place in Scotland, Wales and Northern Ireland.
But while this may help many adults give up, there are some groups who will need much greater assistance, says ASH.
Around a quarter of all adults smoke but among the most disadvantaged, such as single parents on benefit, the rates are as high as 70 per cent.
“It’s a response to stress,” said ASH director Deborah Arnott. “If your life is very stressful then smoking seems to help in some way.”
She said such disadvantaged groups should be prescribed nicotine patches for longer periods than the usual maximum of 12 weeks to help them quit.
“It’s the nicotine they are addicted to, but it’s the smoke that’s killing them,” she said.
Prime Minister Gordon Brown cut the value added tax on nicotine replacement products to five per cent in his last budget as chancellor of the exchequer.
The tax break will last for a year but ASH says the price reduction should be made permanent to help the most addicted and disadvantaged.

Source: www.smh.com.au June 30, 2007

November 9, 2006

Men diagnosed with cancer are less likely to survive the disease if they were smokers or heavy drinkers. Smoking and drinking are well-known risk factors for cancer, but researchers have begun looking into how these addictions affect survivability, as well. Researcher Young Ho Yun and colleagues at the National Cancer Center in Goyang, South Korea tracked 14,578 cancer patients for about nine years and compared mortality data to patients’ history of smoking and alcohol use.
The researchers found that former smokers were more likely to die from any kind of cancer than nonsmoking cancer patients, possibly because smoking causes tumors to grow more aggressively. Smokers also may be less likely to get cancer screening tests, the authors noted, so their disease is often further advanced when treatment begins.
Among patients with head, neck, or liver cancer, heavy drinkers were more likely to die than nondrinkers, with risk increasing with consumption levels.
“Our findings suggest that groups at high risk of cancer need to be educated continually to improve their health behaviors — not only to prevent cancer, but also to improve prognosis,” the study authors noted.

Source: Journal of Clinical Oncology Nov. 1, 2006.

Reference:
Park, S.M., Lim, M.K., Shin, S.A., Yun, Y.H. (2006) Impact of Prediagnosis Smoking, Alcohol, Obesity, and Insulin Resistance on Survival in Male Cancer Patients: National Health Insurance Corporation Study. Journal of Clinical Oncology, 24(31): 5017-5024.

The truth youth anti-smoking campaign has the power to save hundreds of thousands of lives and billions of dollars in smoking related health care costs and productivity losses, according to the Citizens’ Commission to Protect the Truth, a group composed of every former U.S. Secretary of Health, Education and Welfare and Health and Human Services with the exception of Michael Leavitt; every former U.S. Surgeon General; and every former Director of the Centers for Disease Control and Prevention.
A recent study published in the American Journal of Preventive Medicine indicated that the medical care costs averted by the truth® campaign – due to prevention of smoking – were far greater than the costs of the campaign itself and found that for every dollar invested in truth®, it is estimated that society saved over $6.80. The study focused on the period of 2000–2002. During this period of time, the truth® campaign has been credited with reducing the number of children and teen smokers by 300,000.
We believe that if the truth® campaign continues for another five years (2009-2014) with similar effectiveness, there will be up to 500,000 fewer youth smokers with savings of up to $9.0 billion in future medical costs.
The Commission based its analysis on the findings of the study presented in the May 2009 issue of the American Journal of Preventive Medicine, which found that the decrease in the number of youth who initiated smoking as a result of truth® during the period of 2000–2002 may result in averting up to $5.4 billion in future medical costs.
According to the U.S. Centers for Disease Control and Prevention, one-third of young smokers will die prematurely from smoking-related diseases. Since 80% of adult smokers began using tobacco products before the age of 18, the hundreds of thousands of children who opt not to smoke because of their exposure to truth® will almost certainly not become adult smokers.
“Ending smoking by American children and teens is crucial to the health and cost of healthcare to our nation. The truth® campaign provides a return on investment that would make the greediest corporate CEOs salivate. The truth® campaign is one of the most effective investments in the history of public health,” said Joseph A. Califano, Jr., Commission Chairman and former U.S. Secretary of Health, Education, and Welfare who started the national anti-smoking campaign in 1978. “truth® is the only national smoking prevention campaign not directed by the tobacco industry which exposes the tactics of the tobacco industry, the truth about addiction, and the health effects and social consequences of smoking.”
The American Legacy Foundation’s life-saving truth® campaign is the largest national youth smoking prevention campaign and an extraordinary public health story. The campaign is a national peer-to-peer intervention that works. In its first two years, truth® was responsible for 22% of the overall decline in youth smoking—a decrease which represents approximately 300,000 fewer smokers. Peer reviewed studies, both old and new, underscore that truth® can inoculate teens against tobacco addiction. The truth® campaign’s successes are unassailable.
Source : Citizens Commission to Protect the Truth April 19, 2009

Nicotine addiction relies on brain receptors that have been difficult to fully study and characterize. Scientists at the University of Colorado in Boulder have demonstrated that an immunolabeling technique can effectively analyze receptor subunits.

Background: Nicotine’s effects on the brain are triggered upon its binding to nicotinic acetylcholine receptors, each of which consists of five subunits: two alphas, one beta, one delta and one gamma. Different combinations of these subunits produce different receptor subtypes, which may vary in their pharmacology, biophysical properties, and distribution. To more fully understand how to interfere with nicotine’s effects in the brain, scientists must first understand where these different receptors are and how they work. Two of the most important subunits, a4 and b2, have been hard to study because current study methods can only locate the fully assembled receptor unit. Researchers wanted to know if an alternative strategy of immunolabeling (i.e., using antibodies to tag individual proteins), which has been fraught with technical challenges, would be able to identify, map, and quantify separate subunits.

Study Design: Scientists at the University of Colorado worked with brain sections of mice genetically engineered to express particular a4 and b2 subunit combinations. Using a sensitive immunolabeling technique, they explored the expression of the a4 and b2 subunits at both the gene and protein levels. Additional mice strains, missing the subunits under study, were used as controls.

What They Found: The two predominant nicotinic receptor subtypes (a4 and b2) were reliably detected using immunolabeling. Expression of the a4 subunit protein was almost universally dependent on b2, whereas most, but not all, b2 subunit protein expression was a4-dependent.

Comments from the Authors: Immunolabeling using specific antibodies offers a powerful approach for mapping the distribution of nicotine receptor subunits and can produce reliable quantitative results.

What’s Next: Similar studies can be designed to locate other nicotine receptor subtypes. In many cases, the antibody recognition sites are inside the cell membrane. It will likely take alternative biochemical approaches to uncover these less accessible sites. A better understanding of receptor composition and function may eventually have important implications for developing interventions at the receptor level.

Source: The study, led by Dr. Paul Whiteaker of the Institute for Behavioral Genetics at the University of Colorado, Boulder, with Dr. Jon Lindstrom of the University of Pennsylvania, was published in volume 499, number 6, pages 1016-1038 (2006) of the Journal of Comparative Neurology.

Research Summary
There is compelling evidence that second hand smoke can trigger heart attacks, according to a new report from the Institute of Medicine (IOM), and people with heart conditions are urged to avoid exposure to tobacco smoke, the Associated Press reported Oct. 15.
The report, requested by the U.S. Centers for Disease Control and Prevention (CDC), said there is no safe level of exposure to second hand smoke, and that people with cardiovascular disease could risk heart attack with less than an hour’s exposure to environmental tobacco smoke, which restricts blood vessels and increases clotting.
“If you have heart disease, you really need to stay away from second hand smoke. It’s an immediate threat to your life,” said researcher Neal Benowitz of the University of California at San Francisco.
Benowitz added that everyone, in fact, should avoid second hand smoke, since many people who have heart disease are not aware of the problem if they have never had a heart attack. “Even if you think you’re perfectly healthy, second hand smoke could be a potential threat to you,” he said.
“The evidence is clear,” said CDC head Thomas Frieden. “Smoke-free laws don’t hurt business … but they prevent heart attacks in non-smokers.”
Researchers found “clear and consistent” evidence that smoking bans cut the rate of heart attacks, according to statistician Stephen Feinberg of Carnegie Mellon University, a member of the IOM committee that compiled the report.
Source: Associated Press Oct.15th 2009

Research Summary
A recent University of California at Riverside study found that second hand smoke from tobacco can lead to nonalcoholic fatty liver disease (NAFLD), which can cause fat to accumulate in the liver of people even if they drink moderately or don’t drink alcohol at all.
Researchers studied mice exposed to second hand smoke for a year and found that fat accumulated in their liver cells, a sign of NAFLD.
The researchers focused their attention on two main fat metabolism regulators that are also found in human cells: the protein that stimulates synthesis of fatty acids in the liver and AMPK (adenosine monophosphate kinase), which regulates that protein. They found that AMPK activity is inhibited when exposed to second hand smoke, leading the other protein to synthesize more fatty acids. The result is NAFLD, according to the report.
“Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development,” said Manuela Martins-Green, who led the study.
Source: Journal of Hepatology September 2009.

The heart attack rate fell 10 percent in England and 14 percent in Scotland after the U.K. countries imposed bans on public smoking, the Similar results are expected from a study in Wales.
“We always knew a public smoking ban would bring rapid health benefits, but we have been amazed by just how big and how rapid they are,” said John Britton, director of the U.K. Center for Tobacco Control Studies at Nottingham University. The research is expected to boost calls for further curbs on secondhand smoke, such as banning smoking in cars with children.
“Exposure to cigarette smoke induces rapid changes in blood chemistry, making it much more prone to clotting,” explained Ellen Mason, a senior cardiac nurse at the British Heart Foundation. “In someone who has narrowed or damaged coronary arteries, smoke exposure can tip the balance and cause a heart attack.”
The findings echo those in other nations where public smoking has been banned, such as France, Ireland and Italy.

Source: Sunday Times reported Sept. 13th.2009

Research Summary
A genetic study has found that children who were exposed to secondhand smoke are more likely to develop lung cancer as adults, according to researchers from the National Cancer Institute and the Mayo Clinic.
Childhood exposure to secondhand smoke raised lung-cancer risk even among study subjects who never smoked themselves. Researchers drew their conclusions in part from analysis of a gene called MBL2, known to increase susceptibility to respiratory diseases.
Source: Cancer Epidemiology, Biomarkers and Prevention. December 2009

Research Summary
Continuing to use nicotine patches or gums after cancer surgery — to say nothing of smoking — makes chemotherapy less effective, according to researchers at the University of South Florida.
The Associated Press reported April 2 that a study of lung-cancer patients found that nicotine appears to protect cancer cells from chemotherapy drugs like gemcitabine, cisplatin, and taxol. Srikumar Chellappan of the University of South Florida and colleagues studied the impact of nicotine on non-small cell lung cancer, the most common form of the disease.
“Our findings are in agreement with clinical studies showing that patients who continue to smoke have worse survival profiles than those who quit before treatment,” the study noted. “They also raise the possibility that nicotine supplementation for smoking cessation might reduce the response to chemotheraputic agents.”
Source: The research appears in the online edition of Proceedings of the National Academy of Sciences. Reported in Join Together April 2006

Babies born to women who smoke during pregnancy are more likely to have heart defects that are not related to genetics, Reuters reported April 9.
Researcher Sadia Malik of the University of Arkansas for Medical Sciences and colleagues compared more than 3,000 infants born with heart defects to a similar group of infants without heart problems. They found that heart defects were more common among children of women who smoked during the month before they became pregnant or during the first trimester of their pregnancy. Moreover, the risk of babies being born with heart problems was higher when mothers smoked more.
“If even a fraction of congenital heart defects and other birth defects could be prevented by decreasing maternal tobacco use, it would result in improved reproductive outcomes and a saving of millions of health care dollars,” the researchers said.
Source: April 2008 issue of the journal Pediatrics.

A new study found a link between secondhand smoke and sudden infant death syndrome (SIDS), the Toronto Globe and Mail reported Feb. 21.
The study was conducted by researchers at Toronto’s Hospital for Sick Children and the University of Maryland.
In analyzing 44 SIDS deaths, researchers found twice the amount of nicotine levels in the lung tissue of babies whose parents acknowledged that they were smokers than in babies who died of other causes.
“It’s biochemical proof that smoke is associated with SIDS,” said Gideon Koren, lead investigator and senior scientist at the hospital’s research institute. “Some parents may feel guilty, and probably we underestimate the contribution of smoking to the risk of SIDS.”
Koren said additional research is needed to determine which of the toxic substances in tobacco smoke increases the risk for SIDS.
The study’s findings also are raising questions as to whether parents should be held responsible for exposing their babies to tobacco-filled air at home.
“In light of this new research, we and other agencies will be looking at it and rethinking our position to see if a stronger position is more feasible,” said Gail Vandermeulen of the Ontario Association of Children’s Aid Societies.
Source: Journal of Pediatrics February. 2002

The children of women who smoke during pregnancy are at increased risk of suffering strokes or heart attacks later in life, a new study concludes.
Reuters reported March 2 that children of smokers — studied as young adults — were found to have thicker walls around the carotid arteries in their necks, making them more vulnerable to stroke and heart attacks. Children of women who smoked the most during pregnancy had the thickest arterial walls, researchers found.
“There is the possibility that the compounds in tobacco smoke go through the placenta and directly damage the cardiovascular system of the fetus,” said researcher Cuno Uiterwaal at the University Medical Center Utrecht in the Netherlands. “The damage appears to be permanent and stays with the children.”
Source: Findings presented at a recent American Heart Association conference in Orlando. March 5, 2007

A study from the United Kingdom finds that children of mothers who smoke have smaller lung volumes and are more at risk for serious lung disease later in life, Reuters reported Feb. 26.
The study by researchers at the University of Bristol and the University of Glasgow involved 2,000 men and women in their 30s, 40s, and 50s whose parents smoked and took part in a study in the 1970s.
After conducting respiratory tests, the researchers found that children of mothers who smoked had smaller lungs, regardless of whether they also smoked. In addition, these children were more at risk for chronic obstructive pulmonary disease (COPD). If they themselves smoked, the risk was as high as 70 percent.
“Our results suggest that the effects of maternal smoking on lung size are permanent,” said Dr. Mark Upton, lead author of the study.
Children from households where the father smoked, but not the mother, showed poorer lung function, but not as great as those whose mothers smoked.
Source: American Journal of Respiratory and Critical Care Medicine. Feb. 15, 2004

Children exposed to secondhand smoke at home are more likely to carry the streptococcus pneumonia bacteria in their nose and throat, according to Israeli researchers.
A study involving more than 200 children and their mothers found that 76 percent of children exposed to secondhand smoke carried the bacteria in their noses and throats, compared to 60 percent of those not exposed to smoking. The bacteria can cause minor illnesses like ear infections or more dangerous conditions like sinusitis, pneumonia, and meningitis.
Among the mothers, 32 percent of smokers carried the bacteria, compared to 15 percent of nonsmokers exposed to tobacco smoke and 12 percent of nonsmokers not exposed to secondhand smoke.
“Since carriage in the nose is the first step in causing disease, the increased rate of carriage suggests more frequent occurrence of the disease. Indeed, active and passive smoking are associated with increased rate of respiratory infectious diseases,” said lead study author David Greenberg, M.D. “This should definitely encourage the parents not to smoke in the presence of their child, especially if this child has predisposing factors such as asthma.”
Source: Clinical Infectious Diseases. April 1, 2006

Researchers have found that infants as young as three months old accumulate nicotine and carcinogens in their bodies when they are exposed to tobacco smoke, the Guardian reported May 12.
Authors of the study — the first to test smoking exposure on children so young — said that parents who smoking around infants could raise children’s’ risk of addiction, cancer, and other health problems later in life. “The take-home message is that parents should not smoke around their children, because they will suffer from the exposure,” said Stephen Hecht of the University of Minnesota cancer center.
The study of 144 children (ages three months to one year) who lived with family members who smoked found that 98 percent had nicotine in their urine, and 93 percent had cotinine, a marker for nicotine metabolism. Further, 47 percent of the infants had detectable levels of NNAL, a carcinogenic metabolite of cigarette smoke.
“Persistent exposure to environmental tobacco smoke in childhood could be related to cancer later in life,” said Hecht
Source: Cancer Epidemiology Biomarkers and Prevention. May 2006

Infants with at least one parent who smokes have higher levels of a nicotine metabolite in their bodies than the children of nonsmokers, the Guardian reported June 19.
Researchers from the University of Leicester and Warwick Medical School said the study showed that smoking parents are turning their infants into passive smokers, putting them in danger of breathing problems and crib death. “Babies and children are routinely exposed to cigarette smoke by their [caregivers] in the home without the legislative protection available to adults in public places,” the authors stated.
Babies whose mothers smoked had cotinine levels four times higher than children whose parents were both nonsmokers, while babies with fathers who smoked had cotinine levels twice as high.
Cotinine levels were higher among babies who shared a bed with their parents, and during the winter. “Higher cotinine levels in colder times of year may be a reflection of the other key factors which influence exposure to passive smoking, such as poorer ventilation or a greater tendency for parents to smoke indoors in winter,” the authors said.
Source: Archives of Diseases in Childhood. June 2007

Research Summary
Within five years of quitting former female smokers have no greater risk of dying from coronary heart disease than nonsmokers, according to a new study.
HealthDay News reported May 6 that while risk for other smoking-related health problems lingers longer, heart health seems to bounce back more quickly.
Lung-cancer risk persisted 30 years after quitting, however, and former smokers face higher odds of dying from chronic obstructive pulmonary disease for more than 20 years after quitting, the study found.
The study was conducted by researcher Stacey Kenfield of the Harvard School of Public Health and colleagues. “It’s never too early to stop, and it’s never too late to stop,” said Kenfield.
“This shows the power of quitting smoking,” said Jay Brooks, study co-author and chairman of hematology/oncology at Ochsner Health System in Baton Rouge, La. “We’ve known this for a number of years, but the beauty of this study is it is a very large and well-studied group of people. When I tell people to quit smoking, I say the effect of the heart precedes that of the lungs. If you’ve smoked, you need to be cognizant that you’re still at an increased risk of lung cancer.”
Source: May 7, 2008 issue of the Journal of the American Medical Association.

• Compared to 12- and 13-year olds who have frequent family dinners, those who have infrequent family dinners are six times likelier to use marijuana, four times likelier to use tobacco, and three times likelier to use alcohol.
• Compared to teens who attend religious services at least weekly, those who never attend services are more than twice as likely to try cigarettes, and twice as likely to try marijuana and alcohol.
• Compared to teens who have frequent family dinners, those who have infrequent family dinners are one and a half times likelier to report getting grades of C or lower in school. 

Source: www.casacolumbia.org   Sept.2009

A recent study published in the Journal of Epidemiology and Community Health has revealed that women who continue to smoke during pregnancy are more likely to have children with behavioral problems. Disturbances caused can show signs as early as when the child is three years old.
For the sake of the study, over 14,000 mothers and child pairs were observed. The pairs were picked from the millennium cohort study. All the children observed had been born between 2000 and 2001. Professor Kate Pickett from the Hull York medical school, University of York, carried out the research.
Mothers, who were categorized as light or heavy smokers with regards to the number of cigarettes they smoked each day during pregnancy, were given a questionnaire which required them to score their children’s behavior. While 12.5% women said they smoked lightly and 12.4% said they had stopped smoking altogether when pregnant, 10% admitted to smoking heavily all throughout the term.
Based on the data collected, the study confirmed that children whose mothers smoked heavily were two times more prone to behavioral problems, a thing which kept going down as the number of cigarettes smoked during pregnancy went down. According to the study, smoking when pregnant, damages the developing structure and functioning of the fetus’s brain. Boy fetuses are more prone to damage.
Source:www.topnews.net.nz 3/11/2009

A tiny genetic mutation is the key to understanding why nicotine–which binds to brain receptors with such addictive potency–is virtually powerless in muscle cells that are studded with the same type of receptorBy all rights, nicotine ought to paralyze or even kill us, explains Dennis Dougherty, the George Grant Hoag Professor of Chemistry at Caltech and one of the leaders of the research team. After all, the receptor it binds to in the brain’s neurons–a type of acetylcholine receptor, which also binds the neurotransmitter acetylcholine–is found in large numbers in muscle cells. Were nicotine to bind with those cells, it would cause muscles to contract with such force that the response would likely prove lethal. Obviously, considering the data on smoking, that is not what happens. The question has long been: Why not?

“It’s a chemical mystery,” Dougherty admits. “We knew something subtle had to be going on here, but we didn’t know exactly what.” That subtlety, it turns out, lies in the slight tweaking of the structure of the acetylcholine receptor in muscle cells versus its structure in brain cells.
The shape of the acetylcholine receptor, and the way the chemicals that bind with it contort themselves to fit into that receptor, is determined by a number of different weak chemical interactions. Perhaps most important is an interaction that Dougherty calls “underappreciated”–the cation-π interaction, in which a positively charged ion and an electron-rich π system come together.

Back in the late 1990s, Dougherty and colleagues had shown that the cation-π interaction is indeed a key part of acetylcholine’s ability to bind to the acetylcholine receptors in muscles. “We assumed that nicotine’s charge would cause it to do the same thing, to have the same sort of strong interaction that acetylcholine has,” says Dougherty. “But we found that it didn’t.”
This would explain why smoking doesn’t paralyze us; if the nicotine can’t get into the muscle’s acetylcholine receptors, it can’t cause the muscles to contract.

But how, then, does nicotine work its addictive magic on the brain? It took another decade for the scientists to be able to peek at what happens in brain cells’ acetylcholine receptors when nicotine arrives on the scene. Turns out that in brain cells, unlike in muscle cells, nicotine makes the exact same kind of strong cation-π interaction that acetylcholine makes in both brain and muscle cells. “In addition,” Dougherty notes, “we found that nicotine makes a strong hydrogen bond in the brain’s acetylcholine receptors. This same hydrogen bond, in the receptors in muscle cells, is weak.”

The cause of this difference in binding potency, says Dougherty, is a single point mutation that occurs in the receptor near the key tryptophan amino acid that makes the cation-π interaction. “This one mutation means that, in the brain, nicotine can cozy up to this one particular tryptophan much more closely than it can in muscle cells,” he explains. “And that is what allows the nicotine to make the strong cation-π interaction.”

Dougherty says the best way to visualize this change is to think of the receptor as a box with one open side. “In muscle cells, this box is slightly distorted, so that the nicotine can’t get to the tryptophan,” he says. “But in the brain, the box is subtly reshaped. That’s the thing: It’s the shape, not the composition, of the box that changes. This allows the nicotine to make strong interactions, to become very potent. In other words, it’s what allows nicotine to be addictive in the brain.”

“Several projects in our labs are converging on the molecular and cellular mechanisms of the changes that occur when the brain is repeatedly exposed to nicotine,” adds study coauthor Henry Lester, the Bren Professor of Biology at Caltech. “We think that the important events begin with the rather tight and selective interaction between nicotine and certain receptors in the brain. This Nature paper teaches us how this interaction occurs, at an unprecedented level of resolution.”
Dougherty notes that these findings might one day lead to better drugs to combat nicotine addiction and other neurological disorders. “The receptor we describe in this paper is an important drug target,” he says. “It might help pharmaceutical companies develop a better drug than nicotine to do the good things nicotine does–enhance cognition, increase attention–without being addictive and toxic.”

Source: Xiu et al. Nicotine binding to brain receptors requires a strong cation–π interaction. Nature, March 26, 2009; DOI: 10.1038/nature07768 Science Daily 29.03.09

The National Cancer Institute (NCI) released a report today, co-edited by University of Minnesota professor Barbara Loken, that reaches the government’s strongest conclusion to date that tobacco marketing and depictions of smoking in movies promote youth smoking. “There is now incontrovertible evidence that marketing of tobacco, and the depiction of smoking in the movies, promote youth smoking and can cause young people to begin smoking,” said Loken, professor of marketing at the Carlson School of Management and one of the report’s five scientific editors.
The 684-page monograph, “The Role of the Media in Promoting and Reducing Tobacco Use,” presents definitive conclusions that a) tobacco advertising and promotion are causally related to increased tobacco use, and b) exposure to depictions of smoking in movies causes youth smoking initiation. The report also concludes that while mass media campaigns can reduce tobacco use, youth smoking prevention campaigns sponsored by the tobacco industry are generally ineffective and may even increase youth smoking.
“The role of marketing in the success of the tobacco companies is conclusive,” according to Loken. “The report’s recommendations offer the best approach to employ marketing techniques and the media to help prevent a further increase in youth smoking.”
The NCI report reaches six major conclusions:
1. Cigarettes are one of the most heavily marketed products in the United States.
2. Tobacco advertising targets psychological needs of adolescents, such as popularity and peer acceptance. Advertising creates the perception that smoking satisfies these needs.
3. Even brief exposure to tobacco advertising influences adolescents’ perceptions about smoking, smokers, and adolescents’ intentions to smoke.
4. The depiction of cigarette smoking is pervasive in movies, occurring in 75 percent or more of contemporary box-office hits, with identifiable brands in about one-third of movies.
5. A comprehensive ban on tobacco advertising and promotion is an effective policy intervention that prevents tobacco companies from shifting marketing expenditures to permitted media.
6. The tobacco industry works hard to impede tobacco control media campaigns, including attempts to prevent or reduce their funding.
“This direct link between marketing and tobacco use is very powerful.” Loken said, “Anti-tobacco ads before films and a comprehensive ban on tobacco advertising are two effective strategies found to curb effects of tobacco images on youth. Now we need to use marketing to steer youth and others away from tobacco.”
The report provides the most current and comprehensive analysis of more than 1,000 scientific studies on the role of the media in encouraging and discouraging tobacco use. The report is Monograph 19 in the NCI’s Tobacco Control Monograph series examining critical issues in tobacco prevention and control. Research included in the review comes from the disciplines of marketing, psychology, communications, statistics, epidemiology and public health.Source: National Cancer Institute Report. National Press Club Release 21 August

New research suggests that it takes less exposure to tobacco to increase the risk of colorectal cancer among women than men.
Researchers Joseph C. Anderson, M.D., of the University of Connecticut and Zvi A. Alpern, M.D. of Stony Brook University conducted a large cross-sectional study, analyzing data on patients who underwent colonoscopies. Utilizing a measurement called “pack years” — determined by multiplying the number of cigarettes smoked per day by the number of years smoked — researchers compared the amount of tobacco exposure in men and women to increased colorectal cancer risk.
The analysis, controlling for age, body mass index and family history, showed that women who smoked up to 30 pack-years had an 82 percent greater risk for significant colorectal neoplasia than nonsmoking women, while men who smoked up to 30 pack-years showed 21 percent greater risk than nonsmoking men. Female smokers faced double the risk or more of colorectal cancer if they smoked less than 30 pack years, while men achieved the same level of risk only when they smoked more than 30 pack years.
The study was presented at the American College of Gastroenterology’s annual scientific meeting.
 
Source: Reported in Join Together Oct. 7 2008

Research SummaryJust as smoking causes hardening of the arteries, quitting smoking can improve arterial health, although recovery from arterial stiffness may take up to a decade, Reuters reported March 19.
Researcher Noor Ahmed Jatoi and colleagues compared current smokers, ex-smokers and people who never had smoked. “We categorized ex-smokers according to how long they were off cigarettes — under one year, more than one but less than 10 years and more than 10 years,” said Jatoi.
The researchers found that arterial health improved over with time once smokers quit, but only reached normal levels after more than a decade of abstinence.
The study was published in the journal Hypertension.

Source: Reported in Join Together March 23 2007

Source:Reported in Join Together April 2006

PURPOSE: To determine the risk for malignant primary adult-onset glioma (MPAG) associated with cigarette smoking and other lifestyle behaviors in a large, multiethnic, managed-care cohort. METHODS: The study population included a cohort of 133,811 subscribers to the Kaiser Permanente Medical Care Program of Northern California who had received a multiphasic health checkup and questionnaire between 1977 and 1985, were at least 25 years old at their start of follow-up, and had no prior history of benign or malignant brain tumors. In this cohort, patients were followed for up to 21 years for the development of MPAG. RESULTS: Risk for MPAG among women increased with increasing packs of cigarettes smoked per day (p-for-trend = 0.04), adjusting for cigar and pipe smoking, patient age, sex, race, education, alcohol use and coffee consumption. A similar pattern was not observed for men. Individuals who smoked marijuana at least once a month, adjusting for cigarette smoking (packs smoked per day) and for the factors noted above, had a 2.8-fold (CI = 1.3-6.2) increased risk for MPAG. Relative risk for MPAG increased with increasing consumption of coffee (p-for-trend = 0.05). CONCLUSIONS: Cigarette smoking was associated with an increased risk for MPAG among women but not among men. Individuals who smoked marijuana at least once a month had an increased risk for MPAG, although no dose-response relation was observed. Drinkers of >7 cups of coffee per day had a 70% increased risk for MPAG and smaller risk elevation for lower consumption. Alcohol usage was not associated with an increased risk for MPAG.
Source:   J Neurooncol. 2004 May;68(1):57-69

In a new study, researchers have determined that prenatal exposure to cigarette smoking, when combined with a specific genetic variant, places children at increased risk for aggressive behavior and other behavioral problems.
The study, led by scientists at the Institute for Juvenile Research at the University of Illinois at Chicago, identified a long-lasting influence on a child’s behavior precipitated by the monoamine oxidase A (MAOA) gene variant in conjunction with prenatal exposure to tobacco. MAOA is an enzyme which regulates key neurotransmitters in the brain. 
The genetic variant responsible for increased risk of behavioral problems differs between boys and girls, researchers said. In boys exposed to tobacco smoke prenatally, the low-activity MAOA (MAOA-L) gene variant was associated with increased disruptive social interactions, aggressive behavior, and serious rule-violating.
Among girls, the high-activity MAOA (MAOA-H) gene variant was associated with increased disruptive behavior. In addition, girls with both the MAOA-H variant and prenatal exposure to cigarette smoke had an increased “hostile attribution bias” — a tendency to perceive anger in a range of facial expressions — that was not seen among boys.
There was a higher risk of disruptive behavior for both boys and girls the more their mother smoked during pregnancy, according to the study.
“The tendency to over-perceive anger suggests the possibility that the combination of prenatal tobacco exposure and the MAOA risk variant affects the brain’s processing of emotional cues,” said Lauren Wakschlag, the study’s principal investigator. “Clearly, close attention to sex differences in these patterns will be critical for future studies,” she said.

Source:Join Together. March 16th 2009

Cigarette smoking is more strongly associated with head and neck cancers than drinking alcohol, according to a new study. The study found that smoking is responsible for a quarter of head and neck cancers among individuals who do not drink alcohol.

At least 75 percent of head and neck cancers are caused by a combination of cigarette smoking and drinking alcohol, but researchers have not known the individual contributions of these risk factors because people who smoke are more likely to drink than the general population and vice versa. In a new study, researchers sought to tease out the independent effect of each risk factor on head and neck cancer development.
Mia Hashibe, Ph.D., of the International Agency for Cancer Research in Lyon, France, and colleagues examined head and neck cancer risk among smokers who never drank alcohol and people who drink but never used tobacco products. They pooled data from 15 case–control studies, which included 10,244 head and neck cancer patients and 15,227 controls. About 16 percent of the patients and 27 percent of the controls never drank, and about 11 percent of the patients and 38 percent of the controls never smoked.
Cigarette smoking was associated with an increased risk of head and neck cancer–especially cancer of the larynx–among patients who never drank alcohol. About 24 percent of head and neck cancers were due to smoking among patients who never drank.
Drinking alcohol was also associated with greater risk of head and neck cancers among never smokers, but mainly for patients who drank three or more drinks per day. They had twice the risk of head and neck cancers as people who never drink. Only seven percent of head and neck cancers were due to drinking among never smokers.
“The major strength of our pooled analyses was assembly of a very large series of never users of tobacco and never drinkers among head and neck cancer patients and control subjects, which allowed us to examine head and neck cancer risks in detail and to explore differences in risks by cancer subsite, geographic region, and sex,” the authors write.
 
Source:  Journal of the National Cancer Institute  2007, May 16.  99: 777-789

Research Summary
Teenagers expect and want adults to discourage them from using tobacco, according to new research from the
Researcher Maria Nilsson evaluated the impact of an anti-smoking program, Tobacco-Free Duo, which started in 1993. The program targets children between the ages of 13-15 and includes adults supporting the teenagers in staying tobacco-free.
Nilsson found that smoking rates declined among adolescents in the program over a seven-year period, while no corresponding change was observed at the national level. In addition, one in four tobacco-using adults participating in the program stopped smoking in order to take part.
“Children expect adults to work against tobacco. They say this is important and that grown-ups can make a difference by showing a clear and positive commitment,” said Nilsson.
Survey results on 15-year-old smokers showed that close relationships with caring adults played an important role in getting teenagers to smoke less or stop smoking all together.
Source: Promoting Health in Adolescents: Preventing the Use of Tobacco. Umea University in Sweden, Science Daily reported May 5.

Smoking appears to be associated with an increased risk of acute and chronic pancreatitis, according to a new report. In addition, the risk of developing the disease may be higher in those who smoke more.

The occurrence of pancreatitis (an inflammation of the pancreas usually characterized by abdominal pain) has increased in recent decades, according to background information in the article. Acute and chronic pancreatitis are believed to be commonly caused by gallstone disease and excessive alcohol use, respectively. Studies have suggested that smoking may be associated with damage to the pancreas, but since smoking may be associated with alcohol use and risk of gallstone disease, it is difficult to note whether smoking is an independent risk factor for the disease.

Janne Schurmann Tolstrup, M.Sc., Ph.D., of the National Institute of Public Health, University of Southern Denmark, Copenhagen, and colleagues analyzed results from physical examinations and lifestyle habit self-administered questionnaires of 17,905 participants (9,573 women and 8,332 men) to determine if smoking was associated with an increased risk of acute or chronic pancreatitis independent of alcohol consumption and gallstone disease. Participants were followed up for an average of 20.2 years.

“Overall, 58 percent of the women and 68 percent of the men were current smokers, 15 percent of the women and 19 percent of the men were ex-smokers and 28 percent of the women and 13 percent of the men had never smoked,” the authors write. “Participants who at baseline reported smoking or being previous smokers had higher risks of developing acute and chronic pancreatitis compared with non-smokers.” By the end of the study, 235 participants (113 women and 122 men) had developed acute (160 cases) or chronic (97 cases) pancreatitis, with some participants having developed both. About 46 percent of pancreatitis cases were attributable to smoking in this group.

Although alcohol intake was associated with increased risk of pancreatitis, the risk of pancreatitis associated with smoking was independent of alcohol and gallstone disease.
“Apart from the epidemiologic evidence of an association between smoking and development of acute and chronic pancreatitis, a biological effect of smoking seems plausible because both animal studies and human studies have demonstrated changes of the pancreas and in pancreatic functioning after exposure to tobacco smoke,” they conclude.
This study was supported by grants from the Danish National Board of Health and the Danish Medical Research Council.

Source: Tolstrup et al. Smoking and Risk of Acute and Chronic Pancreatitis Among Women and Men: A Population-Based Cohort Study. Archives of Internal Medicine, 2009; 169 (6): 603 DOI: 10.1001/archinternmed.2008.601 ScienceDaily (Mar. 28, 2009)

ScienceDaily (Jan. 29, 2005) — Children who are exposed to environmental tobacco smoke (passive smoking) are at a higher risk of developing lung cancer as adults, says a paper in this week’s BMJ.

Those children exposed to passive smoking on a daily basis and for many hours are the most vulnerable – facing over treble (3.63) the risk of those who grew up in smoke-free environments.
Children experiencing passive smoke a few times a week are one and a half (1.45) times more likely to develop lung cancer, and those exposed daily but not for many hours faced twice (2.08) the risk.
In one of the most comprehensive studies into passive smoking of its kind, researchers looked at 303,020 people across Europe who had never smoked, or had stopped smoking by at least ten years. Within this group, 123,479 provided information on exposure to passive smoke, and researchers followed these participants’ progress for an average of seven years.
Of those who had known exposure to passive smoke (but were not smokers themselves), 97 had developed lung cancer, 20 more had upper respiratory cancers such as cancer of the larynx, and 14 died from chronic obstructive pulmonary disease during the seven follow-up years.
Former smokers faced up to twice the risk of respiratory diseases from passive smoke than those who’d never smoked. This may be because their lungs are already damaged, making them more at risk to the effects of environmental tobacco smoke, say the researchers.
This study significantly reinforces previous research into the cancerous effects of passive smoke, the authors conclude.

Source: British Medical Journal (2005, January 29). Passive Smoking In Childhood May Increase Risk Of Lung Cancer In Later Life. ScienceDaily. Retrieved May 12, 2009, from http://www.sciencedaily.com¬ /releases/2005/01/050128223746.htm

A new report from Perth’s Telethon Institute for Child Health Research has found a strong link between childhood ear infections and exposure to tobacco smoke.

The families of 100 Aboriginal children and 180 non-Aboriginal children participated in the Kalgoorlie Otitis Media Research Project, allowing the collection of social, demographic, environmental and biological data to investigate the causes of otitis media (middle ear infections). The children had regular ear examinations from birth until 2 years of age.
Chief Investigator Dr Deborah Lehmann, who heads the Institute’s infectious diseases research, said ear infections were the most common reason that young children see a doctor and can cause life-long problems.

“Up to 20 per cent of children have more than three ear infections between 1 and 2 years of age. If their hearing is damaged, it can seriously affect their educational outcomes and social circumstances in adulthood,” Dr Lehmann said.
“In Aboriginal children, these ear infections typically start at a younger age, are much more common and more likely to result in hearing loss.”
Key findings from the project include:
  Otitis media was diagnosed at least once in 74% of Aboriginal children and 45% of non-Aboriginal children.
  64% of Aboriginal children and 40% of non-Aboriginal children were exposed to environmental tobacco smoke.
  If we eliminated exposure to tobacco smoke we estimate that we could reduce ear infections by 27% in Aboriginal children and 16% in non-Aboriginal children
  The impact of passive smoking in the home on ear infections was reduced if the children also attended day care.
Dr Lehmann said there is evidence that passive smoking can increase the adherence of bacteria in the respiratory passages and depress the immune system.
“These results highlight the importance of reducing children’s exposure to passive smoking, and this is particularly important for Aboriginal people where the rates of both smoking and otitis media are high,” she said.

“Few Aboriginal children have access to formal childcare despite studies showing that it is an effective way to improve early development and educational outcomes for disadvantaged children. The fact that it could also reduce the burden of ear infections in Aboriginal children adds weight to calls for appropriate childcare facilities to be provided.”
The results are published in the latest edition of the Medical Journal of Australia.

Source: Telethon Institute for Child Health Research (2008, May 19). Ear Infections In Children Linked To Passive Smoking. ScienceDaily. Retrieved May 12, 2009, from http://www.sciencedaily.com¬ /releases/2008/05/080519110703.htm

Marijuana worsens breathing problems in current smokers with chronic obstructive pulmonary disease (COPD), according to a new study.  The study found that among people 40 and older, smokers were two-and-a-half times as likely as nonsmokers to develop COPD, while smoking cigarettes and marijuana together boosted the odds of developing COPD to three-and-a-half times the risk of someone who did not smoke either cigarettes or marijuana–in other words, adding marijuana smoking to cigarette smoking increased the risk by one-third, says Wan Tan, M.D., of St. Paul’s Hospital in Vancouver, British Columbia.
The odds of cigarette smokers having any respiratory symptoms was 2.36 times that of nonsmokers, while the odds of someone who smoked both cigarettes and marijuana having respiratory symptoms was 18 times that of someone who smoked neither–an eightfold jump in risk, Dr. Tan says.
“This study suggests an interaction between cigarettes and marijuana smoking. These findings have not been reported before, and they have a big public health implication,” Dr. Tan says.
A majority of cigarette smokers in the study were also marijuana smokers. In both younger and older adults in the study, 30% smoked both cigarettes and marijuana. Among younger cigarette smokers, 76% also smoked marijuana, while 58% of older cigarette smokers also smoked marijuana.
The findings come from a study of 648 adults ages 18 and older who answered questions on smoking, including their cigarette and marijuana use, and respiratory symptoms. Study subjects ages 40 and older had lung function tests.
The Vancouver researchers decided to study both marijuana and cigarette smoking because both cigarette and marijuana smoking is prevalent in their area, says Dr. Tan. They found that 49% of participants ages 18 to 39 and 46% of those 40 and older had smoked marijuana at least once. Among 18-39 year-olds, 17% said they currently smoked marijuana, compared with 13% in the 40+ age group. In the younger group, 31% said they had ever smoked cigarettes, and 16% were current smokers. In the 40+ group, 52% were ever-smokers while 16% were current smokers.

Source: American Thoracic Society (2007, May 23). Marijuana Worsens COPD Symptoms In Current Cigarette Smokers. ScienceDaily. Retrieved May 12, 2009

A new study finds that the development of bullous lung disease occurs in marijuana smokers approximately 20 years earlier than tobacco smokers.  A condition often caused by exposure to toxic chemicals or long-term exposure to tobacco smoke, bullous lung disease (also known as bullae) is a condition where air trapped in the lungs causes obstruction to breathing and eventual destruction of the lungs.
At present, about 10% of young adults and 1% of the adult population smoke marijuana regularly. Researchers find that the mean age of marijuana-smoking patients with lung problems was 41, as opposed to the average age of 65 years for tobacco-smoking patients.
The study “Bullous Lung Disease due to Marijuana” also finds that the bullous lung disease can easily go undetected as patients suffering from the disease may show normal chest X-rays and lung functions. High-resolution CT scans revealed severe asymmetrical, variably sized bullae in the patients studied. However, chest X-rays and lung functions were normal in half of them.
Lead author Dr. Matthew Naughton says, “What is outstanding about this study is the relatively young ages of the lung disease patients, as well as the lack of abnormality on chest X-rays and lung functions in nearly half of the patients we tested.”
He added, “Marijuana is inhaled as extremely hot fumes to the peak inspiration and held for as long as possible before slow exhalation. This predisposes to greater damage to the lungs and makes marijuana smokers are more prone to bullous disease as compared to cigarette smokers.”
Patients who smoke marijuana inhale more and hold their breath four times longer than cigarette smokers. It is the breathing manoeuvres of marijuana smokers that serve to increase the concentration and pulmonary deposition of inhaled particulate matter – resulting in greater and more rapid lung destruction.

Source: Respirology .Blackwell Publishing (2008, January 27). Marijuana Smokers Face Rapid Lung Destruction — As Much As 20 Years Ahead Of Tobacco Smokers. ScienceDaily. Retrieved May 12, 2009

New research suggests that smoking increases the production of osteopontin in the lungs, which contributes to the development of smoking-related lung disease.
Prasse et al. report their findings in the May 2009 issue of The American Journal of Pathology.   Nearly one billion people worldwide smoke tobacco products. Long-term exposure to compounds found in smoke can lead to both cardiovascular and lung disease. Although lung exposure to cigarette smoke leads to immune cell recruitment and tissue fibrosis, how cigarette smoke causes these changes is largely unknown.
To determine if osteopontin, a molecule that attracts immune cells, mediates cell recruitment in smokers, Prasse et al. compared osteopontin levels from smokers with different types of lung diseases, healthy smokers, and healthy non-smokers. They found high levels of osteopontin expression in patients with interstitial lung disease, whereas healthy smokers had lower levels, and healthy non-smokers produced no osteopontin. Osteopontin expression could be stimulated directly by nicotine treatment.
In addition, expressing osteopontin in rat lung resulted in recruitment of immune cells, resulting in symptoms similar to smoking-related interstitial lung diseases. These results indicate that osteopontin may be pathogenic in smoking-initiated lung disease.
The article from Prasse et al “suggest[s] that chronic nicotine stimulation induced by cigarette smoking promotes macrophage and Langerhans cell accumulation in the lung via an increase in [osteopontin production].” Osteopontin and cellular receptors for nicotine may therefore be new targets for treating smoking related lung disease.

Source: American Journal of Pathology (2009, May 2). New Mediator Of Smoking Recruits. ScienceDaily. Retrieved May 12, 2009,

Alcoholics who smoke appear to lose more brain mass than alcoholics who don’t smoke, according to a study at the San Francisco VA Medical Center.

It is already well-known that the brains of long-term alcoholics atrophy and shrink, the study authors say, but the new findings are the first evidence that cigarette smoking might contribute to that atrophy, particularly in grey matter of the parietal and temporal lobes.
Fifty to 90 percent of alcoholics also are smokers, according to Dieter Meyerhoff, PhD, a radiology researcher at SFVAMC and the principal investigator of the study
“Just looking at the amount of tissue mass lost due to either drinking or smoking, alcoholics who smoke show a greater loss in some regions of the brain compared to alcoholics who don’t smoke,” says Meyerhoff, who also is a professor of radiology at the University of California, San Francisco.
The study, which was published in the August 2005 issue of Alcoholism: Clinical and Experimental Research, compared 37 recovering alcoholics between the ages of 26 and 66 with a control group of 30 healthy light drinkers. The researchers used magnetic resonance imaging, a safe, non-invasive imaging technique, to measure brain volumes of the study participants.
They discovered that the more severe the tobacco habit, the greater the brain injury. “In smoking alcohol-dependent individuals, smaller regional [brain] volumes are related to greater cigarette-smoking severity,” according to the study findings, with severity measured by level of nicotine dependence, cigarettes smoked per day, and years of smoking.
The alcoholics (24 smokers and 13 non-smokers) averaged around 400 drinks per month for three years prior to the study; the light drinkers (seven smokers and 23 non-smokers) averaged between four and 11 drinks per month before the study and had no history of alcohol abuse or dependence. The alcoholics were sober for approximately one week before the study began.
The study uncovered no apparent differences in brain volume between smoking and non-smoking light drinkers.
Another key finding was that among non-smoking alcoholics, there was a direct relationship between brain volume and cognitive function: the higher the volume, the better the function. However, no such relationship was apparent among smoking alcoholics, according to co-author Timothy Durazzo, PhD, an associate radiology researcher at SFVAMC. Nor has such a relationship been measured before in previous studies on alcohol abuse and brain volume, he says.
“And this makes us wonder if what has been reported in the literature of alcoholism could have been obscured or distorted by combining smokers and non-smokers in the same studies,” Durazzo adds.
In their paper, the researchers speculate that smoking “disrupts these [brain] structure-function relationships,” possibly through its detrimental effects on brain volume or on brain neurochemistry.
Meyerhoff and his co-authors emphasize that their results are retrospective — that is, they discovered the apparent effects of smoking during statistical analysis of the participants in an earlier study they conducted on alcoholism and its effects on the brain. They then went back, re-classified each study participant as smoking or non-smoking, and analyzed brain volumes accordingly.
The authors say that if replicated in other studies, their results will raise several potentially important questions. The first is whether recovering alcoholics should also be treated for smoking — and if so, at what point during their treatment. At present, alcohol treatment programs such as Alcoholics Anonymous do not discourage smoking or even address the issue, they say.
Beyond that, says Durazzo, there is the potential effect of smoking on cognitive dysfunction, which is common among older long-term alcoholics. “Right now, our study participants are relatively young, around 50,” he notes. “But will the combination of smoking and drinking, or continued smoking during abstinence from alcohol, put them at greater risk for cognitive dysfunction as they age?” Finally, says Meyerhoff, there is the question of whether smoking has an effect on physical recovery from alcohol abuse. “In alcoholics who stop drinking, we know that there is recovery from at least some of these injuries to the brain — but is this recovery affected by continued smoking?” Meyerhoff and his team are conducting a study to explore that question right now.
In the future, the researchers plan a prospective study that will use MRI to compare brain volumes between smoking and non-smoking light drinkers and smoking and non-smoking alcoholics, with the hope of replicating the results of their current retrospective study.

Source: University of California – San Francisco (2005, September 29). Smoking Seems To Increase Brain Damage In Alcoholics. ScienceDaily. Retrieved May 31, 2009, from http://www.sciencedaily.com¬ /releases/2005/09/050929081514.htm

A new global study has found that lifestyle risk factors such as alcohol consumption and cigarette smoking are important risk factors for bowel cancer. Researchers have shown that people who consume the largest quantities of alcohol (equivalent to > 7 drinks per week) have 60% greater risk of developing the cancer, compared with non-drinkers.

Smoking, obesity and diabetes were also associated with a 20% greater risk of developing bowel cancer – the same risk linked with consuming high intakes of red and processed meat.
Approximately one million new cases of bowel (colorectal) cancer are diagnosed worldwide each year, and more than half a million people die from this type of cancer. In Australia alone, it is the most commonly occurring cancer with more than 12,000 new cases diagnosed each year.
According to lead researcher Associate Professor Rachel Huxley at The George Institute, the most startling finding of this study was, “The strong, and largely, unknown association between high intakes of alcoholic beverages with risk of colorectal cancer. Most people probably know that being overweight and having poor dietary habits are risk factors for the disease, but most are probably unaware that other lifestyle risk factors such as alcohol consumption, cigarette smoking and diabetes are also important culprits.”
Australia’s National Health and Medical Research Council recommend individuals shouldn’t be drinking more than two standard drinks per day.
On a positive note, researchers also demonstrated that physical activity lowered an individual’s risk of the disease but surprisingly, there was little evidence to indicate that high intakes of fruit and vegetables were protective against bowel cancer.
“These findings strongly suggest that a large proportion of colorectal cancer cases could potentially be avoided by making relatively modest lifestyle adjustments such as drinking less, quitting smoking, eating healthily and being a little more active”, said Associate Professor Huxley. “Such changes would also have huge benefits in terms of reducing an individuals’ risk of developing other major forms of illness including cardiovascular disease.”
The study reviewed more than 100 published studies that had reported on the association between major and modifiable risk factors for colorectal cancer including alcohol, smoking, diabetes, physical activity and various dietary components.

Source: Parkin DM, Bray F, Ferlay J, et al. Global cancer statistics, 2002. CA Cancer J Clin 2005;55:74-108.

New research suggests that the combination of drinking alcohol and smoking cigarettes increases the risk of throat and stomach cancers.
Researchers investigated risk factors for three kinds of cancers: esophageal adenocarcinoma (throat cancer), gastric cardia adenocarcinoma (stomach cancer) and esophageal squamous cell carcinoma (which resembles head and neck cancer).
Past studies have linked cancer of the esophagus to drinking and smoking, but the new research found that people who drank four glasses of alcohol daily had five times the risk of developing esophageal squamous cell carcinoma than nondrinkers. Smoking was related to increased risk of developing all three types of cancer, with risk of throat cancer the most elevated.
“It appeared that current smokers have the highest risks, and former smokers have an intermediate risk compared with never-smokers,” said study author Jessie Steevens, an epidemiologist at Maastricht University in the Netherlands.
The findings were presented at a meeting of the American Association for Cancer Research.
Source: Reuters November 17, 2008

Nicotine is thought to exert its effects on the brain by binding to receptors in the brain called nicotinic acetylcholine receptors (nAChRs). However, tobacco smoke contains thousands of chemicals besides nicotine, some of which may also bind to the nAChRs or cause molecules normally found in the body to bind to these receptors. To study the effects of denicotinized cigarettes—cigarettes from which nicotine has been removed—on a specific type of nAChR (a4b2* nAChRs), researchers funded in part by NIDA used a brain imaging technique known as positron emission tomography (PET) to visualize these receptors in the brains of smokers during withdrawal and after smoking either low-nicotine or denicotinized cigarettes. Before the PET imaging, all volunteers stopped smoking for approximately 2 days. The volunteers underwent an hour of PET imaging while still undergoing withdrawal and then were assigned to perform one of three activities: smoke a low-nicotine cigarette, smoke a denicotinized cigarette, or not smoke; they then underwent approximately 4 more hours of PET imaging. Withdrawal symptoms were monitored during all imaging sessions. The imaging results showed not only that “inhalation of nicotine during cigarette smoking is solely responsible for occupancy of brain a4b2* nAChRs,” but also that the imaging “demonstrated significant a4b2* nAChR occupancy from smoking a denicotinized cigarette,” state the authors. This result challenges the assumption that denicotinized cigarettes do not affect the brain’s nicotine receptors, the authors further explain. Interestingly, whether or not the receptors were occupied did not correlate with withdrawal symptoms, indicating that factors other than nicotine binding to the receptors play a role in the relief of withdrawal symptoms provided by smoking.

Source: Brody et al. Brain nicotinic acetylcholine receptor occupancy: Effect of smoking a denicotinized cigarette. Int J Neuropsychopharmacol. 2009;12(3):305–316.

Men diagnosed with cancer are less likely to survive the disease if they were smokers or heavy drinkers, Reuters reported Nov. 7.
Smoking and drinking are well-known risk factors for cancer, but researchers have begun looking into how these addictions affect survivability, as well. Researcher Young Ho Yun and colleagues at the National Cancer Center in Goyang, South Korea tracked 14,578 cancer patients for about nine years and compared mortality data to patients’ history of smoking and alcohol use.
The researchers found that former smokers were more likely to die from any kind of cancer than non-smoking cancer patients, possibly because smoking causes tumors to grow more aggressively. Smokers also may be less likely to get cancer screening tests, the authors noted, so their disease is often further advanced when treatment begins.
Among patients with head, neck, or liver cancer, heavy drinkers were more likely to die than non-drinkers, with risk increasing with consumption levels.
“Our findings suggest that groups at high risk of cancer need to be educated continually to improve their health behaviors — not only to prevent cancer, but also to improve prognosis,” the study authors noted.
The research appears in the Nov. 1, 2006 issue of the Journal of Clinical Oncology.

A new Harvard study concludes that smokers with multiple sclerosis (MS) experience more rapid progression of the disease than non-smokers, Reuters reported July 14.
Smokers also were 2.4 times more likely to have a progressive form of MS rather than the relapsing/remitting type, and 2.5 times more likely to have developed secondary progressive MS after an initial diagnosis of the relapsing/remitting version of the disease. Researchers found that smokers had more disability, severe disease and brain atrophy than non-smokers with MS, and had a greater degree of damaged brain tissue and brain atrophy over time.
Researcher Alberto Ascherio of the Harvard School of Public Health put a positive spin on the findings, noting that MS patients who quit smoking could slow progression of the disease.
Source: Archives of Neurology. July 2009

By Patrick Zickler
NIDA NOTES Staff Writer

Smokers who want to quit can get help with a variety of treatments, including counselling, nicotine replacement therapy (patches, gum, lozenges, or inhalers and medications. Some smokers use these treatments and succeed; for many. however, the discomfort of withdrawal and craving for nicotine lead to relapse. Recent NIDA funded research suggests that our genes may partly explain this variable success.

The research evaluated the effect of an enzyme, designated CYP2B6, on craving and relapse. This enzyme breaks down nicotine in the brain. Some peoples’ genes produce a more active form of the enzyme. while others have a less active form. Dr. Caryn Lerman at the NIDA- and NCI supported Transdisciplinary Tobacco Use Research Centre (TTURC) at the University of Pennsylvania, found that among smokers enrolled in a smoking cessation program, those with the genetic variant that decreases activity of CYP2B6 reported greater craving than did those with the more active form of the enzyme. Moreover, those with the less active enzyme were 1.5 times more likely to resume smoking during treatment.

The same enzyme helps break down bupropion, an antidepressant medication that acts on the brain’s dopamine system—where nicotine exerts much of its addictive influence—and helps some smokers quit. Dr. Lerman, along with colleagues at Georgetown University in Washington, DC., the State University of New York at Buffalo, and Brown University in Providence, Rhode Island, also investigated the relationship of CYP2B6 activity with bupropion treatment. They found that bupropion nearly tripled the success rate for women with the less active enzyme.

These findings provide initial evidence that smokers who have decreased CYP2B6 activity experience greater craving for nicotine than those with the more active form of this enzyme,” Dr. Lerman says. “Perhaps of greater interest is the preliminary evidence that, among women, bupropion may overcome the effect this genetic predisposition has on relapse.”

Genes, Treatment, and Abstinence

Most people—about 70 percent of the U.S. population—inherit two copies of the ‘C’ variant of the gene that influences CYP2B6 activity. The rest of the population inherits from one or both parents the less common form of the gene—the “T’ variant associated with decreased CYP2B6 activity. Among the 426 participants (232 men, 194 women) in the TTURC study, 128 (29.6 percent) had one or two copies of the T form of the gene. All participants received counselling to quit smoking; 229 received bupropion (300 mg/day) and 197 received placebo throughout the 10-week study. The participants provided weekly reports on craving and smoking rates. Abstinence (7 consecutive days without smoking) was verified with blood tests. At the end of treatment, participants who received counselling and bupropion had higher abstinence rates than those who received counselling and placebo. With one exception. participants with the less active enzyme had lower abstinence rates than those with the more active enzyme. Women with the less active enzyme who received bupropion showed the largest treatment effect, with 54 percent achieving abstinence, up from a 19-percent rate among women in the placebo group, notes Dr. Lerman.

This study suggests that properly selected treatment matched to a patient’s characteristics can improve a smoker’s chance of quitting

Theories To Explain Outcomes

The higher abstinence rate with bupropion for women with the lower activity enzyme may he due, in part, to reduced susceptibility to low moods that accompany nicotine withdrawal; overall. women reported more negative feelings than did men when asked to rate their mood during withdrawal. “This rate may reflect better management of the negative moods and craving that abstinence can create. But more study is needed to clarify the mechanisms by which bupropion influences smokers’ success in quitting”, Dr. Lerman says.
Researchers theorize that the association between the less active enzyme and increased craving could be the result of nicotine’s remaining longer in the brains of smokers with the less active enzyme. When nicotine lingers in the brains of these smokers, it may change their brain cells more profoundly than those of smokers with the more active enzyme. If so, the changes might produce more severe addiction marked by more intense craving during abstinence and increased risk of relapse.

“This study offers additional evidence of the important role genes play in smoking and treatment,” says Dr. Joni Rutter of NIDAs Division of Neuroscience and Behavioural Research, ‘While illustrating the increased craving and vulnerability to relapse that may be associated with inherited traits, it also suggests that properly selected treatment matched to a patient’s characteristics in this case, Bupropion for some women can improve a smoker’s chance of quitting.’

Source:Lerman, C., et al. Pharmacogenetic investigation of smoking cessation treatment, Pharmacogenetics
12(8):627-634, 2002.

A comprehensive report on smoking and health released by the U.S. Surgeon General finds that smoking causes diseases in nearly every organ of the body.

When the first Surgeon General’s report on smoking was published 40 years ago, it concluded that smoking was a definite cause of cancers of the lung and larynx in men and chronic bronchitis in both men and women. Later reports concluded that smoking caused cancers of the bladder, esophagus, mouth and throat; cardiovascular diseases; and reproductive effects.

The new report, “The Health Consequences of Smoking: A Report of the Surgeon General,” finds that cigarette smoking is also linked to leukemia, cataracts, periodontitis, pneumonia, acute myeloid, abdominal aortic aneurysm, and cancers of the cervix, kidney, pancreas, and stomach.

“We’ve known for decades that smoking is bad for your health, but this report shows that it’s even worse than we knew,” said U.S. Surgeon General Richard Carmona. “The toxins from cigarette smoke go everywhere the blood flows. I’m hoping this new information will help motivate people to quit smoking and convince young people not to start in the first place.”

According to the report, smoking kills an estimated 440,000 Americans each year. Furthermore, the economic toll linked to smoking is $157 billion each year, with $75 billion spent on direct medical costs and $82 billion in lost productivity.

“We need to cut smoking in this country and around the world,” said HHS Secretary Tommy Thompson. “Smoking is the leading preventable cause of death and disease, costing us too many lives, too many dollars, and too many tears. If we are going to be serious about improving health and preventing disease, we must continue to drive down tobacco use. And we must prevent our youth from taking up this dangerous habit.”

NEW YORK (Reuters Health) – Watching a favorite movie star smoke appears to encourage teen girls to adopt the habit themselves, according to new findings released Tuesday.

Investigators found that girls who said their favorite celebrity was someone who had smoked in at least two recent movies were almost twice as likely to start smoking within the next three years as girls whose favorite stars did not smoke in films.

“Really, smoking in movies is just an effective form of marketing,” study author Dr. John Pierce told Reuters Health .

Pierce, based at the University of California in San Diego, added that it is also common for teens to copy their favorite stars’ clothing, hair and jewelry. Those habits are easy to alter as styles evolve, he said, but once teens become hooked on smoking, “that is something that’s very hard to change.”

Pierce noted that the tobacco industry has argued that it does not pay for actors to smoke on screen, and actors do it simply because it makes them feel more comfortable.

If that is the case, then one could argue that the stars themselves are responsible for encouraging teens to smoke, and should be held accountable for that, Pierce noted.

“If it’s the stars, and they’re liable, then they’d better watch out,” he said.

To investigate whether watching stars smoke on-screen influences teens to do the same, Pierce and his colleagues asked 3104 never-smokers between the ages of 12 and 15 to name their two favorite female stars and two favorite male movie stars.

The researchers reviewed the stars’ movies during the past 3 years, and counted them as smokers if they puffed during at least two films. They then re-interviewed teens three years later, to see how many had started smoking.

When Pierce and his team first contacted teens in 1996, the most popular stars among teen girls were Brad Pitt, Sandra Bullock and Leonardo DiCaprio. Favorite actors for boys were Pamela Anderson, Sandra Bullock and Demi Moore. More than 40 percent of girls and 30 percent of boys had favorite stars who smoked.

Favorite stars who did not smoke on-screen included Jim Carrey, Tom Hanks and Tom Cruise.

Although girls appeared to be influenced by the smoking habits of favorite stars, boys were not, the authors report in the American Journal of Public Health.

They note that research has shown that boys tend to prefer action movies, which tend to include less smoking by stars, while girls prefer more smoke-filled romances and dramas.

Pierce explained that his team also measured each child’s susceptibility to smoking — defined as being unwilling to rule out the option of future smoking. This removed the possibility that only those who were susceptible to smoking would have a favorite star who smoked on-screen, he said.

Dr. Stanton Glantz of the University of California in San Francisco, who was not an author of the paper, noted that research shows that the more teens see people smoke, the more likely they are to pick up the habit. The latest findings suggest that policymakers should strictly limit teens’ exposure to on-screen smoking, he said.

Restricting smoking to R-rated movies would apply “the same rules that Hollywood applies to saying the F-word,” Glantz said.

Almost a third (29%) of Welsh girls aged 15 to 16 admit they smoke on a weekly basis, a new study by the National Public Health Service for Wales has revealed. Among boys of the same aged, 20% admitted to smoking regularly. The report examined a range of determinants of health including alcohol, drug use, socio-economic background, exercise and diet.

The South Wales Echo report includes a case study of one 28-year old who started smoking at the age of 14. She comments: “When I was 16 I was going out more and I would smoke about a pack a week. By the time I was 19 I was smoking about five packs a week. Of course I regret it now – my face is a prune! I wish I had never smoked because it’s really hard to stop and I could die of lung cancer.”

Merseyside’s first non-smoking pub has registered “record breaking-profits.” The Ring O’Bells in West Kirby barred smoking in June 2003.

Since then alcohol sales have risen 60 percent and food takings have doubled. The pub’s kitchen had to be refitted to cater for the demand.

Landlord Alan Jones said: “We lost some custom, which was a concern. But our profits have proved us right.”

A new survey reveals that one in five mothers smoke while pregnant. The habit causes low birth-weight babies with dramatically increased chances of mental impairment, disability and sudden death as infants. Baby health charity Tommy’s conducted the poll.

Smoking is also linked to ectopic pregnancy.

Children with asthma who have at least one parent who smokes are twice as likely to have asthma symptoms all year long compared with children of non-smokers, according to researchers from the University of Michigan (U-M) Health System.The involved in-depth telephone interviews with 896 parents of asthmatic children ages 2 to 12 years old in 10 states. “We set out to look at children who have seasonal asthma symptoms, but found that a substantial percentage have symptoms year-round,” said Kathryn Slish, a researcher in the U-M Department of Pediatrics. “We looked more closely and found a strong relationship between parents’ smoking status and the likelihood that their child would have problems all year long.”

“The only other factor that was associated with year-round symptoms was Medicaid insurance coverage,” added Cabana.

With well-publicized information that secondhand smoke can trigger asthma in children, Slish said, “it’s astounding that so many parents smoke around their asthmatic kids, and don’t stop even though their children are having trouble breathing all year.”

The researchers recommended that pediatricians, family physicians, and nurses address the subject of smoking with the parents of any child diagnosed with asthma and to provide resources to encourage them to quit.

The study’s findings were presented May 4 at the Pediatric Academic Societies annual meeting.

A Canadian-led international study finds that the causes of a heart attack are the same for people throughout the world, with cigarette smoking one of the main risk factors, the “There hasn’t been a study like this ever in the world,” said lead investigator Dr. Salim Yusuf, head of the Population Health Research Institute at McMaster University in Hamilton. “The risk factors that we’ve been able to measure account for 90 percent or more of heart disease. The impact of these risk factors in developing heart disease is global. It’s there in every ethnic group, in men, in women, in every region of the world, in young and old. It means we should be able to prevent the majority of premature heart attacks in the world.”

The research concluded that cigarette smoking and a poor ratio of bad to good cholesterol contribute to two-thirds of all heart attacks worldwide.

The five-year study involved 30,000 people in 52 countries. About half of the participants had suffered a heart attack. They were compared to an equal number of people with no heart disease, matched for age, sex, and city of residence.

“So now we’ll say: What causes the risk factor, not what causes the disease. And from a public-health point of view, there should be no more wallowing about that we need more information. We’ve got it,” said Dr. Sonia Anand, a specialist in vascular medicine and a member of the McMaster research team.

The latest figures show that 15 million people died from heart attacks worldwide in 1998. “The important issue is that the risk factors outlined in this study, the vast majority of them are modifiable,” said Toronto cardiologist Anthony Graham, a spokesman for the Heart and Stroke Foundation of Canada. “And what it suggests is that tobacco control is going to be as important in the developing world as it is in the western world.”

The study’s findings are published in issue of the British medical journal

New research from the University of California (UC) Davis School of Medicine and Medical Center found that cancer death rates among African-American males would decline by almost two-thirds if their exposure to cigarette smoke was eliminated.

“African-American men have had the highest cancer burden of any group in this country for decades,” said study author Bruce Leistikow, associate professor of epidemiology and preventive medicine at the UC Davis School of Medicine and Medical Center. “This study demonstrates, for the first time, that this excess cancer burden can be clearly linked to smoking. Smoke exposure appears responsible for African-American males’ high overall cancer mortality rates, not just their lung cancers.”

By analyzing data, Leistikow determined a correlation between annual smoke exposure and non-lung-cancer death rates for black males in the United States for the years 1969 through 2000. “During two decades of a steep rise, and a subsequent decade of steep fall, U.S. black male smoke exposures and non-lung-cancer death rates have moved in near-perfect lockstep up and down. The associations are very strong and have been consistent year-by-year for over 30 years,” Leistikow said.

Leistikow’s research found that smoking exposure is responsible for more than half the non-lung-cancer death rate in African-American males, and up to two thirds of their overall cancer death rate.

“This means that if black-male smoking exposures fall dramatically, that alone is likely to erase the great majority of their cancer burden,” said Leistikow. “Going back to the low black-male cancer burdens seen before the cigarette epidemic appears possible. Indeed, New York and, less so, California appear to be well on their way there.”

The study’s findings are published in the May 2004 issue of the journal Preventive Medicine.

New research from Sweden has shown that smokers puff clouds of poison in to the air which can seriously affect the breathing around them. The discovery has prompted ASH to urge the government to ban indoor smoking in workplaces. Swedish scientists found that endotoxins, which are made by bacteria and occur naturally in the air, are produced by tobacco smoke in high concentrations. Tobacco is known to contain over 4,000 chemicals, including 50 substances known to cause cancer. Low concentrations of endotoxins are not harmful and may even play a role in protecting people against allergies. However, in high concentrations, endotoxins can cause serious inflammatory reactions in the respiratory tract, leading to bronchitis and asthma. The researchers also concluded that tobacco endotoxins appeared to be the most aggressive among the various types that exist. ASH spokeswoman Amanda Sandford noted that the research could lead to a greater understanding of how tobacco smoke can trigger respiratory diseases such as asthma: “There are lots of sources of pollution we don’t have much control over, but we can control tobacco smoke in enclosed areas,” she said. She added that the study reinforced the need for a ban on smoking ban on indoor places.

Source: Morning Star, Times, 23 August, 2004

For recovering alcoholics and ex-smokers, as well as former users of illicit drugs, the mundane trappings of their addictions—ice cubes, ashtrays, straws, needles—exert a strong, long-lasting power to trigger relapse. A new University of Michigan study, published in the current (October 2001) issue of the Journal of Neuroscience, provides experimental evidence supporting a neurological explanation for why cues as innocent as the sound of ice cubes tinkling in a glass can cause “recovered” addicts to experience dangerous drug cravings. “Drug use is known to sensitize’ certain neural systems within the brain, causing changes that are relatively permanent,” says U-M psychologist Kent C. Berridge, co-author of the study with U-M psychologist Cindy L. Wyvell. “This study shows that the brain is vulnerable to cues that trigger irrational ‘wanting,’ even after a long period of remaining drug-free, once sensitized by prior drug use or exposure.” The research was supported by the National Science Foundation and by the National Institute on Drug Abuse.
For the study, Wyvell and Berridge designed an experiment with rats that eliminated several alternative explanations, such as withdrawal symptoms, learned habits or drug pleasure, for the increase in compulsive drug-seeking that is commonly triggered in human addicts by encounters with drug cues.

First, in order to avoid withdrawal symptoms, they trained the rats to press a lever to get a reward of sugar pellets, not an addictive drug. They also taught the rats to associate a 30-second tone with getting sugar pellets, without needing to press the lever. Then they sensitized one group of rats by administering a series of amphetamine injections, while injecting controls with a saline solution. Next, the researchers waited 10 to 14 days to make sure both groups were drug-free, then resumed the experiment. While the rats pressed the lever in hope of getting the sugar reward, they were presented intermittently with the sound cue, to assess the cue’s ability to trigger excessive pursuit of reward.

In the sensitized rats, the cue triggered excessive wanting,” says Berridge. “Whenever a sugar cue (a sound) occurred, rats pressed in a frenzy on a lever that had previously earned them a sugar reward.” In fact, the researchers found that sensitized rats pressed the lever 200 percent more than rats in the control group, an increase equivalent to the behaviour produced in other rats by injecting amphetamine directly into their brains. This showed that sensitization of the brain and direct drug activation of the brain’s dopamine reward-craving system amplified equally the ability of reward cues to trigger excessive ‘wanting.” “Much more remains to be done before we understand how this process works in humans, with drug rewards such as cocaine and heroin, and to a lesser extent, alcohol or nicotine,” says Berridge. ‘But this study is an important step, because it provides the first pure demonstration that neural sensitization causes a specific process— irrational cue-triggered ‘wanting’ for reward—that is a plausible psychological mechanism for relapse. These results from animals based on a natural sugar reward this may be a useful step toward understanding brain mechanisms of cue-triggered relapse in human drug addiction”

New research suggests that a combination of two genes is linked to whether a person can quit smoking and remain tobacco-free through the years.The study by researchers from the Tobacco Use Research Center of the University of Pennsylvania School of Medicine involved 418 smokers who received either bupropion or a placebo with seven sessions of behavioral group counseling. The researchers tracked the smoking status, abstinence symptoms and side effects of participants weekly, as well as at the end of treatment and six months later.The study found that certain variants of the SLC6A3 dopamine transporter gene and the DRD2 dopamine receptor gene resulted in higher abstinences rates and longer relapse times than other variants of these genes.

“While previous research has examined the effects of genes related to dopamine, a chemical in the brain associated with reinforcing the effects of nicotine, this study provides the first evidence that genes that alter dopamine function may influence smoking cessation and relapse during treatment,” said lead author Caryn Lerman, Ph.D., associate director for Cancer Control and Population Science at the Abramson Cancer Center of the University of Pennsylvania and professor in Penn’s School of Medicine and the Annenberg Public Policy Center.

Lerman said the study’s findings could lead to more effective smoking cessation methods. “Future smoking cessation studies should evaluate genetic predisposition, as well as the influence of psychological and environmental factors that may promote relapse,” she said.

The study’s findings are published in the October issue of Health Psychology. 2003

Nursing students are more likely to smoke cigarettes and to be nicotine dependent than medical students, says a study published in Chest (2003;124: 1415 – 20). A survey of more than 500 students in Philadelphia, USA, showed that four times as many nursing students smoked cigarettes as medical students, and twice as many students were former smokers. The rate of smoking among medical students had fallen in the past decade, and those who did smoke were less nicotine dependent than their nursing counterparts.


Source: The Lancet, 18 October 2003

US researchers investigated 3,122 patients with previous MI or stable angina and found that those who smoked were two and a half times more likely to suffer sudden cardiac death than those who had never smoked. However those who had given up were not at increased risk.

Source: General Practitioner, 3 November 2003

A government report on America’s children shows that violent crime, smoking, and heavy drinking among U.S. teenagers are all on the decline, Reuters reported July 18.
However, more children are overweight than ever, the report found. “Most people, about two-thirds, believe that crime is going up among America’s children,” said Dr. Duane Alexander, director of the National Institute of Child Health and Human Development. “The picture painted by this report, based on actual data, paints the opposite picture. “According to the report released by the National Institutes of Health, the Census Bureau, and other agencies, victims reported 413,000 juvenile crimes in 2002, which translates into 17 violent crimes per 1,000 juveniles aged 12 to 17.”This is a 67-percent drop from the 1993 high, and the lowest rate recorded since the national victimization survey began in 1973,” the report stated.The report also found that fewer children are being killed by guns. Last year, firearms were involved in 19 percent of deaths among 15- to 19-year-olds.Exposure to secondhand smoke also fell, the report said, and fewer teens smoked. As recently as 1994, 88 percent of children ages 4 to 11 were exposed to secondhand smoke. The latest report found that rate had dropped to 64 percent. Daily smoking by youth dropped to the lowest rate since 1975, and heavy drinking among teens also declined.source:Reported in Join Together Online. 7.21.2003

Women who smoke are more likely to go through an early menopause, new research has confirmed.   Women smokers may experience the change of life more than two years earlier than non-smokers.  The latest study, published in the journal Reproductive Biomedicine Online, suggest smoking actually harms a woman’s ovaries and affects her fertility.
Researchers from the Civitanova Marche General Hospital in Italy studied 350 women attending the hospital’s menopause clinic.They found that the menopause started at around 47 years of age for smokers compared with 49 years, six months, for non-smokers.Women who had stopped producing eggs before the age of 46 were more likely to be smokers.

                                               Source: Daily Mail, 6/2/04.  http://www.rbmonline.com/4DCGI/Article/Detail?38%091%09=%201149%09 

The Observer notes growing concern over the impact of cigarette smoking in films. Anti-smoking campaigners, backed by Britain’s largest cancer charity, claim the age classification of films should be as sensitive to smoking as to offensive language and obscenities.

‘We are not arguing for a total ban on smoking in films,’ said Deborah Arnott, director of ASH. ‘But there is strong evidence of a causal link between stars’ smoking behaviour and teenage smoking.’

Some of Hollywood’s biggest names, including Zeta-Jones, Nicole Kidman and Pierce Brosnan, have been criticised after recent research showed that smoking on screen is at its most prevalent for 50 years. Nearly 80 per cent of Hollywood films given a 12 rating feature some form of tobacco use while half of all children’s and PG-rated films depict smoking, according to a survey of 775 Hollywood films. 

British Board of Film Classification guidelines now say films with a PG rating must not contain references to illegal drugs or drug use. It also forbids films with a 15 classification from depicting ‘imitable techniques’ such as emphasising fighting or easily accessible lethal weapons, like knives. However, the guidelines contain no references to cigarettes, which kill 120,000 people each year in the UK. ‘There is surely a strong case for upgrading the age classification of a film to at least 15 if it features smoking by aspirational role models for young people, as this is clearly imitable and dangerous behaviour,’ said Arnott.

 Source:http://observer.guardian.co.uk/uk_news/story/0,6903,1168901,00.html

Seeing actors smoke on-screen can raise the risk of young people starting to smoke, suggests a new study that also concludes that many kids decide to smoke based solely on the behaviour of cinematic role models. The Associated press reported June 9 that researchers from Dartmouth Medical School studied 2,600 children ages 10 to 14, all nonsmokers when the study started in 1999. Each was rated by their exposure to smoking in movies. A follow-up survey found that even when controlling for other factors, the youths who were highly exposed to smoking in movies were three times more likely to start smoking themselves, compared to those students whose exposure to on-screen smoking was rated as low.

The researchers said that 52 percent of those who started smoking seemed to have been primarily influenced in their decision by on-screen smoking. In an accompanying commentary, researcher Stanford Glantz said that movies that depict smoking should be rated R by the Motion Picture Association of America.

Smoking among U.S. high school students has fallen to about one in five the lowest level in at least a generation in a drop-off the government attributes to anti-smoking campaigns and higher cigarette taxes.The Centers for Disease Control and Prevention reported Thursday that nearly 22 percent of high school students said they were smokers in 2003. That is down from more than 36 percent in 1997, and the lowest level since the CDC began keeping track in 1975. The drop was so dramatic that for the first time in more than two decades, the percentage of high school smokers is lower than the percentage of adult smokers. That was seen as an especially encouraging sign by the government.

In fact, the CDC study found that anti-tobacco efforts have been successful across the board, from curbing the number of first-time smokers to reducing the ranks of the heaviest smokers.”We are reaching all the youth. If we can stop youth from becoming addicted smokers, eventually we can stop this epidemic,” said Terry Pechanek, associate director of science for the CDC’s Office on Smoking and Health. “We’re making the progress we’ve been working toward for the last 40 years.”

Dr. John Banzhaf III, who helped mastermind lawsuits against the tobacco industry, said the study illustrates “probably the most dramatic progress which has been made in terms of any public health problem, at least in recent memory.” “The question would be whether we have the political will to continue to do it,” said Banzhaf, executive director of Action on Smoking and Health and professor of public interest law at George Washington University Law School.The CDC said that anti-tobacco efforts such as TV ads and school campaigns have been highly successful. Some of the programs were funded by the $206 billion settlement that tobacco companies and states reached in 1998.

Another big reason fewer teenagers are lighting up is the cost of a pack of cigarettes, the CDC said. The agency said cigarette prices went up 90 percent from 1997 to 2003, mostly because of tax increases. Students were classified as current smokers if they had lit up in the preceding 30 days.The study found that the percentage of heavy smokers those who lit up 20 days or more per month fell to 9.7 percent from 16.8 percent in 1999.Also, fewer students are trying cigarettes: A little more than 58 percent of students in 2003 said they had tried smoking, down from more than 70 percent in 1999.Still, the government noted that other studies recently have warned that the rate of decline in student smoking may be slowing.

The CDC blamed that on several factors, including more depictions of smoking in movies and a near doubling of spending on
tobacco advertising from cigarette makers ($5.7 billion in 1997 to $11.2 billion in 2001). Also, states are spending less money from the tobacco settlement on smoking prevention.Trend-setting states that had well-funded programs and subsequent decreases in student smoking now have had those programs crippled by budget cuts, causing a rise in student smoking rates in those areas, said Matt Barry of the Campaign for Tobacco-Free Kids.Philip Morris spokeswoman Jennifer Golisch said the nation’s No. 1 cigarette maker is “very happy” about the study’s results. “As a manufacturer of a product intended for adults, we believe we have a responsibility to help prevent kids from smoking,” she said.

Golisch said Philip Morris does not place its cigarettes in movies or on TV, though some filmmakers or TV producers have used
Philip Morris products without its permission. She also said the company is spending less on cigarette advertising, in part because of restrictions contained in the tobacco settlement.

Source:http://abcnews.go.com/wire/Living/ap20040618_504.html; 18/Jun/2004

Wearing a nicotine patch can boost memory and stop forgetfulness in older people according to a new study by researchers in to old age. Previous evidence found that nicotine might benefit people with a variety of disorders, including schizophrenia, Alzheimer’s, and attention deficit hyperactivity disorder. The latest study is the first to examine the effect of the drug on people with age-associated memory impairment (AAMI), a common condition among the elderly.
In a small study of over 60s the researchers found that using a standard memory test, four weeks of nicotine treatment halved decision times.  Doctors point out that none of the people on the trial had any form of dementia, such as Alzheimer’s, but some memory loss is normal with ageing. While receiving nicotine, patients assessments of their own memories also showed a small but significant improvement, say researchers at Duke University in Durham, USA. Experts think patches could be used over short periods of time for memory enhancement, without a person having to wear a patch regularly.

 Source: Daily Mail, 27 January 2004

In an experiment to test the availability of cigarettes online, four adolescents were able to buy tens of thousands of cigarettes online from dozens of websites, the Durham Herald-Sun reported Sept. 9. The four children, ages 11 to 15, were taking part in a University of North Carolina at Chapel Hill study when they used credit cards and money orders to try to buy cigarettes from 55 Internet vendors. Over a four-month period in 2001, they succeeded 94 percent of the time using credit cards and 90 percent of the time using money orders. Just one package was marked as containing tobacco products, and only one required an adult signature for delivery. A number of vendors sent free cigarettes and promotional materials to the children.

“Although it is against the law for stores to sell cigarettes to minors in every state in America, there is currently no federal law that bans Internet and mail-order cigarette sales to minors,” lead study author Kurt Ribisl said. “Congress has been considering legislation to ban cigarette sales to minors for more than four years. This study clearly shows that Internet cigarette vendors are not adequately verifying the age of their customers and that federal action is urgently needed.” In the wake of the report, Rep. Marty Meehan (D-Mass.) introduced legislation to regulate Internet cigarette sales and collect excise takes on such sales.

There are now at least 353 online cigarette retailers, and their sales could top $5 billion by the end of 2005, Ribisl said. Most are located in low-tax states like Virginia, North Carolina. One of the biggest online retailers is New York‘s Seneca Indian tribe, which sells cigarettes tax-free from its reservation.

Britain‘s largest tobacco company British American Tobacco (BAT) stands accused of adding sweeteners to cigarettes in an underhand attempt to entice youngsters to smoke, reports the Independent. Apparently, BAT whose products include Lucky Strike and Rothmans has been conducting scientific trials on animals in Canada. The additives that are believed to have been tested include chocolate, wine, cocoa, maple syrup and vanilla.
The experiment has drawn a furious response from Director of ASH, Deborah Arnott. “Adding sweets to tobacco is appalling. It shows that we need more tobacco regulation to prevent anything being added that could make tobacco more attractive, or smother, or easier to use. These are the sort of ingredients that could make cigarettes more attractive to children, why would they want to test these sort of additives?” she asked.

The controversial trials were outlined in the journal Food and Chemical Toxicology. BAT admitted it had indeed commissioned the work to see if cigarettes with additional ingredients had different effects on health compared to cigarettes without additives. The study, conducted over a 90 day duration and used laboratory rats in Canada because testing tobacco on live animals in Britain has been outlawed since 1997.
 
A BAT spokesman admitted that food additives such as cocoa butter and liquorice are already used in brands such as Lucky Strike to add a subtle taste. The spokesman added: “The amounts are tiny but they allow you to play very subtly with the taste of cigarettes. They (the additives) are handy, they are useful, they are food-type ingredients.”