Study suggests willpower isn't the only player
In this New Year, it is time to get smoking stopped! And perhaps our genes can help us understand how. In a recent study, it has been found that some smokers have much more difficulty kicking the habit than others. Now, a new review of prior research identifies a potential culprit: genes.
Researchers analyzed genetic differences cited in 22 studies involving nearly 9,500 white smokers. Of particular interest were variations in genes involved in processing dopamine, a neurotransmitter that helps to regulate the brain's reward and pleasure centers.
Experts believe that the nicotine found in tobacco boosts dopamine in the brain, leading to addiction.
The researchers wondered if variants in genes that regulate dopamine might be associated with the ability to put out the butts for good.
In the end, the scientists focused on a DNA sequence called Taq1A. They found that smokers who carried a variation of that sequence -- called A2/A2 -- appeared to have an easier time quitting smoking than those who carried other variations of the Taq1A sequence.
"This variant has been studied for years, but this study provided more convincing evidence on the role of this genetic variant in smoking cessation by analyzing a significant large number of smoke samples," said study co-author Ming Li, a professor in the department of psychiatry and neurobehavioral sciences at the University of Virginia.
The findings were published Dec. 1 online in Translational Psychiatry.
Li, working with researchers from Zhejiang University School of Medicine in Hangzhou, China, noted that roughly 6 million people die worldwide every year because of smoking.
The studies included in the current analysis were conducted between 1994 and 2014, and numbered from fewer than 100 participants to more than 2,000.
Quitting success varied widely, ranging from less than 10 percent to nearly 67 percent, the researchers reported.
Ultimately, the team found there was a "significant association" -- but no definitive proof -- between having the A2/A2 DNA variant and an increased ability to successfully quit.
The authors said the finding should encourage more research into the genetics behind efforts to quit smoking. Such research could eventually lead to the development of personalized treatments that target each smoker's inherited predispositions, they suggested.
However, Li's team cautioned that "research on this problem remains...Read more..
Children who are raised in households with dogs or farm animals during their first year of life may have a lower risk of asthma a few years later, a new study suggests.
In the study, the researchers looked at early exposure to dogs and farm animals and the rate of asthma among about 377,000 preschool-age and 276,000 school-age children in Sweden.
Among the school-age kids in the study, those who had been exposed to dogs during their first year of life were 13 percent less likely to have asthma at age 6, compared with the school-age kids who had not been exposed to dogs in their first year of life, the researchers found.
Based on the new findings, researchers can confidently "say that Swedish children with dogs in their homes are at lower risk of asthma at age 6, and that this risk reduction is seen also in children to parents with asthma," said study author Tove Fall, an associate professor of Uppsala University in Sweden.
The researchers also found that, the school-age kids who were exposed to farm animals during their first year of life were 52 percent less likely to have asthma at age 6 than those who had not been exposed to farm animals during their first year of life.
Among the preschool-age children, those who were exposed to farm animals during their first year were 31 percent less likely to have asthma when they were between 1 and 5 years old, compared with the kids who were not exposed to farm animals during their first year of life, according to the study, published on November 2, 2015 in the Journal JAMA Pediatrics.
In the study, the researchers looked at diagnoses of asthma obtained from the National Patient Register in Sweden. They also examined data on prescribed asthma drugs dispensed at pharmacies in Sweden. The researchers also looked at whether the kids' parents were registered as dog owners during the child's entire first year of life, and whether the parents reported that they worked with farm animals. The data in the study were analyzed from January 2007, through September 2012.
The researchers said they don't know for sure what exactly may explain the link between early exposure to animals and a reduced risk of asthma.
"It might be due to a single factor, or more likely, a combination of several factors related to a dog ownership lifestyle or dog-owners' attitudes, such as kids' exposure to household dirt and pet dust, time spent outdoors or being physically active," Fall told Live Science. "As a parent in...Read more..
If post-bronchodilator spirometry is required for the diagnosis of chronic obstructive pulmonary disease (COPD), why doesn’t every single primary care physician do it?
A University-based Primary Care Clinic (PCC) analysis revealed that only 19% of patients with COPD had undergone spirometry testing, which determines how well the lungs work by measuring oxygen flow. With COPD being the third leading cause of death in United States, this is certainly a startling statistic. Sandra Adams, MD, from The University of Texas Health Science Center at San Antonio (UTHSCSA) in Texas, presented a way to combat the lack of testing at the CHEST 2015 meeting in Montréal, Canada.
“This is what it’s really all about… the patients,” Adams began the presentation. Between 2012 and 2013, only 64% of the participants reported having spirometry testing within the last 16 years in order to confirm the condition.
Most people would probably say to look at the physicians and institutions where spirometry rates were the lowest. “I actually took a different approach and went to the ones with the highest rates,” Adams expounded. After gathering information on why the high raters used spirometry, as they should, the researchers moved on to those failing to use it. Some of the physicians with low rates voiced the ‘if it quacks like a duck’ viewpoint when it comes to COPD. So the team didn’t hesitate to show them instances where COPD was actually not the correct diagnosis in cases following the mantra.
Improving confidence and knowledge when it comes to spirometry testing were important endpoints, but Adams explained that they “actually wanted to change behavior.”
The team implemented the WipeCOPD program which was designed so that it’s easy and “the clinician doesn’t have to think about.” The interactive program consists of 60 to 90 minutes of continuing education modules per month along with 30 minutes of “live” training sessions on how to perform spirometry moderated by a COPD expert. “The hardest part was getting them in the first module,” Adams said. But after clinicians started the first module, the amount continuing was high.
The rate of spirometry rates increased following the WipeCOPD interventions. It went from the initial 19% (14 out of 75 clinicians) to 56% (176 to 312 clinicians) in just five months. The third-quarter of the study is still in the process, however, rates are clocking in around 82%.
While smoking is linked to an increased risk of developing diabetes, this risk appears to drop over the long term once cigarette use stops, a review of evidence suggests.
Researchers analyzed data on almost 5.9 million people in 88 previous studies examining the connection between smoking, second-hand smoke exposure and diabetes. They estimated that roughly 28 million type 2 diabetes cases worldwide – or about 11.7 percent of cases in men and 2.4 percent in women – could be attributed to active smoking.
The more cigarettes smokers consumed, the more their odds of getting diabetes increased.
If they quit, ex-smokers initially faced an even higher risk of diabetes, but as more years pass without cigarette use their odds of getting the disease gradually diminished, the analysis found.
“The diabetes risk remains high in the recent quitters,” said lead study author An Pan, of Huazhong University of Science and Technology in China. Weight gain linked to smoking cessation may be at least partly to blame for the heightened diabetes risk in those first months after giving up cigarettes, Pan added.
“However, the diabetes risk is reduced substantially after five years,” Pan said by email. “The long-term benefits – including benefits for other diseases like cancer and heart disease – clearly outweigh the short-term higher risk.”
Worldwide, nearly one in 10 adults had diabetes in 2014, and the disease will be the seventh leading cause of death by 2030, according to the World Health Organization.
Most of these people have type 2 diabetes, which is associated with obesity and aging and happens when the body can't properly use or make enough of the hormone insulin to convert blood sugar into energy. Left untreated, diabetes can lead to nerve damage, amputations, blindness, heart disease and strokes.
Plenty of research has established a connection between smoking and diabetes, although the reason is still unclear.
For the current analysis, Pan and colleges focused on exploring the link between the amount and type of smoke exposure and diabetes risk, as well as the potential for this risk to diminish with smoking cessation.
Overall, the pooled data from all the studies showed the risk of diabetes was 37 percent higher for smokers than non-smokers, the study team reports in The Lancet Diabetes and Endocrinology.
Exactly how smoking might lead to diabetes isn’t firmly established, but it’s possible smoking might cause...Read more..
Personalized medicine was a key theme here at the European Respiratory Society (ERS) International Congress 2015, especially for complicated diseases like asthma, chronic obstructive pulmonary disease (COPD), and interstitial lung fibrosis.
"We're using platforms that measure genes and proteins and metabolomic consequences of the disease, and trying to work backward from those profiles to mechanistic pathways. We've got new ways of getting at these complex diseases; it's going to be quite a major part of the respiratory research activity at the meeting," Stephen Holgate, MD, chair of the ERS scientific council, told Medscape Medical News.
Late-breaking abstracts on therapies for asthma and COPD were highlights of the first day of the conference, which was expected to attract approximately 20,000 attendees to the 435 scientific and educational sessions.
Lung cancer was another focus. "A lot is going on in the lung cancer area, with quite a lot of new targeted therapies. The whole personalized medicine agenda is quite interesting," said Kate Hill, PhD, senior research fellow at the University of Leeds and director of the June Hancock Mesothelioma Fund in the United Kingdom.
"That is exciting because lung cancer has been a little out of the realm of ERS for the past few years," said Bettina Korn, RGN, MSc, respiratory clinical nurse specialist and end-of-life care coordinator at St. James's Hospital in Dublin, Ireland.
Pediatric lung health was also highlighted, and research on the subtyping of wheezing in young children was presented. "The role of viral infections is a prominent part of that, but gene–environment interactions in children might also lead to the onset of asthma," said Dr. Holgate. A new technology to measure airway response in young children was also discussed.
The theme of air pollution carried over from last year's conference in Munich.
Smog and Airway Diseases
Investigations into the mechanisms behind injury due to air pollution, especially in pregnant women and young children, and the way exposure to air pollution can lead to asthma and other airway diseases was be presented.
"It's imposed on an individual, unlike smoking, which you can avoid, so it affects 100% of the population. We're interested in doing more on air pollution to create a greater imperative for local governments to take more responsibility," said Dr. Holgate.
A symposium featured a debate about the pros and cons of e-cigarettes, which will...Read more..
After children head back to school, they go straight into peak virus season. If your child patients have asthma, this can exasperate the condition. It’s important to anticipate heightened symptoms and have a plan in place, says Giovanni Piedimonte, MD, Institute Chair for Pediatrics and staff physician for the Cleveland Clinic’s Center for Pediatric Pulmonary Medicine.
Fall and winter are the worst seasons for children with asthma because they become exposed to many more respiratory viruses as school resumes and they return to classrooms, Dr. Piedimonte says.
He warns parents and other doctors that children’s asthma may flare up in late August and September because of two key factors:
1. Viral infections are more prevalent in the community, and that continues into the fall and winter.
2. Children return to school and are in close quarters with other students with viruses.
“The fall/winter season is when we experience a very significant increase in asthma attacks,” says Dr. Piedimonte.
“That’s because viruses become highly prevalent in the population and typically cause upper respiratory infections. This, in turn, triggers asthma attacks.”
Throughout the changes of the seasons, children may have various allergies, depending on pollination and the blooming of various flowers and grasses. Allergic reactions can also spark asthma attacks, alone or in combination with other environmental factors like viruses and indoor and outdoor pollution.
Viruses are the real culprits
However, during the summer season, there are fewer asthma attacks because children are not exposed to as many potential viral infections and spend less time in the more densely populated school setting.
While some children and adults may suffer because of higher levels of humidity and pollution in the summer, the fall/winter season remains the most challenging because of the increase in exposure to viruses, Dr. Piedimonte says. Studies show that viruses cause more than 80 percent of asthma attacks, he says.
Here’s the usual progression, according to Dr. Piedimonte:
• For the first three to five days, a child has an upper respiratory infection (URI), with a runny nose, congestion, sneezing and, sometimes, a low-grade temperature.
• During the URI, the virus may spread down to the lower airways.
• That generates inflammation and triggers obstruction of the airways, which are more reactive (“twitchy”) in children with...
Researchers from Brown University examined healthy patients’ and smoking patients’ lung samples in order to demonstrate that the expression of the pathways in immune responses is decreased in COPD patients. The researchers examined the relationship between NLRX1, the protein known to inhibit the MAVS/ RIG-1-like helicase pathway, in the clinical stage of current and former smokers with COPD.
The team found that measured levels of the protein are a sign of cigarette induced emphysema, similar to the lung destruction that is seen in patients with COPD.
“This is a new school of thought in terms of what causes emphysema and a new school of thought regarding how cigarette smoke does what it does,” corresponding author and pulmonologist Jack A. Elias, MD, dean of medicine and biological sciences at Brown University, explained in a press release. “We’re showing that a lot of what's going on is related to mitochondria.”
Then, the investigators repeated a similar experiment in mice models. They were able to show a direct relationship between cigarette exposure, NLRX1, and the MAVS/ RIG-like helicase pathway. In this experiment, when the mice were exposed to smoke, they demonstrated lower levels of NLRX1 expression than the control mice which were not exposed. Mice that were biologically engineered to lack the gene for NLRX1 developed an advanced degree of emphysema when exposed to the cigarette smoke.
“Our observation is that NLRX1 is a critical inhibitor of MAVS/ RIG-like helicase signaling that is affected by cigarette smoking exposure,” said study lead author Min-Jong Kang, a researcher at both Yale and Brown, continued in the statement. “We observed that the levels of this molecule could explain diverse aspects of disease severity and patient’s symptoms.”
Through even more experiments, the authors of the study solidified their hypothesis that NLRX1 is connected to the MAVS/ RIG-like helicase pathway in the context of cigarette smoke exposure in both human and mice models.
However, there are still unanswered questions. Specifically, the researchers have yet to determine exactly how cigarette smoke suppresses NLRX1 in human subjects. One difference the scientists noted between humans and mice models of this experiment is that...
A bacterial enzyme may be a future candidate in smoking cessation, according to a new study led by researchers at The Scripps Institute. Findings from the study are published in the Journal of the American Chemical Society.
Current smoking cessation aids have proven to be ineffective in at least 80–90% of smokers. This novel enzyme therapy would be to eliminate nicotine before it reaches the brain as to not trigger a smoker into relapse. The NicA2 enzyme is found in the, which is originally from soil in a tobacco field. The bacteria consumes nicotine as its one source of carbon and nitrogen. Researchers set out to test its potential efficacy as a therapeutic agent.
The team combined serum from mice with a nicotine dose equivalent to one cigarette. When the enzyme was added, they found the nicotine's half-life was cut from 2–3 hours to just 9–15 minutes. A higher dose of the enzyme could decrease the half-life of nicotine even more and prevent it from reaching the brain. The team then tested the enzyme to assess its practicality as a drug candidate. The enzyme remained stable in the lab for over three weeks at 98 degrees Fahrenheit. Also, the scientists did not find any toxic metabolites produced when the enzyme broke down nicotine.
Future studies will include improving the enzyme's serum stability so that a single injection can last up to a month, researchers concluded.Read more..