CT Scans Indentify Smokers At Risk Of Emphysema

Using CT scans to measure blood flow in the lungs of people who smoke may offer a way to identify which smokers are most at risk of emphysema before the disease damages and eventually destroys areas of the lungs, according to a new study published in PNAS

The study found that smokers who have very subtle signs of emphysema, but still have normal lung function, have very different blood flow patterns in their lungs compared to non-smokers and smokers without signs of emphysema.This difference could be used to identify smokers at increased risk of emphysema and allow for early intervention.

As many as 24 million Americans have chronic obstructive pulmonary disease (COPD) -- a group of serious lung diseases that includes emphysema -- and COPD is the fourth leading cause of death nationwide. Because COPD is a group of different diseases, identifying more effective treatments may hinge on distinguishing between these diseases and targeting them separately.

The team used multi-detector row CT imaging to measure blood flow patterns in the lungs of 41 study participants -- 17 non-smokers and 24 smokers. All the participants had normal lung function, but 12 of the smokers had very subtle signs of emphysema. The CT scans showed that these 12 individuals had the most disrupted patterns of blood flow compared to the other participants.

The findings also support the idea that abnormal blood flow occurs before emphysema develops.

"Although the underlying causes of emphysema are not well understood, smoking increases the risk of developing the disease," said lead study author Eric Hoffman, Ph.D., UI professor of radiology, internal medicine and biomedical engineering.

"Our study suggests that some smokers have an abnormal response to inflammation in their lungs; instead of sending more blood to the inflamed areas to help repair the damage, blood flow is turned off and the inflamed areas deteriorate."

The cellular pathway that turns off blood flow is helpful when an area of the lung has become permanently blocked and cannot be rescued. In that case, the lung "optimizes gas exchange" and stops supplying the area with blood. However, lung inflammation caused by smoking can be resolved and resultant damage repaired by increased blood flow, which brings oxygen and helpful cellular components to the site of injury.

This study suggests that the ability to distinguish when to turn off or when to ramp up blood flow is defective in some people -- probably due to genetic differences. If this genetic difference is coupled with smoking, which increases lung inflammation, that could increase the risk of developing emphysema.



CT Scans Indentify Smokers At Risk For Emphysema

Be cool without dying: New technique reduces tobacco smoke damage to lungs

Researchers in Australia have demonstrated that blocking a certain protein can reduce or prevent cigarette smoke-induced lung inflammation in mice. Inflammation underlies the disease process of chronic obstructive pulmonary disease (COPD) and many other smoking-related ailments.

The findings have been published online ahead of print publication in the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine.

Cigarette smoking causes lung inflammation, which can lead to oxidative stress, emphysema, small airway fibrosis, mucus hypersecretion and progressive airflow limitation. Since the inflammatory reaction to cigarette smoke responds poorly to current anti-inflammatory treatments, there is intense research to identify more effective therapies for cigarette smoke-induce lung damage.

Granulocyte macrophage-colony stimulating factor (GM-CSF) is of special interest because it governs the growth, activation and survival of leukocytes directly implicated in the pathogenesis of COPD.

Cigarette smoke triggers the release of GM-CSF and other cytokines and chemokines which cause activation and recruitment of more inflammatory cells into the lung,thereby perpetuating the inflammatory response and exacerbating ongoing inflammation. These activated and recruited inflammatory cells also release proteases such as matrix metalloproteinase (MMP)-12, which destroy the lung tissue, resulting in emphysema.

The research team from the University of Melbourne set out to determine whether blocking GM-CSF could reduce the inflammation and other deleterious effects of cigarette smoke exposure in mice.

To do so, they exposed a group of mice, half of which had been treated with a GM-CSF blocking agent, anti-GM-CSF, and half of which were controls, to the equivalent of nine cigarettes of smoke each day for four days. At the end of four days, the mice were killed and their lung tissue was examined for the presence of inflammatory cells.

"We found that anti-GM-CSF strongly reduced the number of potentially harmful white blood cells that infiltrate the lung after smoke exposure, as well as inhibiting the pro-inflammatory cytokine tumor necrosis factor (TNF)-, the chemokine macrophage inflammatory protein-2 (MIP-2), which coordinates the movement of white blood cells into the lung. It also inhibited the protease MMP-12, which is known as one of the main enzymes able to destroy lung tissue," said lead researcher on the study, Ross Vlahos, Ph.D., a senior research fellow with the lung disease research group at the University of Melbourne. "Cigarette smoke-exposed mice that were treated with an anti-GM-CSF had significantly less lung inflammation in comparison to untreated mice. This indicates that GM-CSF is a key mediator in smoke-induced lung inflammation and its neutralization may have therapeutic implications in diseases such as COPD."

These results, though preliminary, may illuminate a new pathway toward fighting smoke-related disease, specifically COPD. "Short-term models often translate into benefits in longer-term models. We still need to develop new methods and agents to test this idea long term and we also need to learn if it is effective in reversing longstanding disease," explained Dr. Vlahos.

In future research, Dr. Vlahos hopes to test whether GM-CSF could be a key target in other disease processes. "We want to understand exactly how blocking GM-CSF alters disease processes at the cellular and molecular levels so we can use this fine detail to make other treatments."

But this research is no free pass for patients to continue smoking, he warned: "Our treatment deals with cigarette smoke-induced lung inflammation involved in COPD, not cancer and other smoking-related ailments. Quitting remains the best and only cure for smoking-related lung disease."

Be cool without dying: New technique reduces tobacco smoke damage to lungs in mice

Young Britons More Likely To Take Up Smoking Thanks To Movies

Children in England see much more smoking in movies compared to their counterparts in the US and are more likely to pick up the habit as a result, finds research published in Tobacco Control.

The UK film classification system, which rates more films as suitable for young people than its US counterpart, is to blame, say the authors.

The research team assessed the number of on-screen smoking/tobacco occurrences in 572 top grossing films in the UK, which included 546 screened in the US plus 26 high earning films released only in the UK.

Because 79% of the films rated only for adults in the US ('R') were classified as suitable for young people in the UK, this meant that young Britons were exposed to 28% more smoking impressions in '15' or '12A' rated movies than their US peers, calculate the authors.



Young Britons More Likely To Take Up Smoking Thanks To Movies

Studies Find DNA Regions Linked To Nicotine Dependence

Americans are bombarded with antismoking messages, yet at least 65 million of us continue to light up. Genetic factors play an important role in this continuing addiction to cigarettes, suggest scientists at Washington University School of Medicine in St. Louis.

In two studies in the January 2007 issue of Human Molecular Genetics, the scientists show that certain genetic variations can influence smoking behaviors and contribute to a person's risk for nicotine dependence.

The smoking-related genes identified normally facilitate communication between nerve cells in the brain. One gene in particular, the alpha-5 nicotinic cholinergic receptor (CHRNA5) gene, was a very strong indicator of risk for nicotine dependence. Individuals with a specific variation in the gene seemed to have a two-fold increase of developing nicotine dependence once exposed to cigarette smoking. CHRNA5 is from a class of receptors that plays a role in dopamine pathways in the brain, which are linked to a person's experience of pleasure.

The researchers also identified genes related to gamma aminobutyric acid (GABA) receptors, another set of proteins vital to nerve cell function. Both GABA and nicotinic receptors had been suspected of involvement in nicotine addiction, but these findings strengthen those suspicions.

The studies also identified a gene not previously known to be involved with nicotine dependence. Called the Neurexin 1 (NRXN1) gene, it helps regulate the balance between excitatory mechanisms — those that increase communication between nerve cells — and inhibitory mechanisms — those that slow firing between nerve cells.

"An imbalance between excitatory and inhibitory activity in the brain may predispose people to addiction, such as alcoholism, drug dependence or nicotine dependence," says Laura Jean Bierut, M.D., associate professor of psychiatry and principal investigator of both studies. "The Neurexin gene we've identified is really a key factor in the balance between inhibition and excitatory activity in neurons."

Bierut suspects a large number of genes are involved in nicotine dependence, and she says understanding how they work may make it possible to develop new treatments for smoking cessation.

The research team analyzed data from almost 2,000 participants in two ongoing studies. One, called the Collaborative Genetic Study of Nicotine Dependence, is a U.S.-based sample that includes both addicted smokers and "social" smokers from St. Louis, Minneapolis and Detroit. The other is an Australian study of smokers of European ancestry called the Nicotine Addiction Genetics study.

The scientists combined two approaches for analyzing genetic information. One approach scanned the entire human genome for suspicious areas of DNA while the second approach closely examined specific target genes.

"The combination of these two approaches represents the most powerful and extensive study on nicotine dependence to date and is an important step in a large-scale, genetic examination of nicotine dependence," says Elias A. Zerhouni, M.D., the director of the National Institutes of Health, which funded the studies. "As more genomic variations are discovered that are associated with substance abuse, we can better understand addictive disorders."

The researchers identified an area of DNA variation that seems to alter the function of a nicotinic receptor protein. That small variation makes a big difference in risk for nicotine dependence.

Current drug treatments for nicotine dependence continue to be only marginally successful, and Bierut believes using information about genetic traits to tailor medications to individuals could make them significantly more effective. "The type of variant you have at this particular receptor — the alpha-5 nicotinic receptor — may actually predict whether or not you will do well on nicotine replacement therapy," she says.

Proving that, however, will require more studies, and the researchers have launched a new project to study DNA in a sample of both low-level smokers and heavier smokers. They are also working with colleagues at the University of Colorado to develop a mouse with the same variant in the CHRNA5 gene that seems to increase the risk of nicotine dependence. That would allow them to compare the effects of nicotine in mice with and without the genetic variation.

Tobacco use, primarily through cigarette smoking, is a leading cause of death and disability. Each year, approximately 440,000 Americans die of smoking-related illnesses, and worldwide, deaths attributed to tobacco total about 5 million. Although the prevalence of cigarette smoking has decreased over the last 30 years in the United States, the rate of smoking cessation among adults has been slowing since the mid-1990s. In addition, adolescents continue to start smoking, with 21 percent of high school students reporting they have smoked a cigarette sometime in the last month.

More than half of the people who smoke at least five packs in their lives — 100 cigarettes — go on to become nicotine dependent. But about 15 percent of people who smoke that amount won't develop any symptoms of nicotine dependence. "These people can give up smoking at any time," Bierut says. "They have no cravings. They smoke socially."

Earlier research suggested that smoking behaviors tend to cluster in families, and large studies of twins previously concluded that the clustering is partly related to genetic factors. An important aspect of these latest studies is that rather than comparing smokers to non-smokers, the researchers compared addicted smokers to non-addicted smokers.

"You're not at risk for nicotine dependence unless you've smoked," Bierut says. "You have to study smokers to identify the people who are at risk of becoming nicotine dependent versus those who smoke but can give it up at any time."

Bierut says it's important to find genetic factors related to nicotine dependence because so much of the population continues to smoke, in spite of the overwhelming evidence that it's harmful. And she believes some of the genes her research team has identified will help scientists to develop therapies for smokers who just can't seem to quit with existing treatments.

[ScientificBlogging]

Secondhand smoke raises risk of hardened arteries among teenagers

Frequent exposure to environmental tobacco smoke among 13-year-olds is associated with an increased risk of future blood vessel hardening and greater risks of other heart disease factors, according to new research published in Circulation: Cardiovascular Quality and Outcomes, a journal of the American Heart Association.

"Although previous research has found that passive smoke may be harmful for blood vessels among adults, we did not know until this study that these specific effects also happen among children and adolescents," said Katariina Kallio, M.D., Ph.D., lead author of the study and research fellow at the Research Centre of Applied and Preventive Cardiovascular Medicine at the University of Turku in Turku, Finland.

"These findings suggest that children should not face exposure to tobacco smoke at all," Kallio said. "Even a little exposure to tobacco smoke may be harmful for blood vessels. We need to provide children a smoke-free environment." [full story]

New smoking cessation therapy proves promising... assuming you still want your nicotine addiction

A novel technology for delivering nicotine to the lungs may soon give smokers a new way to kick the habit. When compared to the nicotine vapor delivery system used in the Nicotrol/Nicorette inhaler, the new technology proved more effective at delivering nicotine to the blood stream.

"We wanted to replicate the experience of smoking without incurring the dangers associated with cigarettes, and we wanted to do so more effectively than the nicotine replacement therapies currently on the market," said Jed Rose, Ph.D., director of the Duke Center for Nicotine and Smoking Cessation Research where the technology is being developed.

The Nicotrol inhaler is a smoking cessation therapy that delivers nicotine vapor to the mouth and upper airways, but little of it reaches the lungs. Duke's new technology combines the vapor phase of pyruvic acid, which occurs naturally in the body, and nicotine. [ScienceCodex]

All fascinating, but why so much research to keep people addicted to nicotine? As I have said many times, the stop smoking propaganda seems designed to make people's addiction more socially acceptable - and keep the profits rolling - rather than curing the nicotine addiction.

Study reveals a need to evaluate and regulate 'electronic cigarettes'

Electronic cigarettes should be evaluated, regulated, labeled and packaged in a manner consistent with cartridge content and product effect – even if that effect is a total failure to deliver nicotine as demonstrated in a study supported by the National Cancer Institute and led by a Virginia Commonwealth University researcher. The research was published in the Online First issue of the journal Tobacco Control. The article will appear in the February print issue of the journal.

Electronic cigarettes consist of a battery, heater and cartridge containing a solution of nicotine, propylene glycol and other chemicals and have been marketed to deliver nicotine without tobacco toxicants. Despite no published data concerning safety or efficacy, these products are sold in shopping malls and online. Further, "electronic cigarettes" currently are unregulated in the U.S., unlike other products intended to deliver nicotine to smokers such as lozenges, gum and patches.

"Consumers have a right to expect that products marketed to deliver a drug will work safely and as promised. Our findings demonstrate that the 'electronic cigarettes' that we tested do not deliver the drug they are supposed to deliver. It's not just that they delivered less nicotine than a cigarette. Rather, they delivered no measurable nicotine at all. In terms of nicotine delivery, these products were as effective as puffing from an unlit cigarette," said principal investigator Thomas Eissenberg, Ph.D., professor in the VCU Department of Psychology.

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Perhaps the good preofessor forgot to put a cartridge in his e-cigarette! Yes, e-cigs need regulating as they deliver a drug, and yes, this is a ploy by tobacco and pharmaceuticals to barge out of their profitable market an upstart product. They should bring out their own e-cigarettes but, for big tobacco, it would ruin their market and, for big pharma, it would expose the lie that NRT are some kind of medicine rather than just another profitable delivery system of a drug that is otherwise classed a poison. Go figure.