More Evidence Links Smoking Cessation to Lowered Diabetes Risk

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...

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Asthma, COPD Therapies Raise Curtain at ERS Conference

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...

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Why Fall Is Worst Season for Your Child’s Asthma

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...

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A Near Definitive Link Between Cigarette Smoke and Chronic Obstructive Pulmonary Disease

Patients with chronic obstructive pulmonary disease (COPD) often display inhibited mitochondrial protein pathways, according to a study published in the Journal of Clinical Investigation

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...

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Why Bacteria May Be a Future Smoking Cessation Aid

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.


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Blood lipid profile tied to childhood asthma and bronchial responsiveness

Blood lipid profiles are associated with childhood asthma, airway obstruction, bronchial responsiveness, and aeroallergen sensitization, researchers from Denmark report.

Dr. Hans Bisgaard from the University of Copenhagen told Reuters Health by email that he was surprised by the "significant association between serum lipids and asthma and allergy. This association is similar to the association found between serum lipids and other chronic inflammatory disorders."

Previous studies examining the relationship between the blood lipids and asthma have yielded ambiguous results, despite the association of hypercholesterolemia with a skewing of the adaptive immune response toward a TH2-oriented response, which is also seen in asthma and related disorders.

Dr. Bisgaard's team investigated the possible relationship between blood lipid levels, asthma, lung function, sensitization and allergic rhinitis in 296 7-year-old children born to mothers with a diagnosis of asthma.

Increasing LDL-cholesterol levels were associated with a 93% increase in the odds of concurrent asthma after adjustment and a significantly increased risk of airway obstruction, the researchers reported July 3 in the Journal of Allergy and Clinical Immunology.

In contrast, high HDL-cholesterol levels were associated with significantly improved airway flow, decreased bronchial responsiveness, 73% lower odds of sensitization against aeroallergens, and a non-significant reduced risk of allergic rhinitis.

High triglyceride levels were significantly associated with a doubling of the risk of aeroallergen sensitization, but not with the other measures.

Dr. Bisgaard said there are no immediate clinical implications of these findings.

"The study is seeking to understand the origins and mechanisms of chronic inflammatory disorders such as asthma and allergy," he said. "This insight will build the foundation for future prevention and treatment."

The researchers add, "Further longitudinal studies are required to evaluate a potential modifiable link between an unhealthy blood lipid profile and asthma and allergic sensitization."

Dr. Yang-Ching Chen from Taipei City Hospital in Taiwan, who was not involved in the new work, also found a link between LDL-cholesterol and asthma in an earlier study.

"Our data identified a trend of increasing levels of total cholesterol and LDL-cholesterol in the group order obese asthmatics > non-obese asthmatics > obese controls > non-obese...

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COPD Foundation Release: FDA Approves First COPD Biomarker

The COPD Foundation is extremely pleased to announce that a new clinical biomarker, plasma fibrinogen, has been approved for use in interventional clinical trials in patients with chronic obstructive pulmonary disease, the nation’s 3rd leading cause of death. This is the first COPD biomarker to receive qualification by the U.S. Food and Drug Administration (FDA) and is the result of six years of work by the COPD Biomarker Qualification Consortium (CBQC).

“Individuals working in the pharmaceutical industry, universities and the patient community have spent several million dollars and countless hours assembling and analyzing data that has led to the FDA’s monumental decision to approve this first COPD biomarker. Ultimately this clinical biomarker will enable future drug development to benefit patients.”

The CBQC, which includes representatives and resources from university and government research, pharmaceutical and patient communities, was created by the COPD Foundation in 2010, with encouragement from the FDA and the National Heart, Lung and Blood Institute, to develop a “biomarker qualification process” for COPD. Biomarkers are medical processes that researchers use to measure disease severity or to determine if a new drug or treatment is effective. Being able to use a biomarker qualified by the FDA assures drug developers that any potential new drug applications will not be rejected simply because of how the drug’s efficacy was measured or how patients were selected.

“This is a major triumph and, on behalf of the entire COPD community, I extend a heart-felt thank you to the FDA and congratulate the CBQC on its commitment and tireless leadership that allowed us to reach this significant milestone,” said John W. Walsh, co-founder and president of the COPD Foundation. “Individuals working in the pharmaceutical industry, universities and the patient community have spent several million dollars and countless hours assembling and analyzing data that has led to the FDA’s monumental decision to approve this first COPD biomarker. Ultimately this clinical biomarker will enable future drug development to benefit patients.”

COPD causes serious long-term disability and as many as 24 million Americans have the disease, but approximately half of them remain undiagnosed. On average, one American dies from COPD every 4 minutes yet in the last 3 decades, only one new class of drug has been approved for COPD.

For more information...

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In old age, current and former smokers face early lung disease

There may be 35 million older Americans with undiagnosed lung disease due to cigarette smoking, a new study suggests.

They don't meet the criteria for a diagnosis of chronic obstructive pulmonary disease (COPD), but they still suffer significant lung disease and impairment, the researchers report in JAMA Internal Medicine.

"We think we can increase their quality of life by treating them before they get worse," said Dr. James Crapo, the study's senior author from National Jewish Health in Denver.

Currently, about half of U.S. residents age 49 and older are current or former cigarette smokers, the researchers write.

About one in five U.S. adults currently smoke.

COPD, the third leading cause of death in the U.S., is often related to smoking, they add. The disease worsens with age and makes it more and more difficult to breathe.

Typically, the condition is diagnosed through spirometry, which measures lung function. But Crapo points out that lung function can be impaired to lesser degrees before people qualify for a COPD diagnosis.

For the new study, the researchers looked at data from people across the U.S. that had been gathered through spirometry, CT imaging scans of the chest, a walking test and questionnaires.

The researchers compared 4,388 people with normal spirometry tests to 794 people with mild COPD and 108 people who never smoked.

Overall, about 54 percent of people who had normal spirometry scores had signs of lung disease or impairment, the researchers found.

"I think to say they don’t have the disease is wrong," Crapo said.

Compared to the never smokers, those with normal spirometry but impaired lung function had worse quality of life scores, more trouble walking and evidence of airway thickening and emphysema on their CT scans.

The researchers suggest the current diagnostic criteria for COPD may not be picking up everyone with lung disease. Also, the criteria might not detect disease that is progressing in younger smokers.

"We don’t know how to prevent it yet, but the first step is identifying it early," Crapo said. "Then, trying to stop it from progressing."

For now, Crapo said old Americans may qualify for a free CT scan of their chest through Medicare, the public insurance program for older and disabled Americans.

While that scan can help doctors look for cancer, Crapo said it also reveals signs of COPD, such as thickening air walls.

"If you’re one of those people who smoked heavily in...

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