Many people who suffer from chronic shortness of breath tend to live sedentary lives – sitting or laying down for significant blocks of time each day. Over time, this behavior pattern leads to reduced cardiovascular fitness, degraded muscle function, bone mass loss, and has been shown in previous studies to increase the likelihood of exacerbation events (shortness of breath attacks significant enough to require an emergency room visit and/or hospitalization).
Therefore, for COPD patients and people who live with persistent breathlessness, respiratory care professionals highly recommend starting and maintaining a daily physical activity program that involves activities that require more walking and standing than sitting or laying.
To kick start this higher level of physical activity in moderate to severe COPD patients, pulmonologists can prescribe pulmonary rehabilitation. This treatment option has been shown in many studies to improve exercise capacity, reduce shortness of breath, reduce hospitalizations and improve overall patient quality of life.
However, 99% of COPD patients in the U.S. cannot gain entry to a pulmonary rehab program given the limited number of available outpatient programs and the restrictive reimbursement rules that govern admission (similar issues exist in many countries around the globe).
Further, for the lucky few who do gain entry, pulmonary rehab programs typically only last 8-12 weeks and the benefits gained during rehab only persistent long-term if the exercise, breathing technique and nutrition recommendations continue to be practiced post-rehab. Unfortunately, many COPD patients who successfully complete a pulmonary rehab program do not continue the practices and principles gained during rehab and therefore lose the conditioning benefits within one year.
As our readers know, we are strong advocates for pulmonary rehabilitation and believe COPD patients should demand their pulmonologist refer them to a program in their local area. We also believe that it is feasible for many COPD patients to start and maintain an at-home rehab-style program on their own if they can’t gain entry to a program in their area or if they have already completed a program and are on their own at this point. We created the Breathe Better for Life program based on the principles of pulmonary rehabilitation for this very purpose. To learn more, visit www.breathebetterforlife.com.
That said, given the overall low level of daily physical activity among COPD patients in general, pulmonology researchers continue to search for additional ideas beyond pulmonary rehabilitation that will help COPD patients achieve and maintain a higher level of daily physical activity for the long-term. To that end, a new Austrian research study published this month online ahead of print in the journal Respiratory Research examined a new and interesting option – Nordic Walking.
In particular, the researchers desired to know whether a 12 week Nordic Walking program would provide lasting conditioning benefits and increase daily activity levels of the COPD patients participating in the study. (Breyer MK, et al. Nordic Walking improves daily physical activities in COPD: a randomized controlled trial. Respiratory Research. 2010, 11:112 doi: 10.1186/1465-9921-11-112. epub ahead of print)
What is Nordic Walking, you ask? Simply put, it is an exercise technique that involves walking outdoors utilizing poles that look a lot like ski poles but have been modified to provide shock absorption and slip resistance. According to the research team, the specialized walking poles increase walking speed and muscle use.
In the study, the research team selected 60 COPD patients and divided them into two groups of 30 - a Control group who received “usual care” (meaning they received no exercise intervention), and a Walking group who participated in a 12 week Nordic Walking program. The Nordic Walking program involved walking outdoors at a brisk pace with the specialized poles for 1 hour, 3 days a week over the 12 week period.
The study subjects’ level of daily activity, movement intensity, exercise capacity and perceived breathlessness among other measures were all established at the outset of the study. Then at the end of the 12 week training period for the Walking group, these measures were taken again for both the Control group and the Walking group to determine the effectiveness of the training program itself. To determine whether there were lasting benefits from the Nordic Walking program, the researchers again measured the COPD patients on these same measures at 3 months and 6 months after the training program ended.
The study results showed significant improvements in the Nordic Walking group with regard to movement intensity, daily activity level, exercise capacity and perceived breathlessness. These improvements were evident at the end of the 12 week training program and were largely still present at the 3 month and 6 month post-training evaluation checkpoints.
For example, the Walking group’s mean time spent each day either walking or standing at the end of the 12 week training program increased by over 50% compared to readings taken at the beginning of the study, and the higher level of daily activity was still around 50% higher than baseline when measured again 6 months after the training program completed. The research team noted one likely reason for the maintained higher level of daily activity of the Walking group at 6 months post-training program was that 63% of the Walking group continued their Nordic Walking program on their own after the official training program ended.
In contrast to these results, the Control group saw the mean time they spent walking or standing drop by about 10% from their readings at the beginning of the study to their readings at the end of the study. Overall, the Walking group was approximately 70% more active each day than the Control group at the 6-month post-training program evaluation checkpoint.
By way of further example, at the end of the 3-month training period the Nordic Walking group members were able to walk 17% further in the 6-minute walk test (the main diagnostic tool used by the researchers to measure exercise capacity) compared to their baseline results at the outset of the study. At 6 months after the training program ended, the Nordic Walking group’s mean 6-minute walk distance was still 13% higher than it had been at baseline. By comparison, the Control group members’ 6-minute walk distance declined 3% at the 9 month evaluation checkpoint (6 months after the Walking group completed its 12 week training program) compared to their mean baseline results.
The paper’s authors concluded, “Nordic Walking has proven to be a simple, safe, and effective physical training modality for patients with COPD. Indeed, this is the first study demonstrating that Nordic Walking is feasible in patients with COPD and can improve COPD patients’ daily physical activity levels. In addition to the positive short-term effects of Nordic Walking on the physical exercise performance and daily symptoms of COPD patients, Nordic Walking created a long term effect on the training results even after an un-coached observation period of six months.”
So, Nordic Walking may be an interesting method for improving daily activity among COPD patients. It certainly seems like the combination of outdoor walking and the use of the specialized walking poles might at a minimum spice up a basic walking program and thereby make it a more interesting form of exercise to continue for a longer period of time.
Tuesday, August 31, 2010
Thursday, August 26, 2010
New study shows dietary counseling improves COPD patient body weight and physical performance
Earlier this month we reported the results of a study that showed combining nutritional supplementation with low intensity exercise training improved physical performance among malnourished/underweight COPD patients. In that study, the researchers theorized that the combination of an anabolic stimulus (exercise) with high-energy content nutritional supplementation sparked improvements in physical performance more than nutritional supplementation alone has shown in previous studies. Click here to read the article.
Now, a new Swedish study published online ahead of print reports that dietary counseling offered as part of a pulmonary rehab program improved physical performance and increased positive changes in body weight among underweight COPD patients. What’s striking about the results is that none of the COPD patients received nutritional supplementation or participated in an exercise program as part of the study. (Farooqi N, et al. Changes in body weight and physical performance after receiving dietary advice in patients with chronic obstructive pulmonary disease (COPD), 1-year follow-up. Archives of Gerontology and Geriatrics. 2010, doi: 10.1016/j.archger.2010.06.005)
While the results of these two studies seem to contradict each other on the surface, we believe they depict complementary results. Certainly, there are many studies on exercise training for COPD patients that clearly show improved physical performance with no nutrition counseling or supplementation involved. On the nutrition front, the research team in the Archives of Gerontology and Geriatrics study acknowledged that the results of the COPD patients in their study would likely have experienced even greater improvements if nutritional supplementation had been provided.
But it is interesting to note that the study subjects’ body weight and physical performance did improve at 3-months and 12-months after the initial dietary counseling based on that counseling alone. The research team speculated that the reason for the successful outcome of their study may be rooted in the longer follow-up period (12 months). By way of explanation, the article authors said, “This study differs from most of the previous nutritional studies in COPD patients, in that the nutritional intervention consisted of dietary advice alone rather than of oral nutritional supplements and that the follow-up time was longer. To achieve substantial changes in physiological functions by nutritional intervention, a longer follow-up period might be beneficial.”
In other words, past studies might have shown greater improvements in COPD patient performance and body weight due to nutritional intervention if the previous research teams had followed up with patients on their progress over a longer period of time. Most studies tend to look at performance improvement at 3-months or 6-months after interventions (exercise or nutrition). Part of the reason for shorter duration studies is to discern whether the examined interventions offer immediate, statistically significant improvements. Additionally, it is expensive to conduct longer-term studies and patient participation over longer time periods tends to wane (which skews and/or dilutes research results).
In this particular research project, 41 COPD patients were recruited after being referred to a pulmonary rehabilitation program at a Swedish hospital (20 women, 21 men). The study subjects received a nutritional assessment from a trained dietician and then were provided counseling on specific foods/portions to improve their diet. Over the course of the study, 7 patients dropped out.
The dietician analyzed each patient’s current total energy (calorie) intake as compared to the total energy intake necessary to achieve ideal body weight (IBW). The dietician did this by asking each COPD patient to recall what and how much they ate within the previous 24-hour period. The dietician then calculated each patient’s corresponding consumed calories based on their self-reported dietary intake.
At the outset of the study, the results of this analysis showed the mean energy intake of the COPD patients was 76% of the amount required for ideal body weight (meaning the patients on average were not consuming enough calories each day to reach their ideal body weight – and indeed the mean average body weight of the study subjects was 95% of their ideal body weight at the beginning of the study).
The dietician’s recommended diet plan (foods/portions) was intended to boost energy intake and bring the study subjects closer to their ideal body weight over time. For the underweight patients in the study (the significant majority of the study subjects), the recommendations including eating breakfast, lunch, dinner and 3-4 snacks each day. Foods rich in protein and calories were recommended (including meat, poultry, fish, egg, dairy products) and advice on complementing their diet with nutrient-fortified foods was provided. Then, the patients were sent on their way to follow their recommended diet plans.
The researchers had the patients return at 3 months and at 12 months after their initial dietician consultation for follow-up consultations. For those follow-up visits, each patient was provided a 3-day food log to record their dietary intake for the 3 days leading up to each follow-up visit. Again, the dietician examined the energy (calorie) content of the food logs and calculated the patients’ intakes in relation to the energy required to achieve ideal body weight.
The 3-month results showed that energy intake by the participating COPD patients rose to 90% of the energy required to achieve ideal body weight (an 18% improvement over the baseline measurement). At 12-months, this calculation climbed slightly higher to 91% (20% over the baseline measurement). As a result of the higher caloric intake over the 12-month period, the COPD patients in the study saw their mean body weight rise to 97% of ideal body weight.
The researchers also evaluated handgrip strength and the distance walked by the study subjects in 12 minutes as measures of physical performance. They took baseline readings for both measures at the outset of the study and again tested the COPD patients at 3 months and 12 months thereafter.
While both measures did improve, the most impressive result from these physical performance measures was that mean distance walked in 12 minutes rose by 18% over the baseline measure at 3-months and by 16% at 12-months. That’s pretty remarkable given that no exercise component was included in either the rehab program or as part of the follow-up regimen for the study participants.
The researchers suggested that the higher caloric intake resulting from the dietician’s recommendations boosted energy levels and strengthened muscles in the study participants which in turn allowed the COPD patients who completed the study to perform physical activity at a higher level.
So, if you are underweight and suffer from chronic shortness of breath, you might consider asking your physician to at refer you to a local dietician. After doing an initial nutritional assessment of your current diet, the dietician can/should develop a food/portion plan for you designed to boost your caloric intake (taking into account other health factors particular to your own circumstance).
In our opinion, if you do this and combine it with an exercise program you will experience gains in physical strength, endurance, and body weight. If past research is any indication, you should also benefit in terms of reduced shortness of breath and improved sense of well being.
The best resource for an exercise program geared for COPD patients is pulmonary rehabilitation. Ask your doctor for a referral to a program in your area. They are notoriously difficult to get into but you risk nothing by asking. If you can’t gain entry to a rehab program, and you need guidance for an exercise program geared specifically for people with COPD or chronic shortness of breath, we suggest you consider purchasing our Breathe Better for Life guide/CD, www.breathebetterforlife.com. Our guide recommendations are based on guidelines published by the American Thoracic Society, European Respiratory Society and the American College of Sports Medicine. If you decide to follow our recommendations, please consult with your physician first to ensure our recommendations are appropriate for your particular situation.
Alternatively, ask your doctor to recommend an exercise or walking program or consult a fitness instructor at a local health club/community center who is certified to construct exercise programs for people with chronic health conditions.
Now, a new Swedish study published online ahead of print reports that dietary counseling offered as part of a pulmonary rehab program improved physical performance and increased positive changes in body weight among underweight COPD patients. What’s striking about the results is that none of the COPD patients received nutritional supplementation or participated in an exercise program as part of the study. (Farooqi N, et al. Changes in body weight and physical performance after receiving dietary advice in patients with chronic obstructive pulmonary disease (COPD), 1-year follow-up. Archives of Gerontology and Geriatrics. 2010, doi: 10.1016/j.archger.2010.06.005)
While the results of these two studies seem to contradict each other on the surface, we believe they depict complementary results. Certainly, there are many studies on exercise training for COPD patients that clearly show improved physical performance with no nutrition counseling or supplementation involved. On the nutrition front, the research team in the Archives of Gerontology and Geriatrics study acknowledged that the results of the COPD patients in their study would likely have experienced even greater improvements if nutritional supplementation had been provided.
But it is interesting to note that the study subjects’ body weight and physical performance did improve at 3-months and 12-months after the initial dietary counseling based on that counseling alone. The research team speculated that the reason for the successful outcome of their study may be rooted in the longer follow-up period (12 months). By way of explanation, the article authors said, “This study differs from most of the previous nutritional studies in COPD patients, in that the nutritional intervention consisted of dietary advice alone rather than of oral nutritional supplements and that the follow-up time was longer. To achieve substantial changes in physiological functions by nutritional intervention, a longer follow-up period might be beneficial.”
In other words, past studies might have shown greater improvements in COPD patient performance and body weight due to nutritional intervention if the previous research teams had followed up with patients on their progress over a longer period of time. Most studies tend to look at performance improvement at 3-months or 6-months after interventions (exercise or nutrition). Part of the reason for shorter duration studies is to discern whether the examined interventions offer immediate, statistically significant improvements. Additionally, it is expensive to conduct longer-term studies and patient participation over longer time periods tends to wane (which skews and/or dilutes research results).
In this particular research project, 41 COPD patients were recruited after being referred to a pulmonary rehabilitation program at a Swedish hospital (20 women, 21 men). The study subjects received a nutritional assessment from a trained dietician and then were provided counseling on specific foods/portions to improve their diet. Over the course of the study, 7 patients dropped out.
The dietician analyzed each patient’s current total energy (calorie) intake as compared to the total energy intake necessary to achieve ideal body weight (IBW). The dietician did this by asking each COPD patient to recall what and how much they ate within the previous 24-hour period. The dietician then calculated each patient’s corresponding consumed calories based on their self-reported dietary intake.
At the outset of the study, the results of this analysis showed the mean energy intake of the COPD patients was 76% of the amount required for ideal body weight (meaning the patients on average were not consuming enough calories each day to reach their ideal body weight – and indeed the mean average body weight of the study subjects was 95% of their ideal body weight at the beginning of the study).
The dietician’s recommended diet plan (foods/portions) was intended to boost energy intake and bring the study subjects closer to their ideal body weight over time. For the underweight patients in the study (the significant majority of the study subjects), the recommendations including eating breakfast, lunch, dinner and 3-4 snacks each day. Foods rich in protein and calories were recommended (including meat, poultry, fish, egg, dairy products) and advice on complementing their diet with nutrient-fortified foods was provided. Then, the patients were sent on their way to follow their recommended diet plans.
The researchers had the patients return at 3 months and at 12 months after their initial dietician consultation for follow-up consultations. For those follow-up visits, each patient was provided a 3-day food log to record their dietary intake for the 3 days leading up to each follow-up visit. Again, the dietician examined the energy (calorie) content of the food logs and calculated the patients’ intakes in relation to the energy required to achieve ideal body weight.
The 3-month results showed that energy intake by the participating COPD patients rose to 90% of the energy required to achieve ideal body weight (an 18% improvement over the baseline measurement). At 12-months, this calculation climbed slightly higher to 91% (20% over the baseline measurement). As a result of the higher caloric intake over the 12-month period, the COPD patients in the study saw their mean body weight rise to 97% of ideal body weight.
The researchers also evaluated handgrip strength and the distance walked by the study subjects in 12 minutes as measures of physical performance. They took baseline readings for both measures at the outset of the study and again tested the COPD patients at 3 months and 12 months thereafter.
While both measures did improve, the most impressive result from these physical performance measures was that mean distance walked in 12 minutes rose by 18% over the baseline measure at 3-months and by 16% at 12-months. That’s pretty remarkable given that no exercise component was included in either the rehab program or as part of the follow-up regimen for the study participants.
The researchers suggested that the higher caloric intake resulting from the dietician’s recommendations boosted energy levels and strengthened muscles in the study participants which in turn allowed the COPD patients who completed the study to perform physical activity at a higher level.
So, if you are underweight and suffer from chronic shortness of breath, you might consider asking your physician to at refer you to a local dietician. After doing an initial nutritional assessment of your current diet, the dietician can/should develop a food/portion plan for you designed to boost your caloric intake (taking into account other health factors particular to your own circumstance).
In our opinion, if you do this and combine it with an exercise program you will experience gains in physical strength, endurance, and body weight. If past research is any indication, you should also benefit in terms of reduced shortness of breath and improved sense of well being.
The best resource for an exercise program geared for COPD patients is pulmonary rehabilitation. Ask your doctor for a referral to a program in your area. They are notoriously difficult to get into but you risk nothing by asking. If you can’t gain entry to a rehab program, and you need guidance for an exercise program geared specifically for people with COPD or chronic shortness of breath, we suggest you consider purchasing our Breathe Better for Life guide/CD, www.breathebetterforlife.com. Our guide recommendations are based on guidelines published by the American Thoracic Society, European Respiratory Society and the American College of Sports Medicine. If you decide to follow our recommendations, please consult with your physician first to ensure our recommendations are appropriate for your particular situation.
Alternatively, ask your doctor to recommend an exercise or walking program or consult a fitness instructor at a local health club/community center who is certified to construct exercise programs for people with chronic health conditions.
Monday, August 23, 2010
Black currant shown to reduce airway inflammation
In July 2010, a group of New Zealand researchers reported that the berry fruit black currant showed promise in reducing airway inflammation in a human cell study. In particular, one of the chemical compounds present in black currant, proanthocyanidins, was shown to suppress certain proteins in the epithelial cells (the cells that make up the lining of lung tissue) that are responsible for triggering inflammation in response to the presence of allergens in the lungs. (Hurst SM, et al. Blackcurrant proanthocyandins augment IFN-gamma-induced suppression of IL-4 stimulated CCL26 secretion in alveolar epithelial cells. Mol Nutr Food Res. 2010 Jul,54 Suppl 2:S159-170)
The study focused primarily on the black currant’s effectiveness in reducing over-production of white blood cells that lead to inflammation and ultimately trigger asthma attacks, but given that the researchers speculated that black currant may help alleviate airway inflammation in general we thought the study was worthy of your attention.
As the research team explained, “The search for suitable foods as a natural alternative or as a complement to traditional therapies for the prevention and/or alleviation of inflammatory related diseases has become the focus of recent research. In particular, berry fruit consumption has been shown to alleviate lung inflammation in animal models. In this study we provide supportive evidence that blackcurrant-derived polyphenolic compounds, in particular proanthocyanidins, have the potential to modulate cellular events leading to the suppression of IL-4 and IL-13-stimulated CCL26 secretion, a primary eosinophilic chemokine that facilitates chronic lung inflammation in asthma patients.”
In the study, the researchers isolated human epithelial cells in culture. In one set of cell samples, they exposed the cells to black currant prior to introducing cell proteins known as cytokines (specifically, interleukin-4 otherwise known as IL-4, and interleukin-13, or IL-13) that signal secretion of certain white blood cells known as eosinophils (specifically CCL26) that in turn trigger lung inflammation. In effect, the researchers were trying to simulate the cell’s response to the presence of an allergen.
You see, when bacterial or fungal material is inhaled into the lungs, the cells of the lung lining detect their presence and begin secreting the proteins called cytokines that are responsible for signaling the body to produce white blood cells to attack and kill the invading bacteria or fungi.
In asthmatics, there is a miscommunication in the body between these proteins and the white blood cells which results in the production of way-too-many white blood cells. This in turn inflames the lung tissue (in effect hardening the cells due to the overload of the white blood cells crowding around). The hardening of the cells causes the cells themselves to enlarge and results in airways that constrict or narrow. This makes it extremely difficult to breathe. Scientists are not certain of the root cause that drives this miscommunication in asthmatics but suspect that the epithelial cells in asthmatics are damaged/altered by a yet-unknown source.
There is a similar mechanism in COPD patients that involves essentially the same process but typically different cytokines and different white blood cells. In the case of COPD, scientists believe the main reason for the miscommunication between the epithelial proteins and white blood cells is damage/alteration of epithelial cell structure caused by long-term exposure to cigarette smoke and other harmful airborne pollutants.
So, getting back to the study, the research team compared the black currant/cytokine exposed samples to cell samples that were exposed to cytokines alone. Then, the researchers counted the number of white blood cells (CCL26) generated in each set of cell samples. They determined that the black currant/cytokine exposed cell samples had notably fewer counts of the white blood cells compared to the cells exposed only to cytokines.
While the researchers speculated on a few reasons why black currant (and other berry fruits) may help reduce airway inflammation, there is no scientific consensus as to the precise mechanism. The article authors’ speculations included the possibility that the antioxidant properties of berry fruits such as black currant may cause certain fruit chemical compounds to bind to the cytokines thereby reducing the number of cytokines available to signal white blood cell production.
If you are interested in trying black currant, it is available in produce stores as raw fruit or juice. There are also a wide variety of black currant oil nutritional supplements available on the market. This particular study made no recommendations regarding consumption levels or dosage levels so we don’t have a dosage recommendation to offer but we did find the following dosage information on healthline.com, “As a dietary supplement, black currant is available in 500 milligram and 1,000 milligram capsules that typically contain black currant seed oil, vegetable glycerine, and gelatin. Black currant is likely safe when used at a maximum dose of 1,000 milligrams (500-1,000 milligrams are often used per day). Black currant juice is also commercially available and has been taken in doses up to 1.5 liters per day, when mixed with apple juice. Maximum doses of black currant seed oil used in clinical trials range from 4.5-6 grams per day up to eight weeks, although there is no proven effective dose, and safety has not been established. Black currant anthocyanins have been taken in doses of 7.7-50 milligrams for up to two months. Based on some herbal textbooks, there is a lack of reported toxicity concerns with black currant consumed as food or ingested in 500 milligram tablets three times a day.”
As we have counseled before regarding other nutritional supplements, please consult your physician prior to consuming black currant to ensure there are no counter-indications related to other medications you take or other aspects of your particular situation.
The study focused primarily on the black currant’s effectiveness in reducing over-production of white blood cells that lead to inflammation and ultimately trigger asthma attacks, but given that the researchers speculated that black currant may help alleviate airway inflammation in general we thought the study was worthy of your attention.
As the research team explained, “The search for suitable foods as a natural alternative or as a complement to traditional therapies for the prevention and/or alleviation of inflammatory related diseases has become the focus of recent research. In particular, berry fruit consumption has been shown to alleviate lung inflammation in animal models. In this study we provide supportive evidence that blackcurrant-derived polyphenolic compounds, in particular proanthocyanidins, have the potential to modulate cellular events leading to the suppression of IL-4 and IL-13-stimulated CCL26 secretion, a primary eosinophilic chemokine that facilitates chronic lung inflammation in asthma patients.”
In the study, the researchers isolated human epithelial cells in culture. In one set of cell samples, they exposed the cells to black currant prior to introducing cell proteins known as cytokines (specifically, interleukin-4 otherwise known as IL-4, and interleukin-13, or IL-13) that signal secretion of certain white blood cells known as eosinophils (specifically CCL26) that in turn trigger lung inflammation. In effect, the researchers were trying to simulate the cell’s response to the presence of an allergen.
You see, when bacterial or fungal material is inhaled into the lungs, the cells of the lung lining detect their presence and begin secreting the proteins called cytokines that are responsible for signaling the body to produce white blood cells to attack and kill the invading bacteria or fungi.
In asthmatics, there is a miscommunication in the body between these proteins and the white blood cells which results in the production of way-too-many white blood cells. This in turn inflames the lung tissue (in effect hardening the cells due to the overload of the white blood cells crowding around). The hardening of the cells causes the cells themselves to enlarge and results in airways that constrict or narrow. This makes it extremely difficult to breathe. Scientists are not certain of the root cause that drives this miscommunication in asthmatics but suspect that the epithelial cells in asthmatics are damaged/altered by a yet-unknown source.
There is a similar mechanism in COPD patients that involves essentially the same process but typically different cytokines and different white blood cells. In the case of COPD, scientists believe the main reason for the miscommunication between the epithelial proteins and white blood cells is damage/alteration of epithelial cell structure caused by long-term exposure to cigarette smoke and other harmful airborne pollutants.
So, getting back to the study, the research team compared the black currant/cytokine exposed samples to cell samples that were exposed to cytokines alone. Then, the researchers counted the number of white blood cells (CCL26) generated in each set of cell samples. They determined that the black currant/cytokine exposed cell samples had notably fewer counts of the white blood cells compared to the cells exposed only to cytokines.
While the researchers speculated on a few reasons why black currant (and other berry fruits) may help reduce airway inflammation, there is no scientific consensus as to the precise mechanism. The article authors’ speculations included the possibility that the antioxidant properties of berry fruits such as black currant may cause certain fruit chemical compounds to bind to the cytokines thereby reducing the number of cytokines available to signal white blood cell production.
If you are interested in trying black currant, it is available in produce stores as raw fruit or juice. There are also a wide variety of black currant oil nutritional supplements available on the market. This particular study made no recommendations regarding consumption levels or dosage levels so we don’t have a dosage recommendation to offer but we did find the following dosage information on healthline.com, “As a dietary supplement, black currant is available in 500 milligram and 1,000 milligram capsules that typically contain black currant seed oil, vegetable glycerine, and gelatin. Black currant is likely safe when used at a maximum dose of 1,000 milligrams (500-1,000 milligrams are often used per day). Black currant juice is also commercially available and has been taken in doses up to 1.5 liters per day, when mixed with apple juice. Maximum doses of black currant seed oil used in clinical trials range from 4.5-6 grams per day up to eight weeks, although there is no proven effective dose, and safety has not been established. Black currant anthocyanins have been taken in doses of 7.7-50 milligrams for up to two months. Based on some herbal textbooks, there is a lack of reported toxicity concerns with black currant consumed as food or ingested in 500 milligram tablets three times a day.”
As we have counseled before regarding other nutritional supplements, please consult your physician prior to consuming black currant to ensure there are no counter-indications related to other medications you take or other aspects of your particular situation.
Thursday, August 12, 2010
Long-term effectiveness of smoking cessation approaches among COPD patients
A new study published in the August edition of the journal Thorax reviews the success rates of different smoking cessation approaches among COPD patients. In doing so, the results of the study seem to indicate that quitting smoking is more challenging for COPD patients than the general population of smokers. In fact, in the two most aggressive approaches evaluated, COPD patients were 27-40% less likely to achieve continuous 12-month smoking abstinence than the general smoking population. The article authors further noted a previous study which showed that COPD patients who are successful in quitting smoking are 30% more likely to relapse than the general smoking population.
Overall, the average continuous 12-month smoking cessation success rates for COPD patients in the nine studies reviewed by the article authors were very low – ranging from 1.4% abstinence among those who received no medical intervention to 12.3% abstinence for COPD patients who received the most aggressive approach (intensive counseling plus pharmacotherapy). (Hoogendoom M, et al. Long-term effectiveness and cost-effectiveness of smoking cessation interventions in patients with COPD. Thorax. 2010 Aug; 65(8):711-718)
In their study, the Dutch research team examined the results of nine previous COPD patient smoking cessation studies conducted over the past 25 years in which continuous smoking abstinence was biochemically verified after 12 months (versus self-reporting by patients). The purpose of their study was to determine the potential patient benefits and health care cost savings among the Netherlands smoking population for each of the smoking cessation options explored.
To be clear, the studies they examined were not exclusively Dutch population studies (meaning the results are not applicable only to smokers in the Netherlands). The researchers took the average results of the nine studies and extrapolated their implications across 50% of the Dutch COPD smoking population (the percentage of the Netherlands COPD smoking population that annually expresses a willingness to quit smoking).
The smoking cessation approaches evaluated were as follows:
1. Usual care – no smoking cessation counseling or pharmacotherapy (control group)
2. Minimal counseling – less than 90 minutes in total and no pharmacotherapy
3. Intensive counseling – 90 minutes or more of counseling and no pharmacotherapy
4. Intensive counseling plus pharmacotherapy – more than 90 minutes of smoking cessation counseling plus any type of pharmacotherapy (meaning they did not distinguish between types of pharmacotherapy).
The results showed that COPD patients who followed usual care had a 1.4% success rate in achieving continuous 12-month smoking abstinence. Those who pursued minimal counseling reached 2.6% while the intensive counseling group reported 6.0% success. The COPD patients who chose the combination of intensive counseling and pharmacotherapy reported the highest average 12-month continuous abstinence at 12.3%. By comparison, general smoking population studies have shown 10% success among those opting for intensive counseling and 17% abstinence among those who received both intensive counseling and pharmacotherapy.
The article authors did not speculate on reasons why COPD patients have lower success rates than smokers who have not yet developed COPD. One would think those who are suffering the greatest adverse health effects of long-term smoking would be more motivated to quit than those who are not yet exhibiting symptoms of lung disease. But regardless of the reasons, the results appear to highlight that long-term smoking cessation is a particularly tough proposition for COPD patients.
The article’s reported results reinforce our belief that respiratory care professionals should provide COPD patients greater access to pulmonary rehabilitation programs regardless of their smoking status. For those who are unaware, in the U.S. (and likely in many other countries around the globe) a very high percentage of pulmonary rehabilitation programs do not admit COPD patients who are active smokers unless they first successfully complete a smoking cessation program (meaning those unwilling to commit to quit are either denied entry or simply decide not to pursue entry).
Given that COPD patients find it harder to quit smoking (and to stay abstinent long-term) than the general smoking population, isn’t it misguided to deny those patients who can’t quit smoking a highly effective therapy for improving physical conditioning, reducing shortness of breath, improving patient quality of life, reducing COPD exacerbations, reducing COPD related hospital admissions and health costs? It’s not like smokers don’t benefit from pulmonary rehab – a number of other studies have demonstrated this fact.
We think it is misguided and it is one of the reasons we created the Breathe Better for Life guidebook and companion CD-ROM…to provide smokers and COPD patients with the knowledge and tools to begin a pulmonary rehab style exercise and nutrition program at home or at a local fitness center in the event they are unable or unwilling to gain entry to a rehab program in their area. To learn more about the Breathe Better for Life, please visit our web site at www.breathebetterforlife.com.
Overall, the average continuous 12-month smoking cessation success rates for COPD patients in the nine studies reviewed by the article authors were very low – ranging from 1.4% abstinence among those who received no medical intervention to 12.3% abstinence for COPD patients who received the most aggressive approach (intensive counseling plus pharmacotherapy). (Hoogendoom M, et al. Long-term effectiveness and cost-effectiveness of smoking cessation interventions in patients with COPD. Thorax. 2010 Aug; 65(8):711-718)
In their study, the Dutch research team examined the results of nine previous COPD patient smoking cessation studies conducted over the past 25 years in which continuous smoking abstinence was biochemically verified after 12 months (versus self-reporting by patients). The purpose of their study was to determine the potential patient benefits and health care cost savings among the Netherlands smoking population for each of the smoking cessation options explored.
To be clear, the studies they examined were not exclusively Dutch population studies (meaning the results are not applicable only to smokers in the Netherlands). The researchers took the average results of the nine studies and extrapolated their implications across 50% of the Dutch COPD smoking population (the percentage of the Netherlands COPD smoking population that annually expresses a willingness to quit smoking).
The smoking cessation approaches evaluated were as follows:
1. Usual care – no smoking cessation counseling or pharmacotherapy (control group)
2. Minimal counseling – less than 90 minutes in total and no pharmacotherapy
3. Intensive counseling – 90 minutes or more of counseling and no pharmacotherapy
4. Intensive counseling plus pharmacotherapy – more than 90 minutes of smoking cessation counseling plus any type of pharmacotherapy (meaning they did not distinguish between types of pharmacotherapy).
The results showed that COPD patients who followed usual care had a 1.4% success rate in achieving continuous 12-month smoking abstinence. Those who pursued minimal counseling reached 2.6% while the intensive counseling group reported 6.0% success. The COPD patients who chose the combination of intensive counseling and pharmacotherapy reported the highest average 12-month continuous abstinence at 12.3%. By comparison, general smoking population studies have shown 10% success among those opting for intensive counseling and 17% abstinence among those who received both intensive counseling and pharmacotherapy.
The article authors did not speculate on reasons why COPD patients have lower success rates than smokers who have not yet developed COPD. One would think those who are suffering the greatest adverse health effects of long-term smoking would be more motivated to quit than those who are not yet exhibiting symptoms of lung disease. But regardless of the reasons, the results appear to highlight that long-term smoking cessation is a particularly tough proposition for COPD patients.
The article’s reported results reinforce our belief that respiratory care professionals should provide COPD patients greater access to pulmonary rehabilitation programs regardless of their smoking status. For those who are unaware, in the U.S. (and likely in many other countries around the globe) a very high percentage of pulmonary rehabilitation programs do not admit COPD patients who are active smokers unless they first successfully complete a smoking cessation program (meaning those unwilling to commit to quit are either denied entry or simply decide not to pursue entry).
Given that COPD patients find it harder to quit smoking (and to stay abstinent long-term) than the general smoking population, isn’t it misguided to deny those patients who can’t quit smoking a highly effective therapy for improving physical conditioning, reducing shortness of breath, improving patient quality of life, reducing COPD exacerbations, reducing COPD related hospital admissions and health costs? It’s not like smokers don’t benefit from pulmonary rehab – a number of other studies have demonstrated this fact.
We think it is misguided and it is one of the reasons we created the Breathe Better for Life guidebook and companion CD-ROM…to provide smokers and COPD patients with the knowledge and tools to begin a pulmonary rehab style exercise and nutrition program at home or at a local fitness center in the event they are unable or unwilling to gain entry to a rehab program in their area. To learn more about the Breathe Better for Life, please visit our web site at www.breathebetterforlife.com.
Sunday, August 8, 2010
Low intensity exercise and nutritional supplementation effective for malnourished COPD patients
A significant percentage of people with COPD are underweight and considered malnourished. For many of these COPD patients, the main reason for the malnutrition stems from a higher than normal metabolism due to the need for their bodies to work harder to generate each breath (even at rest) compared to people with healthy lung function. Additionally, the act of eating food is more demanding and less satisfying for many people with COPD due to difficulty in swallowing, persistent coughing, chronic sputum secretion, and general shortness of breath.
As a result, many underweight COPD patients have suppressed appetites and eat less food than their bodies’ need to meet the heightened energy requirements to simply keep breathing. By eating less food, underweight/malnourished COPD patients also have less energy and therefore are more sedentary. Being sedentary leads in turn to a condition known as muscle wasting where the combination of low nutrient intake and lack of exercise/movement causes the body’s muscles to become weak and dysfunctional.
In past COPD nutrition studies, researchers have sought to test different ways of delivering calorie rich foods and nutritional supplements to help patients add weight, build lean muscle, boost energy, and increase exercise capacity. The results of these studies have been mixed.
A new study published in June 2010 in the journal Respiratory Medicine took a fresh look at this problem and proposed a new solution – combine nutritional supplementation with a low intensity pulmonary rehabilitation exercise program. The study team speculated that nutritional supplementation alone is not sufficient to produce desired conditioning benefits because the body also needs an anabolic stimulus (exercise) to build muscle mass and improve physiologic function.
In the study, a group of Japanese researchers enrolled 32 moderate to severe COPD patients. The patients were divided into two groups. The control group of 15 patients did not receive nutritional supplementation and did not participate in an outpatient pulmonary rehab program. The nutrition/exercise group consisted of 17 patients who underwent a 12 week program of low intensity exercise and oral nutritional supplementation. This group also received other core elements of pulmonary rehabilitation such as breathing training and counseling/education on other aspects of COPD disease management.
The nutritional supplementation provided to the nutrition/exercise group consisted of two 200ml packages of a nutritional drink each day that contained 60% carbohydrates, 25% fat, and 15% protein. The nutrition drink provided an extra 400 calories per day, and included Omega-3 polyunsaturated fatty acids and vitamins (the study does not describe what specific vitamins were supplemented but does indicate that the vitamins incorporated in the drink were primarily antioxidants).
The daily nutrition/exercise group exercise training consisted of 15 minutes of walking, strength training exercises for both upper and lower body, calisthenics and respiratory muscle stretching. The intensity level targeted for these exercises was 40-50% of maximum oxygen consumption (a measure of peak oxygen usage for each patient, established at the outset of the program). At this level, the exercise was considered low intensity.
One interesting note is the nutrition/exercise group only trained in the outpatient pulmonary rehab center one day every two weeks of the 12 week study. The rest of their training was supposed to take place unsupervised at home – which is putting a lot of faith in the exercise compliance of the nutrition/exercise group.
The researchers found that the nutrition/exercise group experienced significant increases from the beginning of the program to the end of the program (as compared to the control group) in quadriceps muscle force, walking endurance, body weight, weight bearing capability, and self-reported health status. For example, the nutrition/exercise group’s mean quadriceps muscle force rose 21% over the course the 12 week program while the control group’s quadriceps force declined by 3%. The nutrition/exercise group’s mean performance on the 6 minute walk test (a measure of walking endurance) improved 6% while the control group declined by 11%. The mean ability to bear weight rose by 15% for the nutrition/exercise group but remained flat for the control group.
Separately, the researchers also measured whether the combination of nutritional supplementation and low intensity exercise reduced airway inflammation in the nutrition/exercise group of COPD patients. The study results demonstrated that the combination of exercise and nutrition supplementation did in fact reduce counts of proteins known as “cytokines” that are general indicators of the presence of tissue inflammation.
In response to inflammation, cytokines are released by cells in the lining of the lungs and signal the body to react to suppress the inflammation. A high cytokine count is indicative of significant inflammation and vice versa. Over the 12 week program, the nutrition/exercise group saw mean cytokine counts for the three types of cytokines evaluated (interleukin-6, interleukin-8, and Tumor Necrosis Factor-alpha) drop 10%, 45% and 22% respectively. By contrast, the control group cytokine counts for these types rose 44%, 58% and 24% respectively. These are significant differences and clearly demonstrate the effectiveness of the nutrition/exercise intervention.
The research team concluded, “our data suggest a potential role for the combination of nutritional support and low-intensity exercise, and that this combination may improve the outcomes of exercise tolerance and health-related QOL (quality of life) in patients with malnourished COPD. Thus a combination of nutritional support and low-intensity exercise may provide a new therapeutic approach for pulmonary cachexia (muscle wasting).”
As a result, many underweight COPD patients have suppressed appetites and eat less food than their bodies’ need to meet the heightened energy requirements to simply keep breathing. By eating less food, underweight/malnourished COPD patients also have less energy and therefore are more sedentary. Being sedentary leads in turn to a condition known as muscle wasting where the combination of low nutrient intake and lack of exercise/movement causes the body’s muscles to become weak and dysfunctional.
In past COPD nutrition studies, researchers have sought to test different ways of delivering calorie rich foods and nutritional supplements to help patients add weight, build lean muscle, boost energy, and increase exercise capacity. The results of these studies have been mixed.
A new study published in June 2010 in the journal Respiratory Medicine took a fresh look at this problem and proposed a new solution – combine nutritional supplementation with a low intensity pulmonary rehabilitation exercise program. The study team speculated that nutritional supplementation alone is not sufficient to produce desired conditioning benefits because the body also needs an anabolic stimulus (exercise) to build muscle mass and improve physiologic function.
In the study, a group of Japanese researchers enrolled 32 moderate to severe COPD patients. The patients were divided into two groups. The control group of 15 patients did not receive nutritional supplementation and did not participate in an outpatient pulmonary rehab program. The nutrition/exercise group consisted of 17 patients who underwent a 12 week program of low intensity exercise and oral nutritional supplementation. This group also received other core elements of pulmonary rehabilitation such as breathing training and counseling/education on other aspects of COPD disease management.
The nutritional supplementation provided to the nutrition/exercise group consisted of two 200ml packages of a nutritional drink each day that contained 60% carbohydrates, 25% fat, and 15% protein. The nutrition drink provided an extra 400 calories per day, and included Omega-3 polyunsaturated fatty acids and vitamins (the study does not describe what specific vitamins were supplemented but does indicate that the vitamins incorporated in the drink were primarily antioxidants).
The daily nutrition/exercise group exercise training consisted of 15 minutes of walking, strength training exercises for both upper and lower body, calisthenics and respiratory muscle stretching. The intensity level targeted for these exercises was 40-50% of maximum oxygen consumption (a measure of peak oxygen usage for each patient, established at the outset of the program). At this level, the exercise was considered low intensity.
One interesting note is the nutrition/exercise group only trained in the outpatient pulmonary rehab center one day every two weeks of the 12 week study. The rest of their training was supposed to take place unsupervised at home – which is putting a lot of faith in the exercise compliance of the nutrition/exercise group.
The researchers found that the nutrition/exercise group experienced significant increases from the beginning of the program to the end of the program (as compared to the control group) in quadriceps muscle force, walking endurance, body weight, weight bearing capability, and self-reported health status. For example, the nutrition/exercise group’s mean quadriceps muscle force rose 21% over the course the 12 week program while the control group’s quadriceps force declined by 3%. The nutrition/exercise group’s mean performance on the 6 minute walk test (a measure of walking endurance) improved 6% while the control group declined by 11%. The mean ability to bear weight rose by 15% for the nutrition/exercise group but remained flat for the control group.
Separately, the researchers also measured whether the combination of nutritional supplementation and low intensity exercise reduced airway inflammation in the nutrition/exercise group of COPD patients. The study results demonstrated that the combination of exercise and nutrition supplementation did in fact reduce counts of proteins known as “cytokines” that are general indicators of the presence of tissue inflammation.
In response to inflammation, cytokines are released by cells in the lining of the lungs and signal the body to react to suppress the inflammation. A high cytokine count is indicative of significant inflammation and vice versa. Over the 12 week program, the nutrition/exercise group saw mean cytokine counts for the three types of cytokines evaluated (interleukin-6, interleukin-8, and Tumor Necrosis Factor-alpha) drop 10%, 45% and 22% respectively. By contrast, the control group cytokine counts for these types rose 44%, 58% and 24% respectively. These are significant differences and clearly demonstrate the effectiveness of the nutrition/exercise intervention.
The research team concluded, “our data suggest a potential role for the combination of nutritional support and low-intensity exercise, and that this combination may improve the outcomes of exercise tolerance and health-related QOL (quality of life) in patients with malnourished COPD. Thus a combination of nutritional support and low-intensity exercise may provide a new therapeutic approach for pulmonary cachexia (muscle wasting).”
Thursday, August 5, 2010
Pursed-lips breathing technique improves inspiratory capacity in COPD patients
An abstract of new study published online ahead of print in the journal Respiration highlights the benefits of a breathing technique known as pursed-lips breathing (often referred to as PLB by respiratory care professionals). Specifically, the researchers reported that inspiratory capacity (the maximum of volume of air inhaled by the lungs from a fully expired state) increased significantly in the 35 severe COPD patients tested during the study. (Visser FJ, et al. Pursed-Lips Breathing Improves Inspiratory Capacity in Chronic Obstructive Pulmonary Disease. Respiration. 2010 July 17 [Epub ahead of print])
Pursed-lips breathing is a highly effective breathing technique taught by respiratory therapists and other pulmonology professionals in pulmonary rehabilitation programs to help COPD reduce the sensation of breathlessness before, during or after exercise or other strenuous activities. Despite its effectiveness, it is remarkable to me how many COPD patients have never used it or heard of it.
PLB has been shown in previous studies to help moderate to severe COPD patients improve pulmonary gas exchange, reduce hyperinflation of the lungs, improve physical function and reduce oxygen desaturation in the lungs. In one recent study, 32 COPD patients who used pursed-lip breathing immediately before walking boosted the time they were about to walk before fatiguing by 16%. (Faager G, et al. Influence of spontaneous pursed lips breathing on walking endurance and oxygen saturation in patients with moderate to severe chronic obstructive pulmonary disease. Clin Rehabil. 2008 Aug;22(8):675-83)
Pursed-lips breathing works like this - first, with your mouth closed you breathe in through your nose for 2-3 seconds. Then, you purse your lips (like you are blowing out candles on a birthday cake or blowing bubbles through the small opening of a bubble wand) and blow air out through your pursed-lips for about twice as long as you inhaled through your nose (approximately 4-6 seconds).
This technique works because narrowing the opening of your mouth when you exhale creates back pressure. Back pressure helps you blow out more used air from your lungs. And that’s the core of the issue when you feel short of breath. While it feels like you can’t breathe in fresh air, the real issue is that you have too much used air trapped in your lungs. Until you can get the used air out, it doesn’t matter how hard you try to breathe in. Your lungs don’t have the capacity to accept a large volume of fresh air when you have used air dominating your airway passages. PLB helps clear out the used air more quickly so that more fresh air (and hence, more oxygen) can be taken in by your lungs. In turn, PLB helps reduce shortness of breath related to walking, climbing stairs, exercising, and other vigorous activities. This is likely the mechanism that increased inspiratory capacity in the COPD patients in the Respiration study mentioned above. By clearing out more old/used air using PLB, the lungs are in a better position to absorb a greater maximum volume of fresh air when inhaling.
A simple example to demonstrate how PLB works – face the palm of one of your hands a couple of inches from the opening of your mouth and exhale for 3 seconds without pursing your lips. Now, exhale again on the palm of your hand using the pursed-lips breathing technique for 3 seconds. If you’ve executed PLB correctly, you should have noticed a significant difference in the force of air hitting your hand when using PLB versus exhaling normally from your mouth.
Though I don’t have COPD nor have I ever smoked cigarettes, I use the pursed-lips breathing technique frequently when I climb long flights of stairs and when I’m feeling short of breath when running or working out in the gym. I have to say I’ve been very impressed at two effects of PLB when I use it. First, I definitely believe it helps me reduce shortness of breath in a relatively short time frame. Second, and more surprising to me, is the sensation I get when using PLB that I am in greater control of my breathing rhythm during vigorous activity which to me has a calming/relaxing effect.
For a printable sheet demonstrating the pursed-lips breathing technique taken from our Breathe Better for Life CD-ROM, click here. For more information about our Breathe Better for Life guidebook and CD-ROM, visit www.breathebetterforlife.com.
Pursed-lips breathing is a highly effective breathing technique taught by respiratory therapists and other pulmonology professionals in pulmonary rehabilitation programs to help COPD reduce the sensation of breathlessness before, during or after exercise or other strenuous activities. Despite its effectiveness, it is remarkable to me how many COPD patients have never used it or heard of it.
PLB has been shown in previous studies to help moderate to severe COPD patients improve pulmonary gas exchange, reduce hyperinflation of the lungs, improve physical function and reduce oxygen desaturation in the lungs. In one recent study, 32 COPD patients who used pursed-lip breathing immediately before walking boosted the time they were about to walk before fatiguing by 16%. (Faager G, et al. Influence of spontaneous pursed lips breathing on walking endurance and oxygen saturation in patients with moderate to severe chronic obstructive pulmonary disease. Clin Rehabil. 2008 Aug;22(8):675-83)
Pursed-lips breathing works like this - first, with your mouth closed you breathe in through your nose for 2-3 seconds. Then, you purse your lips (like you are blowing out candles on a birthday cake or blowing bubbles through the small opening of a bubble wand) and blow air out through your pursed-lips for about twice as long as you inhaled through your nose (approximately 4-6 seconds).
This technique works because narrowing the opening of your mouth when you exhale creates back pressure. Back pressure helps you blow out more used air from your lungs. And that’s the core of the issue when you feel short of breath. While it feels like you can’t breathe in fresh air, the real issue is that you have too much used air trapped in your lungs. Until you can get the used air out, it doesn’t matter how hard you try to breathe in. Your lungs don’t have the capacity to accept a large volume of fresh air when you have used air dominating your airway passages. PLB helps clear out the used air more quickly so that more fresh air (and hence, more oxygen) can be taken in by your lungs. In turn, PLB helps reduce shortness of breath related to walking, climbing stairs, exercising, and other vigorous activities. This is likely the mechanism that increased inspiratory capacity in the COPD patients in the Respiration study mentioned above. By clearing out more old/used air using PLB, the lungs are in a better position to absorb a greater maximum volume of fresh air when inhaling.
A simple example to demonstrate how PLB works – face the palm of one of your hands a couple of inches from the opening of your mouth and exhale for 3 seconds without pursing your lips. Now, exhale again on the palm of your hand using the pursed-lips breathing technique for 3 seconds. If you’ve executed PLB correctly, you should have noticed a significant difference in the force of air hitting your hand when using PLB versus exhaling normally from your mouth.
Though I don’t have COPD nor have I ever smoked cigarettes, I use the pursed-lips breathing technique frequently when I climb long flights of stairs and when I’m feeling short of breath when running or working out in the gym. I have to say I’ve been very impressed at two effects of PLB when I use it. First, I definitely believe it helps me reduce shortness of breath in a relatively short time frame. Second, and more surprising to me, is the sensation I get when using PLB that I am in greater control of my breathing rhythm during vigorous activity which to me has a calming/relaxing effect.
For a printable sheet demonstrating the pursed-lips breathing technique taken from our Breathe Better for Life CD-ROM, click here. For more information about our Breathe Better for Life guidebook and CD-ROM, visit www.breathebetterforlife.com.
Monday, August 2, 2010
Wood smoke exposure, COPD and chronic bronchitis
Outside of the United States a number of research studies have looked at the connection between wood smoke, COPD and chronic bronchitis. While cigarette smoke exposure remains the number one cause of developing COPD worldwide, wood smoke exposure has been identified as a major contributing factor in many countries that utilize wood as a room heating and cooking heat source.
A new study published this month online ahead of print in the American Journal of Respiratory and Critical Care Medicine examines the connection between wood smoke and COPD/chronic bronchitis diagnosis in the United States. In the study, the research team found a significant correlation between wood smoke exposure and COPD/chronic bronchitis diagnosis among current smokers (and further noted higher odds among people of Hispanic origin and men of all origin). (Sood A, et al. Wood Smoke Exposure and Gene Promoter Methylation are Associated with Increased Risk for COPD in Smokers.Am J Respir Crit Care Med. 2010 Jul 1. [Epub ahead of print])
As the study authors explained, “In developed countries, people are exposed to wood smoke in a variety of ways, including smoke from residential heating, cooking stoves, campfires, forest fires, and prescribed fires. Wood burning is an important contributor to particle and gaseous material in ambient air, and in some locations accounts for up to 80% of the airborne particle concentrations during the winter...Wood burning not only increases indoor but also outdoor ‘neighborhood’ pollution; thereby exposing many non-users to wood smoke components… Wood smoke is a complex mixture of numerous volatile and particulate substances constituted by different organic and inorganic compounds known to be toxic or irritating to the respiratory system. Its composition varies with the wood type and the conditions of combustion. More than 200 chemical and compound groups have been identified, most of which are in the inhalable size range…Exposure to wood smoke in developed countries tends to be at sustained low-levels unlike exposure to cigarette smoke that is short-term but intense with a single cigarette…
Our study contrasts with most studies conducted outside the United States that have focused on non-smokers. Our population of relatively older smokers may be particularly susceptible to the adverse respiratory effects of wood smoke exposure, compared to the general population. This conclusion is supported by the observed additive effect between current cigarette smoke and wood smoke exposures on COPD phenotypes. Furthermore, these epidemiological findings are substantiated by our laboratory findings in which pulmonary inflammation and pathological changes were enhanced in mice concurrently exposed to wood smoke and cigarette smoke compared to cigarette smoke alone”.
In the study, researchers examined the medical records of the Lovelace Smoker Cohort. A Cohort is a group of people who have agreed to participate in an ongoing study, typically conducted over a generation. In such studies, subjects submit to periodic medical tests and examinations over time and also answer periodic surveys regarding a variety of health information. The Lovelace Smoker Cohort follows approximately 2,000 New Mexico residents who identified themselves as ever-smokers (study participants enrolled between 2001 and 2007).
The research team sampled approximately 1,800 relevant subjects from the cohort and reviewed surveys completed this sampling to identify those who self-reported exposure to wood smoke (approximately 500 people). Then the researchers examined spirometry results and sputum samples taken periodically for both the group exposed to wood smoke/cigarette smoke and those who were only exposed to cigarette smoke.
They discovered that those who were exposed to wood smoke and reported themselves as current cigarette smokers had a 116% higher odds ratio of being diagnosed with COPD than study subjects who were current smokers but were not exposed to wood smoke. Additionally, those exposed to wood/cigarette smoke had a 46% higher odds ratio of being diagnosed with chronic bronchitis.
Further, the study results revealed that the odds ratio of developing COPD among former smokers exposed to wood smoke was 36% higher than current cigarette smokers not exposed to wood smoke. This result implies that wood smoke is potentially more harmful than cigarette smoke in the odds of developing COPD. However, in contrast of this result, former smokers exposed to wood smoke had a 46% lower odds ratio of developing chronic bronchitis as compared to current smokers exposed to cigarette smoke only. So, there does not appear to be a correlation between wood smoke exposure and chronic bronchitis among former smokers.
Overall, the study seems to indicate that current smokers who regularly utilize wood as a cooking, heating, or brush removal fire source dramatically increase their odds of developing COPD and/or chronic bronchitis. If you are both a current smoker and are exposed to wood smoke frequently, these results suggest you can significantly reduce your odds of developing COPD and chronic bronchitis by halting your exposure to wood smoke. That is not to say that doing so will prevent you from being diagnosed with COPD and/or chronic bronchitis, especially if you are a current smoker. But any positive step you can take to avoid regular exposure to pollutants/irritants (such as wood smoke) that contribute to persistent airway inflammation and sputum production is surely a step in the right direction.
A new study published this month online ahead of print in the American Journal of Respiratory and Critical Care Medicine examines the connection between wood smoke and COPD/chronic bronchitis diagnosis in the United States. In the study, the research team found a significant correlation between wood smoke exposure and COPD/chronic bronchitis diagnosis among current smokers (and further noted higher odds among people of Hispanic origin and men of all origin). (Sood A, et al. Wood Smoke Exposure and Gene Promoter Methylation are Associated with Increased Risk for COPD in Smokers.Am J Respir Crit Care Med. 2010 Jul 1. [Epub ahead of print])
As the study authors explained, “In developed countries, people are exposed to wood smoke in a variety of ways, including smoke from residential heating, cooking stoves, campfires, forest fires, and prescribed fires. Wood burning is an important contributor to particle and gaseous material in ambient air, and in some locations accounts for up to 80% of the airborne particle concentrations during the winter...Wood burning not only increases indoor but also outdoor ‘neighborhood’ pollution; thereby exposing many non-users to wood smoke components… Wood smoke is a complex mixture of numerous volatile and particulate substances constituted by different organic and inorganic compounds known to be toxic or irritating to the respiratory system. Its composition varies with the wood type and the conditions of combustion. More than 200 chemical and compound groups have been identified, most of which are in the inhalable size range…Exposure to wood smoke in developed countries tends to be at sustained low-levels unlike exposure to cigarette smoke that is short-term but intense with a single cigarette…
Our study contrasts with most studies conducted outside the United States that have focused on non-smokers. Our population of relatively older smokers may be particularly susceptible to the adverse respiratory effects of wood smoke exposure, compared to the general population. This conclusion is supported by the observed additive effect between current cigarette smoke and wood smoke exposures on COPD phenotypes. Furthermore, these epidemiological findings are substantiated by our laboratory findings in which pulmonary inflammation and pathological changes were enhanced in mice concurrently exposed to wood smoke and cigarette smoke compared to cigarette smoke alone”.
In the study, researchers examined the medical records of the Lovelace Smoker Cohort. A Cohort is a group of people who have agreed to participate in an ongoing study, typically conducted over a generation. In such studies, subjects submit to periodic medical tests and examinations over time and also answer periodic surveys regarding a variety of health information. The Lovelace Smoker Cohort follows approximately 2,000 New Mexico residents who identified themselves as ever-smokers (study participants enrolled between 2001 and 2007).
The research team sampled approximately 1,800 relevant subjects from the cohort and reviewed surveys completed this sampling to identify those who self-reported exposure to wood smoke (approximately 500 people). Then the researchers examined spirometry results and sputum samples taken periodically for both the group exposed to wood smoke/cigarette smoke and those who were only exposed to cigarette smoke.
They discovered that those who were exposed to wood smoke and reported themselves as current cigarette smokers had a 116% higher odds ratio of being diagnosed with COPD than study subjects who were current smokers but were not exposed to wood smoke. Additionally, those exposed to wood/cigarette smoke had a 46% higher odds ratio of being diagnosed with chronic bronchitis.
Further, the study results revealed that the odds ratio of developing COPD among former smokers exposed to wood smoke was 36% higher than current cigarette smokers not exposed to wood smoke. This result implies that wood smoke is potentially more harmful than cigarette smoke in the odds of developing COPD. However, in contrast of this result, former smokers exposed to wood smoke had a 46% lower odds ratio of developing chronic bronchitis as compared to current smokers exposed to cigarette smoke only. So, there does not appear to be a correlation between wood smoke exposure and chronic bronchitis among former smokers.
Overall, the study seems to indicate that current smokers who regularly utilize wood as a cooking, heating, or brush removal fire source dramatically increase their odds of developing COPD and/or chronic bronchitis. If you are both a current smoker and are exposed to wood smoke frequently, these results suggest you can significantly reduce your odds of developing COPD and chronic bronchitis by halting your exposure to wood smoke. That is not to say that doing so will prevent you from being diagnosed with COPD and/or chronic bronchitis, especially if you are a current smoker. But any positive step you can take to avoid regular exposure to pollutants/irritants (such as wood smoke) that contribute to persistent airway inflammation and sputum production is surely a step in the right direction.
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