One of the most valuable steps anyone who suffers from chronic shortness of breath can undertake is to engage in a regular program of physical activity (including those diagnosed with chronic obstructive pulmonary disease or COPD).
Often the biggest challenge to become more physically active among those with pronounced breathing difficulties is a poor level of conditioning. Shortness of breath often leads people to rest more (meaning sitting or lying for larger segments of the day). The trend towards a more sedentary existence weakens muscles, bones, and the body’s cardiovascular function.
To help COPD patients “kick start” a physical activity program, pulmonology professionals can prescribe a treatment option known as pulmonary rehabilitation. In these programs, respiratory therapists and physicians first assess the baseline physical condition of each patient and then they design a somewhat customized 8-12 week exercise program that includes aerobic exercise (typically walking on a treadmill, riding a stationary cycle, or utilizing a device known as a cycle ergonometer) and strength training (weight lifting). Patients typically visit an outpatient rehab center 2-3 days per week for the 1 hour exercise sessions, and at various points along the way the therapists increase the duration and/or intensity of the exercise to help patients build back strength and endurance. Most rehab programs also include counseling and education sessions regarding breathing techniques, nutrition, smoking cessation, proper use of medications and social support.
Sounds great, right? Well, it is. Literally thousands of studies have been conducted on the effectiveness of pulmonary rehabilitation in reducing COPD patient shortness of breath, improving physical conditioning (strength and endurance), reducing exacerbations (shortness of breath attacks), shortening hospital stays and reducing overall health care costs. You’d think pulmonary rehab would be offered to every COPD patient…but it isn’t. In fact, only 1-2% of COPD patients are admitted to pulmonary rehab programs each year for a variety of reasons (none of them compelling).
At particular disadvantage are COPD patients considered “severe” cases. You see, there is a bit of a goldilocks mentality when it comes to doling out access to pulmonary rehab. If you have mild COPD (Stage I), you are unlikely to be admitted. If you have very severe COPD (Stage IV), you are also unlikely to be admitted. Why? Because Medicare and insurance companies will only reimburse rehab clinics for moderate to severe COPD patients (Stage II and III). And hospitals are not in the business of offering services for which they do not get paid.
Further, there is somewhat of an unspoken bias against admitting severe and very severe patients to begin with among pulmonology professionals. There seems to be an undercurrent that offering pulmonary rehab to severe patients is a waste of resources since their condition is unlikely to improve.
But research studies counter such notions. For example, a recent Nigerian study designed a 6-week pulmonary rehab program for 42 severe/very severe COPD patients. In particular, the study team desired to see whether the program would boost both the physical condition of patients as well as improve quality of life. [1]
Their results were remarkable in that the 6 week program (2 visits weekly for 2 ½ hours each session) delivered clinically significant improvements in distance walked on a timed test (21% improvement). Further, quality of life ratings for dyspnea (perceived shortness of breath), fatigue, emotional support and mastery all improved above the clinically significant threshold established in past research studies. Further still, the percentage of study participants acknowledging depression (40%) and anxiety (32%) both fell to 27% by the end of the study. More remarkable is the fact that the vast majority of these improvements were maintained 4 months after the 6 week program ended.
The study authors concluded, “This study has shown that a successful outpatient based rehabilitation programme is feasible and possible in patients with very severe COPD. Significant improvements can be achieved in shuttle walking distance, quality of life and psychological measurements, and the improvement is maintained for at least three more months without further intervention.”
If you are a COPD patient, we highly recommend you speak to your pulmonologist about gaining entry to a pulmonary rehab program in your area. If they won’t refer you, if you get rejected for admission, or there is no program in your area, we suggest you consider purchasing our Breathe Better for Life guidebook and companion CD-ROM.
We devised a pulmonary-rehab style exercise program based on guidelines established by the American Thoracic Society and the European Respiratory Society. We then augmented these guidelines with the exercise protocol recommended by the American College of Sports Medicine for those with chronic respiratory conditions. The guide and the CD were reviewed and edited by prominent respiratory care professionals, and both resources cover elements of a pulmonary rehab program that go beyond exercise (breathing techniques, airway clearing techniques, nutrition, proper use of inhaler medications, and other topics). To learn more about Breathe Better for Life, visit www.breathebetterforlife.com.
If you decide to follow our exercise program please consult your physician first to ensure the program is appropriate for your particular situation. While we did create two different programs based on condition severity (with different starting points, intensities, durations), it is important to include your doctor in your plans to begin an exercise program.
[1] Ige OM, et al. Outpatient Pulmonary Rehabilitation in Severe Chronic Obstructive Pulmonary Disease. Indian J Chest Dis Allied Sci. 2010 Oct-Dec; 52(4)
Welcome!
Welcome! Here we publish our views on new research and insights from the field of pulmonary medicine, most often focusing on topics related to exercise, nutrition, and other self-management techniques for those who suffer from chronic shortness of breath.
Whether you have COPD, currently smoke, or are just concerned about persistent shortness of breath and/or cough, read our articles to explore COPD treatment options and self-management techniques that can help you feel better NOW!
Whether you have COPD, currently smoke, or are just concerned about persistent shortness of breath and/or cough, read our articles to explore COPD treatment options and self-management techniques that can help you feel better NOW!
Thursday, February 17, 2011
Friday, February 11, 2011
Incorrect use of inhalers common among COPD patients
Bronchodilators are common treatment options prescribed by physicians treating patients suffering from chronic shortness of breath. Despite their widespread use, however, a significant percentage of COPD patients do not use their inhalers properly. The result of the misuse is inhalation of either too-little or too-much medication. In either case, patients can become frustrated with the effectiveness and/or side effects of the medications.
This widespread misuse is somewhat understandable given that there are different types of inhalers which carry different usage instructions (dry powder inhalers, metered dose inhalers) and some incorporate nebulizers while others don’t. Further, despite the best efforts of respiratory care professionals, many patients report they do not receive adequate instruction on how to use them properly.
As a case in point, a new study abstract published online ahead of print in the Journal of General Internal Medicine, examined the inhaler use of 40 COPD and 60 asthma patients who had been hospitalized due to their conditions at one of two Chicago area hospitals. The researchers discovered that 86% of the study subjects were improperly using metered dose inhalers while 71% were misusing Diskus brand dry powder inhalers. [1]
The study authors cited two main reasons for the poor rate of correct usage – difficulty with vision, and low health literacy. 43% of the COPD patients in the study had vision worse than 20/50 in both eyes. 61% of COPD patients in the study scored “less-than-adequate” health literacy on a test called The Short Test of Functional Health Literacy in Adults (S-TOFHLA for short).
After administering the vision and health literacy tests, the researchers taught patients the correct methods for using the inhalers (and presumably practiced with them). At the end of the study 100% of the participants correctly used their inhalers. The research team concluded the abstract by acknowledging, “Inhaler misuse is common, but correctable in hospitalized patients with COPD or asthma. Hospitals should implement a program to assess and teach appropriate inhaler technique that can overcome barriers to patient self-management, including insufficient vision, during transitions from hospital to home.”
If you think you might be using your inhaler improperly, the simplest of solutions is to visit your physician/pulmonologist/respiratory therapist and ask them to demonstrate the proper technique. Practice it in front of them to ensure you’ve got it down right and in future office visits, every now and then ask them to evaluate your inhaler technique.
Here is a brief excerpt from our Breathe Better for Life guidebook regarding proper use of metered dose inhalers:
“Many COPD medications need to be inhaled deeply into the lungs. Most people, over 90%, misuse their inhalers. To help you do this effectively, you will most likely need to use a metered-dose inhaler (MDI). If you have an MDI without a spacer, you need to shake the inhaler to prime it. Remove the cap and exhale deeply. Hold the inhaler one to two inches from your mouth (do NOT put it in your mouth). Press down to discharge the medication as you breathe in as deeply as you can. One depression (spray) per breath. Close your mouth and hold your breath for 5–10 seconds (ideally). Then exhale slowly.
If your MDI has a spacer, you want to shake the inhaler to prime it, then attach the spacer. Exhale deeply, then put the spacer between your teeth and seal your lips around it. With your chin up, pump one puff into the spacer. Slowly inhale through your mouth for three to four seconds. (Too rapid of an inhalation will likely result in less medication getting to the lungs, where it is absorbed and utilized by the airways.)
Remove the spacer from your mouth, and with your mouth closed, hold your breath for 10 seconds (ideally). Then exhale slowly. If you take a second puff, wait at least 30 seconds before doing so.”
If you’d like a more robust explanation and demonstration of the proper use of inhalers, our Breathe Better for Life companion CD-ROM includes easy-to-understand pictorial, narrated, step-by-step instructions on the proper use of metered dose inhalers, dry powder inhalers and nebulizers. As many of you know the Breathe Better for Life guidebook and CD-ROM also contains specific exercise, nutrition, breathing technique and airway clearing technique recommendations and demonstrations. You can learn more about Breathe Better for Life by visiting www.breathebetterforlife.com.
[1] Press VG, et al. Misuse of Respiratory Inhalers in Hospitalized Patients with Asthma or COPD. J Gen Intern Med. 2011 Jan 20 [Epub ahead of print]
This widespread misuse is somewhat understandable given that there are different types of inhalers which carry different usage instructions (dry powder inhalers, metered dose inhalers) and some incorporate nebulizers while others don’t. Further, despite the best efforts of respiratory care professionals, many patients report they do not receive adequate instruction on how to use them properly.
As a case in point, a new study abstract published online ahead of print in the Journal of General Internal Medicine, examined the inhaler use of 40 COPD and 60 asthma patients who had been hospitalized due to their conditions at one of two Chicago area hospitals. The researchers discovered that 86% of the study subjects were improperly using metered dose inhalers while 71% were misusing Diskus brand dry powder inhalers. [1]
The study authors cited two main reasons for the poor rate of correct usage – difficulty with vision, and low health literacy. 43% of the COPD patients in the study had vision worse than 20/50 in both eyes. 61% of COPD patients in the study scored “less-than-adequate” health literacy on a test called The Short Test of Functional Health Literacy in Adults (S-TOFHLA for short).
After administering the vision and health literacy tests, the researchers taught patients the correct methods for using the inhalers (and presumably practiced with them). At the end of the study 100% of the participants correctly used their inhalers. The research team concluded the abstract by acknowledging, “Inhaler misuse is common, but correctable in hospitalized patients with COPD or asthma. Hospitals should implement a program to assess and teach appropriate inhaler technique that can overcome barriers to patient self-management, including insufficient vision, during transitions from hospital to home.”
If you think you might be using your inhaler improperly, the simplest of solutions is to visit your physician/pulmonologist/respiratory therapist and ask them to demonstrate the proper technique. Practice it in front of them to ensure you’ve got it down right and in future office visits, every now and then ask them to evaluate your inhaler technique.
Here is a brief excerpt from our Breathe Better for Life guidebook regarding proper use of metered dose inhalers:
“Many COPD medications need to be inhaled deeply into the lungs. Most people, over 90%, misuse their inhalers. To help you do this effectively, you will most likely need to use a metered-dose inhaler (MDI). If you have an MDI without a spacer, you need to shake the inhaler to prime it. Remove the cap and exhale deeply. Hold the inhaler one to two inches from your mouth (do NOT put it in your mouth). Press down to discharge the medication as you breathe in as deeply as you can. One depression (spray) per breath. Close your mouth and hold your breath for 5–10 seconds (ideally). Then exhale slowly.
If your MDI has a spacer, you want to shake the inhaler to prime it, then attach the spacer. Exhale deeply, then put the spacer between your teeth and seal your lips around it. With your chin up, pump one puff into the spacer. Slowly inhale through your mouth for three to four seconds. (Too rapid of an inhalation will likely result in less medication getting to the lungs, where it is absorbed and utilized by the airways.)
Remove the spacer from your mouth, and with your mouth closed, hold your breath for 10 seconds (ideally). Then exhale slowly. If you take a second puff, wait at least 30 seconds before doing so.”
If you’d like a more robust explanation and demonstration of the proper use of inhalers, our Breathe Better for Life companion CD-ROM includes easy-to-understand pictorial, narrated, step-by-step instructions on the proper use of metered dose inhalers, dry powder inhalers and nebulizers. As many of you know the Breathe Better for Life guidebook and CD-ROM also contains specific exercise, nutrition, breathing technique and airway clearing technique recommendations and demonstrations. You can learn more about Breathe Better for Life by visiting www.breathebetterforlife.com.
[1] Press VG, et al. Misuse of Respiratory Inhalers in Hospitalized Patients with Asthma or COPD. J Gen Intern Med. 2011 Jan 20 [Epub ahead of print]
Tuesday, February 8, 2011
Vitamin E supplementation reduces risk of lung disease by 10% among women in new study
A new study published online ahead of print in the respiratory journal Thorax showed that healthy women who consumed 600 IU of vitamin E every other day had a 10% lower risk of developing lung disease. [1]
The study examined the past health records of nearly 40,00 women who enrolled in a large, ongoing health study called the Women’s Health Study. The researchers split the 40,000 women into two groups of roughly 20,000 – those who consumed 600 IU of vitamin E every other day, and those who received a placebo (100 mg of aspirin every other day). The mean age, weight, smoking status, alcohol use, multivitamin use and other health factors between the two groups were largely the same (a purposeful selection by the researchers to eliminate variables that might skew the study results).
During 10 years of follow up from study enrollment, 760 women receiving vitamin E were diagnosed with lung disease. By way of comparison, 846 of the study participants receiving the placebo were diagnosed with a chronic respiratory condition. From this data, the study authors concluded that those receiving vitamin E had a 10% lower risk of developing lung disease.
As an aside, the researchers pointed out that the strongest contributing health factor in developing lung disease among the study participants was cigarette smoking. Smokers in the study had 4.2 higher odds of developing lung disease than non-smokers. This is not a novel finding as other studies have produced similar results but we offer it as a reminder of the strong correlation between cigarette smoking and lung disease.
In addressing the implications of the lower lung disease risk from consumption of vitamin E, the study authors did not speculate on the mechanisms involved but did relate the findings of other vitamin E/COPD studies, “Observational studies investigating the association of dietary intake and pulmonary function consistently report that higher intake of nutrients with antioxidant properties is associated with better pulmonary outcomes, but causal inferences are limited by concerns about confounding and other biases. Studies comparing patients with COPD with healthy individuals report lower plasma and peripheral skeletal muscle vitamin E (alpha-tocopherol) concentrations in patients and a lower risk of death from respiratory disease with higher serum alpha-tocopherol concentration, but whether nutrition contributed to the onset of COPD is less clear.”
In other words, even though previous studies have hinted at vitamin E’s potential value for people who already have lung disease, there is not yet overwhelming, definitive evidence of its effectiveness. Further, the Thorax study was conducted on healthy women not COPD patients and therefore one cannot necessarily extend vitamin E’s benefits to those who already have respiratory disease.
With that in mind, however, there is a strong and growing body of evidence linking depressed levels of antioxidants (including vitamin E) with oxidative stress and inflammation in humans and laboratory animals with diagnosed respiratory conditions. And many of these studies demonstrate the power of boosting antioxidant blood levels in lowering oxidative stress and inflammation (whether through diet or dietary supplements). For additional articles we've written on antioxidants for healthy respiratory function, type in the keyword "antioxidant" in the search box in the left hand column of this page.
The dosage level consumed by the women in the Thorax study, 600 IU every other day, is well within the tolerable upper daily limits as reported by the National Institutes of Health Office of Dietary Supplements. For more information about vitamin E and potential counter-indications, click here to visit the aforementioned NIH information page on vitamin E. Please also consult your physician to determine whether adding vitamin E to your daily regimen is appropriate.
[1] Agler AH, et al. Randomized vitamin E supplementation and risk of chronic lung disease in the Women’s Health Study. Thorax. 2011 January 21. [Epub ahead of print]
The study examined the past health records of nearly 40,00 women who enrolled in a large, ongoing health study called the Women’s Health Study. The researchers split the 40,000 women into two groups of roughly 20,000 – those who consumed 600 IU of vitamin E every other day, and those who received a placebo (100 mg of aspirin every other day). The mean age, weight, smoking status, alcohol use, multivitamin use and other health factors between the two groups were largely the same (a purposeful selection by the researchers to eliminate variables that might skew the study results).
During 10 years of follow up from study enrollment, 760 women receiving vitamin E were diagnosed with lung disease. By way of comparison, 846 of the study participants receiving the placebo were diagnosed with a chronic respiratory condition. From this data, the study authors concluded that those receiving vitamin E had a 10% lower risk of developing lung disease.
As an aside, the researchers pointed out that the strongest contributing health factor in developing lung disease among the study participants was cigarette smoking. Smokers in the study had 4.2 higher odds of developing lung disease than non-smokers. This is not a novel finding as other studies have produced similar results but we offer it as a reminder of the strong correlation between cigarette smoking and lung disease.
In addressing the implications of the lower lung disease risk from consumption of vitamin E, the study authors did not speculate on the mechanisms involved but did relate the findings of other vitamin E/COPD studies, “Observational studies investigating the association of dietary intake and pulmonary function consistently report that higher intake of nutrients with antioxidant properties is associated with better pulmonary outcomes, but causal inferences are limited by concerns about confounding and other biases. Studies comparing patients with COPD with healthy individuals report lower plasma and peripheral skeletal muscle vitamin E (alpha-tocopherol) concentrations in patients and a lower risk of death from respiratory disease with higher serum alpha-tocopherol concentration, but whether nutrition contributed to the onset of COPD is less clear.”
In other words, even though previous studies have hinted at vitamin E’s potential value for people who already have lung disease, there is not yet overwhelming, definitive evidence of its effectiveness. Further, the Thorax study was conducted on healthy women not COPD patients and therefore one cannot necessarily extend vitamin E’s benefits to those who already have respiratory disease.
With that in mind, however, there is a strong and growing body of evidence linking depressed levels of antioxidants (including vitamin E) with oxidative stress and inflammation in humans and laboratory animals with diagnosed respiratory conditions. And many of these studies demonstrate the power of boosting antioxidant blood levels in lowering oxidative stress and inflammation (whether through diet or dietary supplements). For additional articles we've written on antioxidants for healthy respiratory function, type in the keyword "antioxidant" in the search box in the left hand column of this page.
The dosage level consumed by the women in the Thorax study, 600 IU every other day, is well within the tolerable upper daily limits as reported by the National Institutes of Health Office of Dietary Supplements. For more information about vitamin E and potential counter-indications, click here to visit the aforementioned NIH information page on vitamin E. Please also consult your physician to determine whether adding vitamin E to your daily regimen is appropriate.
[1] Agler AH, et al. Randomized vitamin E supplementation and risk of chronic lung disease in the Women’s Health Study. Thorax. 2011 January 21. [Epub ahead of print]
Friday, February 4, 2011
Physical activity level best predictor of mortality in COPD patients
The official journal of the American College of Chest Physicians, Chest, just published an abstract of a new study evaluating a range of potential predictors of mortality among COPD patients. Though the contents of the full study are embargoed until the article has gone to press, the abstract provides some interesting insights worth sharing.
First, as regular readers of our blog and e-letters well know, we are strong proponents for daily physical activity among COPD patients and anyone who suffers from chronic shortness of breath. We favor an exercise program based on the principles and practices of the COPD treatment pulmonary rehabilitation but acknowledge that even a simple walking program can confer conditioning benefits for smokers and those with respiratory conditions.
Many previous respiratory health studies have clearly and unambiguously demonstrated that regular physical activity reduces shortness of breath symptoms, increases cardiovascular conditioning, heightens muscle strength, improves self-reported quality of life, reduces hospital admissions and reduces severe shortness of breath attacks known as exacerbations.
When physicians act to address shortness of breath symptoms they typically favor smoking cessation, inhaler-based medications and antibiotics. These are reasonable and prudent treatment options. Smoking cessation confers significant health benefits in both the short and long run but a minority of smokers achieves successful permanent smoking cessation. Inhaler-based bronchodilators, steroids, and antibiotics offer short-term relief of immediate shortness of breath symptoms but their track record in conferring long term health benefits are spotty at best.
Regular physical activity, on the other hand, can deliver both short-term and long-term benefits provided one begins and maintains a regular program of activity. Previous studies have shown that COPD patients who are the most active (whether they exercise the most or simply are up and walking/moving around more frequently) report the highest quality of life, demonstrate the best exercise capacity and record the lowest sensations of breathlessness compared to those who are the least active.
In the new Chest study abstract, the researchers offered one more compelling reason to become more physically active – COPD patients in their study who were the most active reported the best survival rates over the four year follow up period after study enrollment. In fact, of all the diagnostic measures evaluated by the study team, the level of physical activity was considered the strongest predictor of patients likely to survive. [1]
According to the abstract, the Germany based researchers enrolled 170 stable COPD patients in their study. At the outset, they conducted a battery of diagnostic tests on the patients and recorded their respective readings. Tests included evaluations of respiratory function, cardiovascular function, body mass index, nutrition status, blood levels of inflammation markers, exercise capacity and levels of physical activity.
Forty-eight months after enrolling the patients and conducting the diagnostic tests, the researchers followed up with the patients to determine which were still alive and which had passed away (26 of the 170 patients died during the four year follow up period, roughly 15%).
The researchers then compared the mean diagnostic readings for the survivors and non-survivors and determined that among all the diagnostic measures, physical activity level was the measure with the highest inverse correlation between the two groups (meaning the people who did not survive the four year follow up period had recorded the lowest levels of physical activity in the diagnostic tests).
In fact, the study abstract mentioned that each 8-10% increase in physical activity level was associated with approximately 50% lower risk of death! Pretty compelling reason to get up off the couch and get moving, wouldn’t you say?!
Note: Physical activity level (PAL) in the study was measured by attaching a device to patients called a multisensory armband which records energy expenditure from movement over a defined period of time (typically a number of days). The World Health Organization has established that PAL levels between 1.7 and 2.0 are indicative of moderately active adults based on data accumulated over time utilizing this device and associated energy expenditure/metabolism calculations. Those considered sedentary or inactive have PAL levels between 1.4 and 1.7. In the Chest abstract, each .14 increase in PAL yielded 54% lower hazard ratio of death, hence our approximation of 8-10% movement in PAL (.14/1.7 or .14/1.4).
If you are a COPD patient and spend most of the day sitting or lying down, it is strongly worth your while to consider becoming more active (standing, walking, exercising). Not only will doing so improve how you feel and breathe each and every day, it may also help extend your life!
We realize getting started on a physical activity program may feel daunting. For those of you who feel that way, you are likely concerned about your balance, potential shortness of breath episodes, and lack of current energy. All are reasonable concerns but none of these issues will go away by simply sitting or lying down. They will only get worse.
To address these concerns, respiratory care professionals offer a treatment option known as pulmonary rehabilitation which assists COPD patients get started on a regular exercise program by starting slow and gradually increasing the intensity and duration of exercise for each patient based on their respective individual starting conditioning levels. These programs are highly effective and we strongly recommend you ask your pulmonologist for a referral to a program in your area.
One thing to keep in mind, however. Entry into these programs can be challenging. There are not enough pulmonary rehab programs around the country to serve all the COPD patients who could benefit from the treatment. Further, Medicare and insurance reimbursement only applies to Stage II and Stage III COPD patients in most cases (moderate to severe COPD), and the programs only last 8-12 weeks.
If you can’t gain entry into a pulmonary rehab program in your area, we recommend you consider purchasing our Breathe Better for Life guidebook and companion CD-ROM. We have created an at-home (or fitness center) exercise program based on pulmonary rehabilitation guidelines published by the American Thoracic Society and European Respiratory Society. We augmented these guidelines by incorporating exercise recommendations for people with chronic respiratory problems from the American College of Sports Medicine. Whether you follow our program or simply use the guide as a resource to discuss structuring an exercise program with your physician, we believe Breathe Better for Life provides excellent education for COPD patients and smokers on exercise, nutrition, breathing technique and airway clearing techniques to improve how you breathe and live. You can learn more about Breathe Better for Life by visiting www.breathebetterforlife.com.
[1] Waschki B, et al. Physical activity is the strongest predictor of all-cause mortality in patients with chronic obstructive pulmonary disease: a prospective cohort study. Chest. 2011 Jan 27 [Epub ahead of print].
First, as regular readers of our blog and e-letters well know, we are strong proponents for daily physical activity among COPD patients and anyone who suffers from chronic shortness of breath. We favor an exercise program based on the principles and practices of the COPD treatment pulmonary rehabilitation but acknowledge that even a simple walking program can confer conditioning benefits for smokers and those with respiratory conditions.
Many previous respiratory health studies have clearly and unambiguously demonstrated that regular physical activity reduces shortness of breath symptoms, increases cardiovascular conditioning, heightens muscle strength, improves self-reported quality of life, reduces hospital admissions and reduces severe shortness of breath attacks known as exacerbations.
When physicians act to address shortness of breath symptoms they typically favor smoking cessation, inhaler-based medications and antibiotics. These are reasonable and prudent treatment options. Smoking cessation confers significant health benefits in both the short and long run but a minority of smokers achieves successful permanent smoking cessation. Inhaler-based bronchodilators, steroids, and antibiotics offer short-term relief of immediate shortness of breath symptoms but their track record in conferring long term health benefits are spotty at best.
Regular physical activity, on the other hand, can deliver both short-term and long-term benefits provided one begins and maintains a regular program of activity. Previous studies have shown that COPD patients who are the most active (whether they exercise the most or simply are up and walking/moving around more frequently) report the highest quality of life, demonstrate the best exercise capacity and record the lowest sensations of breathlessness compared to those who are the least active.
In the new Chest study abstract, the researchers offered one more compelling reason to become more physically active – COPD patients in their study who were the most active reported the best survival rates over the four year follow up period after study enrollment. In fact, of all the diagnostic measures evaluated by the study team, the level of physical activity was considered the strongest predictor of patients likely to survive. [1]
According to the abstract, the Germany based researchers enrolled 170 stable COPD patients in their study. At the outset, they conducted a battery of diagnostic tests on the patients and recorded their respective readings. Tests included evaluations of respiratory function, cardiovascular function, body mass index, nutrition status, blood levels of inflammation markers, exercise capacity and levels of physical activity.
Forty-eight months after enrolling the patients and conducting the diagnostic tests, the researchers followed up with the patients to determine which were still alive and which had passed away (26 of the 170 patients died during the four year follow up period, roughly 15%).
The researchers then compared the mean diagnostic readings for the survivors and non-survivors and determined that among all the diagnostic measures, physical activity level was the measure with the highest inverse correlation between the two groups (meaning the people who did not survive the four year follow up period had recorded the lowest levels of physical activity in the diagnostic tests).
In fact, the study abstract mentioned that each 8-10% increase in physical activity level was associated with approximately 50% lower risk of death! Pretty compelling reason to get up off the couch and get moving, wouldn’t you say?!
Note: Physical activity level (PAL) in the study was measured by attaching a device to patients called a multisensory armband which records energy expenditure from movement over a defined period of time (typically a number of days). The World Health Organization has established that PAL levels between 1.7 and 2.0 are indicative of moderately active adults based on data accumulated over time utilizing this device and associated energy expenditure/metabolism calculations. Those considered sedentary or inactive have PAL levels between 1.4 and 1.7. In the Chest abstract, each .14 increase in PAL yielded 54% lower hazard ratio of death, hence our approximation of 8-10% movement in PAL (.14/1.7 or .14/1.4).
If you are a COPD patient and spend most of the day sitting or lying down, it is strongly worth your while to consider becoming more active (standing, walking, exercising). Not only will doing so improve how you feel and breathe each and every day, it may also help extend your life!
We realize getting started on a physical activity program may feel daunting. For those of you who feel that way, you are likely concerned about your balance, potential shortness of breath episodes, and lack of current energy. All are reasonable concerns but none of these issues will go away by simply sitting or lying down. They will only get worse.
To address these concerns, respiratory care professionals offer a treatment option known as pulmonary rehabilitation which assists COPD patients get started on a regular exercise program by starting slow and gradually increasing the intensity and duration of exercise for each patient based on their respective individual starting conditioning levels. These programs are highly effective and we strongly recommend you ask your pulmonologist for a referral to a program in your area.
One thing to keep in mind, however. Entry into these programs can be challenging. There are not enough pulmonary rehab programs around the country to serve all the COPD patients who could benefit from the treatment. Further, Medicare and insurance reimbursement only applies to Stage II and Stage III COPD patients in most cases (moderate to severe COPD), and the programs only last 8-12 weeks.
If you can’t gain entry into a pulmonary rehab program in your area, we recommend you consider purchasing our Breathe Better for Life guidebook and companion CD-ROM. We have created an at-home (or fitness center) exercise program based on pulmonary rehabilitation guidelines published by the American Thoracic Society and European Respiratory Society. We augmented these guidelines by incorporating exercise recommendations for people with chronic respiratory problems from the American College of Sports Medicine. Whether you follow our program or simply use the guide as a resource to discuss structuring an exercise program with your physician, we believe Breathe Better for Life provides excellent education for COPD patients and smokers on exercise, nutrition, breathing technique and airway clearing techniques to improve how you breathe and live. You can learn more about Breathe Better for Life by visiting www.breathebetterforlife.com.
[1] Waschki B, et al. Physical activity is the strongest predictor of all-cause mortality in patients with chronic obstructive pulmonary disease: a prospective cohort study. Chest. 2011 Jan 27 [Epub ahead of print].
Wednesday, February 2, 2011
New study shows N-acetylcysteine’s effect on oxidative stress from cigarette smoke
Each puff of cigarette smoke contains massive numbers of molecules known as free radicals that damage the lining of the airways and allow the toxic chemicals present in cigarette smoke to enter lung tissues. Over time, these toxins damage the tissue’s immune response to invading bacteria and fungi. This results in inflammation of lung tissue, and inflammation is believed to be a prime cause for chronic shortness of breath.
Normally, the body has a supply of neutralizing molecules known as antioxidants that bond to free radicals and essentially render them harmless. Antioxidants are in foods we eat (primarily fruits and vegetables) and can also be consumed in the form of dietary supplements.
But in the vast majority of cigarette smokers, the body’s supply of antioxidants is severely depressed for two reasons. On one hand, the significant counts of free radicals inhaled in cigarette smoke are far larger than even the healthiest of eater’s consumption of antioxidant rich foods. On the other hand, previous research has shown that the average smoker’s diet is low in antioxidant-rich food to begin with. The combination of these two factors (too many free radicals and too few antioxidants) leads to a condition known as oxidative stress.
Respiratory researchers have increasingly turned their attention to the impact of supplementing antioxidants in smokers and those with chronic shortness of breath to see if they can reduce oxidative stress and inflammation (and thereby contribute to improving shortness of breath symptoms).
We have previously written a number of articles regarding a number of recent studies regarding antioxidants that have shown promise in reducing oxidative stress and inflammation among those exposed to cigarette smoke and those with respiratory health conditions, including COPD. One such antioxidant is n-acetylcysteine (often referred to as NAC). NAC has been studied extensively for its anti-inflammatory properties and has also shown effectiveness in boosting exercise tolerance among COPD patients participating in a pulmonary rehabilitation exercise program.
A new research paper published this month online ahead of print in the journal International Immunopharmacology showed further evidence of NAC’s ability to significantly reduce oxidative stress and inflammation due to exposure to cigarette smoke. [1]
In the study, lung tissue from four groups of laboratory mice were examined for differences in oxidative stress and inflammation markers (proteins and white blood cells known to be present in high numbers as a result of oxidative stress and inflammation).
A control group of mice lung tissue received a normal diet and was not exposed to nicotine, NAC or another antioxidant compound known as eugenol. A cigarette group received exposure to nicotine in addition to a normal diet. Another group received nicotine and eugenol and the final group received nicotine and NAC.
The researchers then examined the four groups’ lung tissue counts of cytokines (proteins) and macrophages (white blood cells) to evaluate the relative influence of nicotine, eugenol and NAC.
First, they discovered that nicotine dramatically increased the number of cytokines and macrophages compared to the control group (approximately 3 fold increase), proving once again the impact of the chemicals in cigarette smoke in generating oxidative stress and inflammation.
Further the researchers reported dramatic decreases in the same oxidative stress and inflammation markers in lung tissue treated with nicotine and either NAC or eugenol (the relative performance between NAC and eugenol was about the same). In fact, the study results showed that NAC (and eugenol) lowered the counts of cytokines and macrophages to nearly the same level as the control group, implying that NAC and eugenol effectively negated the impact of nicotine in the mice lung tissue samples.
The researchers concluded, “…we have also demonstrated that, the importance of eugenol and N-acetylcysteine to exert a new anti-inflammatory [effect] to combat against nicotine-induced immune disorder, as our results clearly established that, co-treatment of eugenol or N-acetylcysteine with nicotine can diminish the nicotine-induced enhanced Th1 cytokines (TNF-α and IL-12) release and in mRNA level, as well as, boost up the Th2 (IL-10 and TGF-β) cytokine release and mRNA level up to more or less control level . In summary, our study has enhanced our understanding of the molecular steps leading to nicotine induced weaken of immune functions by murine [mouse] macrophages, and provided additional rationale for the application of anti-inflammatory therapeutic approaches by eugenol and N-acetylcysteine for different inflammatory [condition] prevention and treatment during nicotine-induced toxicity.”
Respiratory health care professionals will caution that these results may or may not translate to humans exposed to nicotine/cigarette smoke. However, there have been promising live human studies involving NAC therapy as an effective treatment option for chronic inflammation and therefore we believe NAC is worth your consideration.
NAC is an amino acid that helps the body produce glutathione – the most abundant antioxidant found in the human body (including lung tissues). NAC is widely available as a stand-alone dietary supplement or in combination with other antioxidant ingredients. As an aside, NAC is the lead ingredient in our respiratory support antioxidant-rich dietary supplement, Resplenish at a daily dosage of 1200mg. To learn more about Resplenish, please visit www.resplenish.com.
Normally, the body has a supply of neutralizing molecules known as antioxidants that bond to free radicals and essentially render them harmless. Antioxidants are in foods we eat (primarily fruits and vegetables) and can also be consumed in the form of dietary supplements.
But in the vast majority of cigarette smokers, the body’s supply of antioxidants is severely depressed for two reasons. On one hand, the significant counts of free radicals inhaled in cigarette smoke are far larger than even the healthiest of eater’s consumption of antioxidant rich foods. On the other hand, previous research has shown that the average smoker’s diet is low in antioxidant-rich food to begin with. The combination of these two factors (too many free radicals and too few antioxidants) leads to a condition known as oxidative stress.
Respiratory researchers have increasingly turned their attention to the impact of supplementing antioxidants in smokers and those with chronic shortness of breath to see if they can reduce oxidative stress and inflammation (and thereby contribute to improving shortness of breath symptoms).
We have previously written a number of articles regarding a number of recent studies regarding antioxidants that have shown promise in reducing oxidative stress and inflammation among those exposed to cigarette smoke and those with respiratory health conditions, including COPD. One such antioxidant is n-acetylcysteine (often referred to as NAC). NAC has been studied extensively for its anti-inflammatory properties and has also shown effectiveness in boosting exercise tolerance among COPD patients participating in a pulmonary rehabilitation exercise program.
A new research paper published this month online ahead of print in the journal International Immunopharmacology showed further evidence of NAC’s ability to significantly reduce oxidative stress and inflammation due to exposure to cigarette smoke. [1]
In the study, lung tissue from four groups of laboratory mice were examined for differences in oxidative stress and inflammation markers (proteins and white blood cells known to be present in high numbers as a result of oxidative stress and inflammation).
A control group of mice lung tissue received a normal diet and was not exposed to nicotine, NAC or another antioxidant compound known as eugenol. A cigarette group received exposure to nicotine in addition to a normal diet. Another group received nicotine and eugenol and the final group received nicotine and NAC.
The researchers then examined the four groups’ lung tissue counts of cytokines (proteins) and macrophages (white blood cells) to evaluate the relative influence of nicotine, eugenol and NAC.
First, they discovered that nicotine dramatically increased the number of cytokines and macrophages compared to the control group (approximately 3 fold increase), proving once again the impact of the chemicals in cigarette smoke in generating oxidative stress and inflammation.
Further the researchers reported dramatic decreases in the same oxidative stress and inflammation markers in lung tissue treated with nicotine and either NAC or eugenol (the relative performance between NAC and eugenol was about the same). In fact, the study results showed that NAC (and eugenol) lowered the counts of cytokines and macrophages to nearly the same level as the control group, implying that NAC and eugenol effectively negated the impact of nicotine in the mice lung tissue samples.
The researchers concluded, “…we have also demonstrated that, the importance of eugenol and N-acetylcysteine to exert a new anti-inflammatory [effect] to combat against nicotine-induced immune disorder, as our results clearly established that, co-treatment of eugenol or N-acetylcysteine with nicotine can diminish the nicotine-induced enhanced Th1 cytokines (TNF-α and IL-12) release and in mRNA level, as well as, boost up the Th2 (IL-10 and TGF-β) cytokine release and mRNA level up to more or less control level . In summary, our study has enhanced our understanding of the molecular steps leading to nicotine induced weaken of immune functions by murine [mouse] macrophages, and provided additional rationale for the application of anti-inflammatory therapeutic approaches by eugenol and N-acetylcysteine for different inflammatory [condition] prevention and treatment during nicotine-induced toxicity.”
Respiratory health care professionals will caution that these results may or may not translate to humans exposed to nicotine/cigarette smoke. However, there have been promising live human studies involving NAC therapy as an effective treatment option for chronic inflammation and therefore we believe NAC is worth your consideration.
NAC is an amino acid that helps the body produce glutathione – the most abundant antioxidant found in the human body (including lung tissues). NAC is widely available as a stand-alone dietary supplement or in combination with other antioxidant ingredients. As an aside, NAC is the lead ingredient in our respiratory support antioxidant-rich dietary supplement, Resplenish at a daily dosage of 1200mg. To learn more about Resplenish, please visit www.resplenish.com.
[1] Kar Mahapatra S, et al. Alteration of immune function and Th1/Th2 cytokine balance in nicotine-induced murine macrophages: Immunomodulatory role of eugenol and N-acetylcysteine. Int Immunopharmacol. 2011 Jan 13 [Epub ahead of print].
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