Many of you have heard of the 1938 Orson Welles’ radio broadcast of the H.G. Wells classic novel, War of the Worlds, and the widespread panic it briefly spurred. Welles’ actors delivered chilling, live reports of invading aliens landing on Earth and causing major mayhem, death and destruction along the way. Many people listening on the radio had no idea that Welles was offering a theatric production and mistakenly believed that real aliens were indeed invading. Calls flooded police stations; people grabbed family, pets and guns and headed for the cellar, others hopped in cars and either fled in abject fear or went in search of aliens to attack. When the broadcast was over and the dust settled, Welles was forced to bashfully go on-air again to explain, NEVER MIND, it was all just an act.
Well believe it or not, a similar theatric production goes on in your lungs daily if you are a smoker or have a respiratory condition such as COPD.
Imagine invading bacteria are inhaled into your lungs (the aliens). Proteins in lung cells called cytokines that are charged with keeping a lookout for troublemakers (radio listeners) sense the invasion and panic. The cytokines start signaling other cytokines, sending out thousands of messages (calls flooding police stations). The message-receiving cytokines in turn call even more cytokines and so on…all putting out alerts for the body to produce white blood cells (policemen) to come and attack the invading aliens. The cells that produce white blood cells receive thousands, tens of thousands, hundreds of thousands, millions of messages from the cytokines to rush to the lungs as fast as possible and take care of the invaders. Soon the lung tissues, as the cytokines and white blood cells gather for the fight, become swelled with the particles and fluids from these defenders of the peace, all running around in a panic about the invading bacteria. They’ve brought enough ammo to wipe out millions of the invaders…but guess what? There may only be a hundred of the bacteria molecules…
You see – it’s a false alarm. An act. An over-reaction.
Cigarette smoke has messed up lung cells’ ability to appropriately detect and respond to invading bacteria. Instead of cytokines accurately sensing the number of invading bacteria/fungi and sending out signals for a proportional response to kill them, the cells fear there is a massive attack and respond with overwhelming force.
The problem with this over-reaction is that when lung tissues swell with fluid and become stiff, the airways narrow and it becomes harder to breathe. This circumstance is referred to as airway inflammation by pulmonology professionals.
Inflammation in the lungs is similar to inflammation in other parts of your body - tissues swell with fluid and become stiff. If you’ve ever sprained an ankle, knee or shoulder, you know how your damaged joint swelled and stiffened for a period of time after the injury. The pressure of the swelled tissue feels uncomfortable, like someone squeezing you. The stiffened joint makes it hard to move, restricting your activity. Well, now imagine those same effects happening to your airways…no wonder it’s hard to breathe!
Can inflammation be stopped or reduced?
Pulmonology researchers and practitioners are in an ongoing search to find effective ways to reduce oxidative stress, relieve inflammation, and prevent/reverse /minimize the damage done by cigarette smoke and other inhaled toxic agents.
If you currently smoke, the number one step you can take to reduce inflammation is to quit. Permanently. Plain and simple, it’s the single best first step you can take.
Outside of smoking cessation, physicians can and often do prescribe some combination of short-acting bronchodilators and corticosteroids for use when patients are experiencing uncomfortable shortness of breath. These medications force open the airways by shutting off the production of cytokines and similar signaling agents in the body…but only for a short time. These pharmaceutical solutions do very little to resolve inflammation long-term and they unfortunately come with common dissatisfying side effects such as persistent dry-mouth.
Physicians often also prescribe antibiotics to help COPD patients and others with respiratory conditions defeat upper respiratory infections caused by bacteria & fungi. Antibiotics do help relieve immediate shortness of breath symptoms by killing off infectious bacteria & fungi, but again, this is only a short-term fix. Antibiotics do not relieve inflammation over the long term.
Beyond Inhalers - Do Your Part!
There are some very specific, research-based action steps you can take on your own to reduce oxidative stress, alleviate inflammation, reduce shortness of breath, and feel better for the long run, including:
• Engage in a regular cardiovascular & strength training exercise program
• Ensure you are receiving adequate exposure to direct sunlight
• Increase antioxidant & key nutrient intake from food
• Increase antioxidant & key nutrient intake from dietary supplements
• Practice proven breathing techniques & airway clearing techniques
To be clear, in no way are these steps meant to replace advice provided by your physician. Further, these action steps will NOT reverse lung disease, repair lung cells, nor improve lung function, but combined they can help make a significant difference in how you feel and breathe, and are steps you can take that complement the medical care you receive from your physician. To learn more about each of these respiratory health self-management action steps, visit our Five Steps to Feel Better Now Plan by clicking here.
Wednesday, October 27, 2010
Wednesday, October 20, 2010
Does frequent chocolate consumption lower your risk of coronary heart disease?
According to a new study published online ahead of print in the journal Clinical Nutrition…quite possibly yes! The research team leading the study found that adults who consumed at least 5 servings of chocolate per week had 57% lower odds of developing coronary heart disease (CHD) compared to those who consumed no candy at all. (Djousse L, et al. Chocolate consumption is inversely associated with prevalent coronary heart disease: The National Heart, Lung, and Blood Institute Family Heart Study. Clin Nutr. 2010 Sep 19. [Epub ahead of print])
Now I’m sure we’ve all seen the screaming headlines in supermarket tabloids that declare, “Chocolate Cures Everything!” And while for some people chocolate might indeed seem like a cure for a broken heart, stress or a craving for sweet-tasting food, does it really offer measurable health benefits?
Well, according to the new study’s authors, it turns out that a number of human subject studies conducted over the past decade have actually demonstrated notable health benefits associated with high chocolate consumption ranging from lower blood pressure, lower cholesterol levels, and lower cardiovascular disease risk in general.
In the Clinical Nutrition study, the Harvard Medical School-based lead investigator examined the medical records of nearly 5,000 adults who participated in broader heart health study known as the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. In particular, the researchers looked at food consumption surveys completed by study participants that highlighted chocolate consumption among other foods. They then compared the incidence of coronary heart disease among the study participants at various levels of chocolate consumption (none, 1-3 times/month, 1-4 times/week, and 5+ times/week).
The study team’s results showed that people who consumed chocolate 1-3 times a month had about the same odds ratio of developing CHD as non-chocolate consumers, while the group that consumed chocolate 1-4 times/week had 26% lower risk of developing CHD, and the group devouring chocolate 5+ times/week showed a 57% lower odds ratio of a CHD diagnosis.
So what’s going on here? How can high chocolate consumption possibly lessen your risk of coronary heart disease? Well, according to the study authors, chocolate (cocoa and dark chocolate in particular), contains high amounts of powerful antioxidant compounds known as polyphenols that are believed to be helpful in reducing the damage done to the human body by molecules known as free radicals.
Free radicals are by-products of the body’s process to utilize oxygen (when cells absorb oxygen, they break off the piece of oxygen they need leaving an unstable oxygen molecule behind – this unstable oxygen molecule is known as a free radical). Free radical damage is believed to be a significant contributing factor in many diseases associated with aging. In addition to free radicals created in the human body through the normal everyday process of absorbing and using energy, free radicals can also be inhaled in massive amounts through cigarette smoke as well as environmental and industrial pollutants. Hence why we bring this study to your attention.
Generally, in non-smoking adults who consume a diet that includes foods high in antioxidant content (whole grains, fruits, vegetables, tea, and red wine to name a few) research evidence shows lower incidence of many types of cardiovascular and respiratory disease. From this study’s results it appears that chocolate can be added to this list.
It should be noted that while the study authors emphasize the value of dark chocolate over milk chocolate in reporting their findings based on previously reported study results, their study participants did not delineate their consumption between the two types of chocolate (and one would presume that most of the study subjects were consuming a fair bit of milk chocolate given that most chocolate candy is milk chocolate-based).
A parting word of caution from the study’s authors though – while chocolate may confer these protective cardiovascular benefits, other forms of candy do not. For example, the investigators evaluated the odds ratio of CHD among people who consumed 5+ servings of non-chocolate candy each week to those who consumed no candy and found the non-chocolate candy group had a 49% HIGHER risk of developing coronary heart disease (as opposed to a 57% LOWER risk among those who consumed chocolate 5+ times/week).
So, if you find yourself craving a sweet-tasting component to your daily diet one would be wise to reach for a chocolate bar instead of a fistful of jelly beans. While chocolate might be a bit messier to eat, your heart will approve of your selection!
Now I’m sure we’ve all seen the screaming headlines in supermarket tabloids that declare, “Chocolate Cures Everything!” And while for some people chocolate might indeed seem like a cure for a broken heart, stress or a craving for sweet-tasting food, does it really offer measurable health benefits?
Well, according to the new study’s authors, it turns out that a number of human subject studies conducted over the past decade have actually demonstrated notable health benefits associated with high chocolate consumption ranging from lower blood pressure, lower cholesterol levels, and lower cardiovascular disease risk in general.
In the Clinical Nutrition study, the Harvard Medical School-based lead investigator examined the medical records of nearly 5,000 adults who participated in broader heart health study known as the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. In particular, the researchers looked at food consumption surveys completed by study participants that highlighted chocolate consumption among other foods. They then compared the incidence of coronary heart disease among the study participants at various levels of chocolate consumption (none, 1-3 times/month, 1-4 times/week, and 5+ times/week).
The study team’s results showed that people who consumed chocolate 1-3 times a month had about the same odds ratio of developing CHD as non-chocolate consumers, while the group that consumed chocolate 1-4 times/week had 26% lower risk of developing CHD, and the group devouring chocolate 5+ times/week showed a 57% lower odds ratio of a CHD diagnosis.
So what’s going on here? How can high chocolate consumption possibly lessen your risk of coronary heart disease? Well, according to the study authors, chocolate (cocoa and dark chocolate in particular), contains high amounts of powerful antioxidant compounds known as polyphenols that are believed to be helpful in reducing the damage done to the human body by molecules known as free radicals.
Free radicals are by-products of the body’s process to utilize oxygen (when cells absorb oxygen, they break off the piece of oxygen they need leaving an unstable oxygen molecule behind – this unstable oxygen molecule is known as a free radical). Free radical damage is believed to be a significant contributing factor in many diseases associated with aging. In addition to free radicals created in the human body through the normal everyday process of absorbing and using energy, free radicals can also be inhaled in massive amounts through cigarette smoke as well as environmental and industrial pollutants. Hence why we bring this study to your attention.
Generally, in non-smoking adults who consume a diet that includes foods high in antioxidant content (whole grains, fruits, vegetables, tea, and red wine to name a few) research evidence shows lower incidence of many types of cardiovascular and respiratory disease. From this study’s results it appears that chocolate can be added to this list.
It should be noted that while the study authors emphasize the value of dark chocolate over milk chocolate in reporting their findings based on previously reported study results, their study participants did not delineate their consumption between the two types of chocolate (and one would presume that most of the study subjects were consuming a fair bit of milk chocolate given that most chocolate candy is milk chocolate-based).
A parting word of caution from the study’s authors though – while chocolate may confer these protective cardiovascular benefits, other forms of candy do not. For example, the investigators evaluated the odds ratio of CHD among people who consumed 5+ servings of non-chocolate candy each week to those who consumed no candy and found the non-chocolate candy group had a 49% HIGHER risk of developing coronary heart disease (as opposed to a 57% LOWER risk among those who consumed chocolate 5+ times/week).
So, if you find yourself craving a sweet-tasting component to your daily diet one would be wise to reach for a chocolate bar instead of a fistful of jelly beans. While chocolate might be a bit messier to eat, your heart will approve of your selection!
Tuesday, October 19, 2010
Further evidence of undetected osteoporosis in COPD patients
For the second time in less than a month, a new study has been published detailing the high rate of osteoporosis in COPD patients and revealing the low rate of testing and detection for this debilitating bone condition among those with lung disease.
For regular readers of our blog and e-letters, you will recall that we published an article earlier this month describing a new study that showed osteoporosis was present in 51% of COPD patients participating in the study. More alarming though was the presence of vertebral fractures in a significant percentage of these patients – many of whom had no idea they had such fractures! Click here to read the article.
Now comes a study published last week online ahead of print in the journal Osteoporosis International that demonstrates both the high incidence of osteoporosis in COPD patients and the poor rate of testing and detection of bone disease in this population – only on a significantly larger scale.
In this new study, a group of researchers from the Dartmouth Medical School examined the records of close to 90,000 male veterans who were newly diagnosed with COPD between 1999 and 2003 and who were receiving medical care through the Veterans Administration. (Morden NE, et al. Skeletal health in men with chronic lung disease: rates of testing, treatment, and fractures. Osteoporos Int. 2010 Oct 9. [Epub ahead of print]).
In particular the research team sought to determine whether the presence of osteoporosis was higher among male COPD patients in comparison to men of similar age in the U.S. population. Their results showed that the male COPD patients in the study had 256% higher incidence of hip fractures and 38% higher incidence of wrist fractures compared to males of similar age in the general U.S. population.
According to the study authors, “The fracture rate in this population was much higher than that reported in the literature for men in the general population between the ages of 65 and 69… The high fracture rate likely results from a confluence of risks that include medication exposure, inactivity, smoking, hypogonadism, underweight or weight loss as well as inadequate nutrition and effects of the chronic inflammation that characterizes COPD.”
Further, the investigators sought to understand the prevalence of bone mineral density testing and treatment for low bone density in the male COPD patients. They found that only 4% of the nearly 90,000 COPD patients had received a bone density test (either concurrent with their COPD diagnosis or thereafter). Of the 4% COPD patients who were tested for low bone density, approximately 75% were prescribed an osteoporosis-related medication – but that still means that only 3% of the total COPD study subjects were prescribed helpful medication.
We ask ourselves, if pulmonologists know that well over 50% of COPD patients likely have osteoporosis, why are they only testing 4% of newly diagnosed patients?
How can this be? It’s probably best to let the researchers speak for themselves, “Juxtaposed to the high rate of fragility fracture, the low rate of bone densitometry [testing] and anti-resporptive treatment in this population is striking. The association between osteoporosis and COPD was recognized as early as 1972, and confirmation of this association has repeatedly appeared in the literature since then. The low rate of treatment observed in this cohort [population] likely reflects the low rate of bone density testing which commonly prompts treatment. Of particular note is the fact that more COPD exacerbations were strongly associated with both higher probability of fracture and lower probability of testing or treatment. This may reflect physician and patient distraction as lung disease is prioritized over bone health or simply a lack of understanding of the association between COPD severity (and related treatments) and fracture.”
In other words, physicians seem more focused on treating lung disease and miss the opportunity to test COPD patients for osteoporosis. While one can understand the prioritization of care when a patient has experienced a COPD-related exacerbation, it is less understandable why there isn’t standard osteoporosis screening as part of the follow up process related to an exacerbation. This is especially puzzling given the observations of the Dartmouth study team, “In addition to being at high risk for osteoporosis and consequent fragility fractures, men with COPD may suffer particularly high mortality following a hip fracture…In addition to higher mortality, patients with COPD may suffer greater morbidity from osteoporosis as vertebral compression fractures may diminish lung volume and compromise already limited respiratory function.”
Therefore, my good friends, you appear to be in the driver’s seat on this topic. If you have COPD and you have not been tested/screened for osteoporosis, we would highly recommend that you asked to be tested. The study highlighted four different screening tests available for assessing osteoporosis risk including: dual energy X-ray studies, ultrasound for bone density measure, CT scan bone density, and bone mineral, single or dual photon.
Separately, you can help support both your respiratory function and bone density by altering your lifestyle by taking these valuable steps:
1. Start and maintain a regular exercise program that includes both cardiovascular training and strength training. Our Breathe Better for Life guide/CD, www.breathebetterforlife.com, provides a specific exercise program regimen formulated specifically for COPD patients and smokers based on the principles and practices of the COPD treatment pulmonary rehabilitation. Even a simple walking program that involves 20-40 minutes of walking 3-5 days each week will provide some protective value for both COPD symptoms and osteoporosis.
2. Increase your exposure to direct sunlight (without sunscreen lotion on that blocks UV-B rays)…meaning get outside with multiple parts of your body exposed to direct sunlight for 20-30 minutes a day (combine that with your walking program and you’re knocking off two important steps in one action!) Sunlight helps your body produce Vitamin D, an important nutrient in supporting healthy respiratory function and bones. COPD patients and smokers are known to be significantly deficient in Vitamin D.
3. Supplement your diet with foods rich in Vitamin D (and/or fortified with Vitamin D). For a good listing of Vitamin D rich foods, click here.
4. Consider adding a Vitamin D3 dietary supplement to your daily routine – we recommend 2,000 IU daily dosage (make sure your Vitamin D3 comes in the form of cholecalciferol). For those interested, we have included this dosage level in our new respiratory support supplement, Resplenish. To learn more about Resplenish, click here.
5. Increase protein sources to your daily diet – three particularly good sources that have been shown in previous studies to be associated with better respiratory function are soy isoflavones (soy bean sprouts, tofu, soy beans), fish and dairy products (both dairy products and fish are also rich sources of Vitamin D). Many COPD patients and smokers are underweight due to lack of adequate protein/nutrient intake. Protein is helpful in maintaining a healthy weight and healthy muscles – which are supportive of healthy bones.
For regular readers of our blog and e-letters, you will recall that we published an article earlier this month describing a new study that showed osteoporosis was present in 51% of COPD patients participating in the study. More alarming though was the presence of vertebral fractures in a significant percentage of these patients – many of whom had no idea they had such fractures! Click here to read the article.
Now comes a study published last week online ahead of print in the journal Osteoporosis International that demonstrates both the high incidence of osteoporosis in COPD patients and the poor rate of testing and detection of bone disease in this population – only on a significantly larger scale.
In this new study, a group of researchers from the Dartmouth Medical School examined the records of close to 90,000 male veterans who were newly diagnosed with COPD between 1999 and 2003 and who were receiving medical care through the Veterans Administration. (Morden NE, et al. Skeletal health in men with chronic lung disease: rates of testing, treatment, and fractures. Osteoporos Int. 2010 Oct 9. [Epub ahead of print]).
In particular the research team sought to determine whether the presence of osteoporosis was higher among male COPD patients in comparison to men of similar age in the U.S. population. Their results showed that the male COPD patients in the study had 256% higher incidence of hip fractures and 38% higher incidence of wrist fractures compared to males of similar age in the general U.S. population.
According to the study authors, “The fracture rate in this population was much higher than that reported in the literature for men in the general population between the ages of 65 and 69… The high fracture rate likely results from a confluence of risks that include medication exposure, inactivity, smoking, hypogonadism, underweight or weight loss as well as inadequate nutrition and effects of the chronic inflammation that characterizes COPD.”
Further, the investigators sought to understand the prevalence of bone mineral density testing and treatment for low bone density in the male COPD patients. They found that only 4% of the nearly 90,000 COPD patients had received a bone density test (either concurrent with their COPD diagnosis or thereafter). Of the 4% COPD patients who were tested for low bone density, approximately 75% were prescribed an osteoporosis-related medication – but that still means that only 3% of the total COPD study subjects were prescribed helpful medication.
We ask ourselves, if pulmonologists know that well over 50% of COPD patients likely have osteoporosis, why are they only testing 4% of newly diagnosed patients?
How can this be? It’s probably best to let the researchers speak for themselves, “Juxtaposed to the high rate of fragility fracture, the low rate of bone densitometry [testing] and anti-resporptive treatment in this population is striking. The association between osteoporosis and COPD was recognized as early as 1972, and confirmation of this association has repeatedly appeared in the literature since then. The low rate of treatment observed in this cohort [population] likely reflects the low rate of bone density testing which commonly prompts treatment. Of particular note is the fact that more COPD exacerbations were strongly associated with both higher probability of fracture and lower probability of testing or treatment. This may reflect physician and patient distraction as lung disease is prioritized over bone health or simply a lack of understanding of the association between COPD severity (and related treatments) and fracture.”
In other words, physicians seem more focused on treating lung disease and miss the opportunity to test COPD patients for osteoporosis. While one can understand the prioritization of care when a patient has experienced a COPD-related exacerbation, it is less understandable why there isn’t standard osteoporosis screening as part of the follow up process related to an exacerbation. This is especially puzzling given the observations of the Dartmouth study team, “In addition to being at high risk for osteoporosis and consequent fragility fractures, men with COPD may suffer particularly high mortality following a hip fracture…In addition to higher mortality, patients with COPD may suffer greater morbidity from osteoporosis as vertebral compression fractures may diminish lung volume and compromise already limited respiratory function.”
Therefore, my good friends, you appear to be in the driver’s seat on this topic. If you have COPD and you have not been tested/screened for osteoporosis, we would highly recommend that you asked to be tested. The study highlighted four different screening tests available for assessing osteoporosis risk including: dual energy X-ray studies, ultrasound for bone density measure, CT scan bone density, and bone mineral, single or dual photon.
Separately, you can help support both your respiratory function and bone density by altering your lifestyle by taking these valuable steps:
1. Start and maintain a regular exercise program that includes both cardiovascular training and strength training. Our Breathe Better for Life guide/CD, www.breathebetterforlife.com, provides a specific exercise program regimen formulated specifically for COPD patients and smokers based on the principles and practices of the COPD treatment pulmonary rehabilitation. Even a simple walking program that involves 20-40 minutes of walking 3-5 days each week will provide some protective value for both COPD symptoms and osteoporosis.
2. Increase your exposure to direct sunlight (without sunscreen lotion on that blocks UV-B rays)…meaning get outside with multiple parts of your body exposed to direct sunlight for 20-30 minutes a day (combine that with your walking program and you’re knocking off two important steps in one action!) Sunlight helps your body produce Vitamin D, an important nutrient in supporting healthy respiratory function and bones. COPD patients and smokers are known to be significantly deficient in Vitamin D.
3. Supplement your diet with foods rich in Vitamin D (and/or fortified with Vitamin D). For a good listing of Vitamin D rich foods, click here.
4. Consider adding a Vitamin D3 dietary supplement to your daily routine – we recommend 2,000 IU daily dosage (make sure your Vitamin D3 comes in the form of cholecalciferol). For those interested, we have included this dosage level in our new respiratory support supplement, Resplenish. To learn more about Resplenish, click here.
5. Increase protein sources to your daily diet – three particularly good sources that have been shown in previous studies to be associated with better respiratory function are soy isoflavones (soy bean sprouts, tofu, soy beans), fish and dairy products (both dairy products and fish are also rich sources of Vitamin D). Many COPD patients and smokers are underweight due to lack of adequate protein/nutrient intake. Protein is helpful in maintaining a healthy weight and healthy muscles – which are supportive of healthy bones.
Sunday, October 17, 2010
New study shows value of combining aerobic exercise with strength training among COPD patients
This week, a new Portuguese research study revealed that moderate to severe COPD patients who underwent an exercise program including both strength resistance training and aerobic exercise training reported higher levels of perceived health status compared to COPD patients who participated in either aerobic training alone or respiratory physiotherapy.
A number of previous studies have shown that the combination of aerobic exercise and strength/resistance training produces higher levels of overall physical conditioning in COPD patients than either of these two forms of exercise alone (i.e. greater endurance, greater muscle strength, greater exercise capacity). This is a key reason why most pulmonary rehabilitation programs include both strength training and aerobic/cardiovascular training in their exercise regimens.
Instead of evaluating objective, physical measures of performance between these three potential COPD treatment options (strength & aerobic exercise, aerobic exercise, physiotherapy), the new Portuguese based research study aimed to understand how COPD patients perceive their own health status through two “quality of life” surveys (the St. George’s Respiratory Questionnaire (view sample survey form by clicking here) and the Short Form [36] Health Survey (view sample survey form by clicking here).
In other words, the study team desired to know, outside of physical performance measures (e.g. did you walk farther, did you walk faster, could you lift more weight), do COPD patients actually feel differently about their own health status depending on which method of rehabilitation they receive?
To test their hypothesis, the research team divided 50 moderate to severe COPD patients into two groups (25 who participated in a 10-week combined strength/aerobic exercise program, 25 in a 10-week aerobic-only exercise group) and compared their survey results to each other and to an additional 50 moderate to severe COPD patients who received 10 weeks of respiratory physiotherapy (essentially physical therapy accompanied by breathing technique and airway clearing technique training – but no explicit exercise program). They administered the two surveys mentioned above prior to the respective treatment programs and then again at the end of the programs. They then measured the differences in the patients’ responses from their pre-program surveys and their post-program surveys and compared the mean (average) results between the three different treatment options. (Pereira AM, et al. Impact of combined exercise on chronic obstructive pulmonary patients' state of health. Rev Port Pneumol. 2010 Sep-Oct;16(5):737-57)
The results clearly showed that COPD patients who received both the strength training and aerobic exercise training reported significantly higher ratings of their perceived health status at the end of their exercise program as compared to the other two groups ON ALL SECTIONS OF BOTH SURVEYS.
For example, in the St. George’s Respiratory Questionnaire, the combined exercise group reported a 64 point increase in their “activity” rating (a section of the questionnaire designed to understand a patient’s ability to participate in activities of daily living) versus a 19 point increase for the aerobic-only exercise group and a 1 point increase for the physiotherapy group.
As another example, on the SF-36 survey, COPD patients receiving both strength and aerobic exercise training reported an 83 point jump in their perceived vitality (a section of the test designed to assess quality of daily living), versus a 14 point rise for the aerobic-only group. On this measure the physiotherapy group showed flat response between pre and post treatment.
These results reinforce the basic underlying principles and practices of COPD treatment pulmonary rehabilitation. Combined strength and aerobic exercise is highly valuable for those who suffer from chronic shortness of breath on two fronts – on physical performance measures and on quality of life perceptions.
If you are a COPD patient and you’d like to try an exercise program, consider asking your pulmonologist for a referral to an outpatient pulmonary rehabilitation program in your area. A note of upfront warning – these programs have very limited admission rates despite their proven effectiveness due to lack of available medical resources to help meet the demand for program participation. Additionally, Medicare and insurance guidelines limit reimbursement for pulmonary rehabilitation to moderate and severe COPD patients only (meaning mild and very severe COPD patients are not eligible for reimbursement – and hence are rarely admitted).
Alternatively, ask your physician to recommend an exercise program appropriate for your situation. If they don’t have such a program to offer you, consider visiting a local fitness center in your area and ask to speak with a fitness instructor certified in structuring exercise programs for people with chronic health conditions.
If none of those options appeal to you but you’d like to learn more about what a pulmonary rehabilitation-style exercise program looks like, we’d recommend you consider purchasing our Breathe Better for Life guide and companion CD-ROM, www.breathebetterforlife.com.
We’ve created an at-home or at-fitness center strength and aerobic exercise program based on pulmonary rehabilitation guidelines published by the American Thoracic Society and the European Respiratory Society. We’ve also tweaked the program to include exercise guidelines issued by the American College of Sports Medicine for elderly patients with chronic respiratory conditions. Our guide provides explicit exercise recommendations and our CD provides explicit, narrated step-by-step instructions for common strength training movements. If you do elect to purchase our guide and follow our exercise program recommendations, we recommend you discuss your plan with your physician prior to engaging in the exercise program to ensure it is appropriate for your particular situation.
A number of previous studies have shown that the combination of aerobic exercise and strength/resistance training produces higher levels of overall physical conditioning in COPD patients than either of these two forms of exercise alone (i.e. greater endurance, greater muscle strength, greater exercise capacity). This is a key reason why most pulmonary rehabilitation programs include both strength training and aerobic/cardiovascular training in their exercise regimens.
Instead of evaluating objective, physical measures of performance between these three potential COPD treatment options (strength & aerobic exercise, aerobic exercise, physiotherapy), the new Portuguese based research study aimed to understand how COPD patients perceive their own health status through two “quality of life” surveys (the St. George’s Respiratory Questionnaire (view sample survey form by clicking here) and the Short Form [36] Health Survey (view sample survey form by clicking here).
In other words, the study team desired to know, outside of physical performance measures (e.g. did you walk farther, did you walk faster, could you lift more weight), do COPD patients actually feel differently about their own health status depending on which method of rehabilitation they receive?
To test their hypothesis, the research team divided 50 moderate to severe COPD patients into two groups (25 who participated in a 10-week combined strength/aerobic exercise program, 25 in a 10-week aerobic-only exercise group) and compared their survey results to each other and to an additional 50 moderate to severe COPD patients who received 10 weeks of respiratory physiotherapy (essentially physical therapy accompanied by breathing technique and airway clearing technique training – but no explicit exercise program). They administered the two surveys mentioned above prior to the respective treatment programs and then again at the end of the programs. They then measured the differences in the patients’ responses from their pre-program surveys and their post-program surveys and compared the mean (average) results between the three different treatment options. (Pereira AM, et al. Impact of combined exercise on chronic obstructive pulmonary patients' state of health. Rev Port Pneumol. 2010 Sep-Oct;16(5):737-57)
The results clearly showed that COPD patients who received both the strength training and aerobic exercise training reported significantly higher ratings of their perceived health status at the end of their exercise program as compared to the other two groups ON ALL SECTIONS OF BOTH SURVEYS.
For example, in the St. George’s Respiratory Questionnaire, the combined exercise group reported a 64 point increase in their “activity” rating (a section of the questionnaire designed to understand a patient’s ability to participate in activities of daily living) versus a 19 point increase for the aerobic-only exercise group and a 1 point increase for the physiotherapy group.
As another example, on the SF-36 survey, COPD patients receiving both strength and aerobic exercise training reported an 83 point jump in their perceived vitality (a section of the test designed to assess quality of daily living), versus a 14 point rise for the aerobic-only group. On this measure the physiotherapy group showed flat response between pre and post treatment.
These results reinforce the basic underlying principles and practices of COPD treatment pulmonary rehabilitation. Combined strength and aerobic exercise is highly valuable for those who suffer from chronic shortness of breath on two fronts – on physical performance measures and on quality of life perceptions.
If you are a COPD patient and you’d like to try an exercise program, consider asking your pulmonologist for a referral to an outpatient pulmonary rehabilitation program in your area. A note of upfront warning – these programs have very limited admission rates despite their proven effectiveness due to lack of available medical resources to help meet the demand for program participation. Additionally, Medicare and insurance guidelines limit reimbursement for pulmonary rehabilitation to moderate and severe COPD patients only (meaning mild and very severe COPD patients are not eligible for reimbursement – and hence are rarely admitted).
Alternatively, ask your physician to recommend an exercise program appropriate for your situation. If they don’t have such a program to offer you, consider visiting a local fitness center in your area and ask to speak with a fitness instructor certified in structuring exercise programs for people with chronic health conditions.
If none of those options appeal to you but you’d like to learn more about what a pulmonary rehabilitation-style exercise program looks like, we’d recommend you consider purchasing our Breathe Better for Life guide and companion CD-ROM, www.breathebetterforlife.com.
We’ve created an at-home or at-fitness center strength and aerobic exercise program based on pulmonary rehabilitation guidelines published by the American Thoracic Society and the European Respiratory Society. We’ve also tweaked the program to include exercise guidelines issued by the American College of Sports Medicine for elderly patients with chronic respiratory conditions. Our guide provides explicit exercise recommendations and our CD provides explicit, narrated step-by-step instructions for common strength training movements. If you do elect to purchase our guide and follow our exercise program recommendations, we recommend you discuss your plan with your physician prior to engaging in the exercise program to ensure it is appropriate for your particular situation.
Friday, October 15, 2010
Antioxidant Quercetin shown to reduce inflammation & oxidative stress
A new study published in the pulmonology journal Respiratory Research demonstrated the effectiveness of the potent antioxidant Quercetin in reducing oxidative stress and inflammation in laboratory mice exposed to a toxic chemical commonly found in cigarette smoke.
Quercetin, a flavinoid found in many plants, has long been studied for its antioxidant properties. Over the past few years, Quercetin has garnered more and more attention from pulmonology researchers seeking methods to help alleviate oxidative stress and inflammation in smokers and people with respiratory health concerns. In several laboratory animal studies and in a few human tissue studies, Quercetin has been shown to reduce inflammation and oxidative stress associated with prolonged exposure to cigarette smoke.
In this new study, the University of Michigan based-investigators sought to confirm previous Quercetin study results by using a different method of exposing laboratory mice to a toxic chemical found in cigarette smoke. (Ganasen S, et al. Respiratory Research. 2010, 11:131)
Instead of exposing laboratory mice to cigarette smoke itself, the investigators instead introduced a specific chemical found in cigarette smoke called lipopolysaccharide (LPS) into the mice via their nasal openings. According to the study authors LPS is, “a cell wall component of gram negative bacteria, is a potent inflammatory molecule and is present in appreciable amounts in cigarette smoke. It is also an active component in environmental and occupational exposures…”
The researchers divided the mice into three groups. One group (the control group) received no exposure to LPS or Quercetin. One group received LPS but no Quercetin (the LPS group). The third group was exposed to LPS and orally fed daily doses of Quercetin at 10mg per kg of body weight (the Quercetin group).
The 8-10 week old mice in the two groups who were exposed to LPS (LPS group & Quercetin group) received the exposure one day a week over a 4 week period. After the 4 week LPS exposure period, mice in the Quercetin group received the potent antioxidant once a day for 10 days. Then the mice were euthanized and their lung cells examined.
To assess the degree of inflammation and oxidative stress, the research team evaluated counts of certain proteins and white blood cells known to be present in high amounts in lung tissue inflamed due to cigarette smoke (e.g. cytokines, chemokines, TBARs). They first discovered that the LPS group mice did indeed evidence a significant degree of inflammation from the 4 week exposure to LPS thus validating their method of exposing lung cells directly to a toxic chemical contained in cigarette smoke.
They further discovered that Quercetin significantly reduced the degree of inflammation and oxidative stress in the Quercetin group when comparing counts of the inflammation/oxidative stress markers mentioned above to mice in the LPS group. As the study authors concluded, “In summary, we have demonstrated that quercetin, a plant polyphenol, reduces oxidative stress, inflammation and MMP levels in elastase/LPS treated mice which show typical features of [poor respiratory function].”
While these results support previous respiratory health studies evaluating the potential of Quercetin as a helpful antioxidant and anti-inflammatory dietary ingredient, there have yet to be live human studies conducted that provide definitive guidance regarding efficacious dosages in humans desiring better respiratory health. That said, Quercetin is readily available in dietary supplement form in daily recommended dosages ranging from 100mg to 500mg. There are also a wide variety of fruits and vegetables that contain high concentrations of Quercetin that can be viewed by clicking here.
We have also included Quercetin at 200mg in our new respiratory support supplement formula, Resplenish along with a dozen other potent antioxidants studied for their respiratory support properties. To learn more about Resplenish, visit www.resplenish.com.
Quercetin, a flavinoid found in many plants, has long been studied for its antioxidant properties. Over the past few years, Quercetin has garnered more and more attention from pulmonology researchers seeking methods to help alleviate oxidative stress and inflammation in smokers and people with respiratory health concerns. In several laboratory animal studies and in a few human tissue studies, Quercetin has been shown to reduce inflammation and oxidative stress associated with prolonged exposure to cigarette smoke.
In this new study, the University of Michigan based-investigators sought to confirm previous Quercetin study results by using a different method of exposing laboratory mice to a toxic chemical found in cigarette smoke. (Ganasen S, et al. Respiratory Research. 2010, 11:131)
Instead of exposing laboratory mice to cigarette smoke itself, the investigators instead introduced a specific chemical found in cigarette smoke called lipopolysaccharide (LPS) into the mice via their nasal openings. According to the study authors LPS is, “a cell wall component of gram negative bacteria, is a potent inflammatory molecule and is present in appreciable amounts in cigarette smoke. It is also an active component in environmental and occupational exposures…”
The researchers divided the mice into three groups. One group (the control group) received no exposure to LPS or Quercetin. One group received LPS but no Quercetin (the LPS group). The third group was exposed to LPS and orally fed daily doses of Quercetin at 10mg per kg of body weight (the Quercetin group).
The 8-10 week old mice in the two groups who were exposed to LPS (LPS group & Quercetin group) received the exposure one day a week over a 4 week period. After the 4 week LPS exposure period, mice in the Quercetin group received the potent antioxidant once a day for 10 days. Then the mice were euthanized and their lung cells examined.
To assess the degree of inflammation and oxidative stress, the research team evaluated counts of certain proteins and white blood cells known to be present in high amounts in lung tissue inflamed due to cigarette smoke (e.g. cytokines, chemokines, TBARs). They first discovered that the LPS group mice did indeed evidence a significant degree of inflammation from the 4 week exposure to LPS thus validating their method of exposing lung cells directly to a toxic chemical contained in cigarette smoke.
They further discovered that Quercetin significantly reduced the degree of inflammation and oxidative stress in the Quercetin group when comparing counts of the inflammation/oxidative stress markers mentioned above to mice in the LPS group. As the study authors concluded, “In summary, we have demonstrated that quercetin, a plant polyphenol, reduces oxidative stress, inflammation and MMP levels in elastase/LPS treated mice which show typical features of [poor respiratory function].”
While these results support previous respiratory health studies evaluating the potential of Quercetin as a helpful antioxidant and anti-inflammatory dietary ingredient, there have yet to be live human studies conducted that provide definitive guidance regarding efficacious dosages in humans desiring better respiratory health. That said, Quercetin is readily available in dietary supplement form in daily recommended dosages ranging from 100mg to 500mg. There are also a wide variety of fruits and vegetables that contain high concentrations of Quercetin that can be viewed by clicking here.
We have also included Quercetin at 200mg in our new respiratory support supplement formula, Resplenish along with a dozen other potent antioxidants studied for their respiratory support properties. To learn more about Resplenish, visit www.resplenish.com.
Monday, October 11, 2010
High level of physical activity, even at advanced ages, is extremely beneficial
In researching articles for our current e-letter editions, we ran across an interesting snippet in Respiratory Report (an e-letter targeted at pulmonology professionals) regarding a new study that shows that maintaining an ongoing regular exercise program late into life provides significant conditioning benefits.
Quoting the Respiratory Report article, “In looking at seniors who ski well into the so-called "golden years," investigators discovered they have twice the oxygen-uptake capacity of same-aged adults who do not exercise.
The research, conducted at Mid Sweden University, was presented at last week's American College of Sports Medicine: Integrative Physiology of Exercise conference.
The results for the active seniors are comparable to values for men who are 40 to 50 years younger but do not exercise to improve their stamina. Analyses of muscle samples at the molecular and cell level reveal a profile similar to what is found in younger men.”
Pretty amazing to discover that in your 60’s, 70’s and 80’s, you can exhibit stamina and strength of non-exercising adults who are 40 and 50 years younger so long as you keep physically active! Not only that, as we previously reported, other studies have shown that starting and maintaining an active exercise program in your 50’s and 60’s, doubles the odds of you reaching age 85! Click here to read the article.
While the study referenced in the Respiratory Report is not specifically related to COPD patients, we thought it worth sharing because we often run into reports of COPD patients and smokers feeling like, “why start an exercise program now. It’s too late.”
Au contraire mon amis! (sorry if that’s improper French diction for…on the contrary my friends). Beginning and maintaining an exercise program for smokers and COPD patients at any age and at any stage of disease is HIGHLY beneficial. Many COPD and smoker research studies prove it. Not only does it improve physical & cardiovascular conditioning, it strengthens muscles, improves balance/coordination, reduces shortness of breath, reduces hospitalizations related to COPD exacerbations, and improves sense of well being/quality of life.
True, exercise will NOT reverse the damage done to your lungs from prolonged exposure to cigarette smoke (nothing can unfortunately) but it can make you feel significantly better nonetheless and help you become more mobile and active and thereby enjoy a more fulfilling life.
To get started, for COPD patients who have been diagnosed with Stage II or Stage III COPD, ask your doctor for a referral to a pulmonary rehabilitation program in your area. The cornerstone element of these programs is guided/observed exercise in which therapists adjust your starting point based on their assessment of your physical condition at admission, and then increase the duration/intensity of your exercise program based on your progress on specific diagnostic measures.
Unfortunately, for Stage I and Stage IV COPD patients, and others concerned with persistent shortness of breath who have not been diagnosed with COPD (such as current/former smokers), entry into an outpatient pulmonary rehab program is next to impossible.
If you fall into this latter category (or if you are Stage II or Stage III and can’t/won’t go to a pulmonary rehab program), we recommend you consider purchasing our Breathe Better for Life guide/CD, www.breathebetterforlife.com. We’ve created a home-based or fitness-center based exercise program based on the same principles and practices that respiratory care professionals use in pulmonary rehabilitation programs. Of course, if you do decide to purchase and follow our exercise program, we recommend you first discuss your exercise plan with your physician to ensure the program is appropriate for your particular circumstance.
The point is – whatever exercise program you follow – start one and keep it going. Next to smoking cessation, it’s the very best thing you can do on your own to improve how you feel and breathe no matter what age you are!
Quoting the Respiratory Report article, “In looking at seniors who ski well into the so-called "golden years," investigators discovered they have twice the oxygen-uptake capacity of same-aged adults who do not exercise.
The research, conducted at Mid Sweden University, was presented at last week's American College of Sports Medicine: Integrative Physiology of Exercise conference.
The results for the active seniors are comparable to values for men who are 40 to 50 years younger but do not exercise to improve their stamina. Analyses of muscle samples at the molecular and cell level reveal a profile similar to what is found in younger men.”
Pretty amazing to discover that in your 60’s, 70’s and 80’s, you can exhibit stamina and strength of non-exercising adults who are 40 and 50 years younger so long as you keep physically active! Not only that, as we previously reported, other studies have shown that starting and maintaining an active exercise program in your 50’s and 60’s, doubles the odds of you reaching age 85! Click here to read the article.
While the study referenced in the Respiratory Report is not specifically related to COPD patients, we thought it worth sharing because we often run into reports of COPD patients and smokers feeling like, “why start an exercise program now. It’s too late.”
Au contraire mon amis! (sorry if that’s improper French diction for…on the contrary my friends). Beginning and maintaining an exercise program for smokers and COPD patients at any age and at any stage of disease is HIGHLY beneficial. Many COPD and smoker research studies prove it. Not only does it improve physical & cardiovascular conditioning, it strengthens muscles, improves balance/coordination, reduces shortness of breath, reduces hospitalizations related to COPD exacerbations, and improves sense of well being/quality of life.
True, exercise will NOT reverse the damage done to your lungs from prolonged exposure to cigarette smoke (nothing can unfortunately) but it can make you feel significantly better nonetheless and help you become more mobile and active and thereby enjoy a more fulfilling life.
To get started, for COPD patients who have been diagnosed with Stage II or Stage III COPD, ask your doctor for a referral to a pulmonary rehabilitation program in your area. The cornerstone element of these programs is guided/observed exercise in which therapists adjust your starting point based on their assessment of your physical condition at admission, and then increase the duration/intensity of your exercise program based on your progress on specific diagnostic measures.
Unfortunately, for Stage I and Stage IV COPD patients, and others concerned with persistent shortness of breath who have not been diagnosed with COPD (such as current/former smokers), entry into an outpatient pulmonary rehab program is next to impossible.
If you fall into this latter category (or if you are Stage II or Stage III and can’t/won’t go to a pulmonary rehab program), we recommend you consider purchasing our Breathe Better for Life guide/CD, www.breathebetterforlife.com. We’ve created a home-based or fitness-center based exercise program based on the same principles and practices that respiratory care professionals use in pulmonary rehabilitation programs. Of course, if you do decide to purchase and follow our exercise program, we recommend you first discuss your exercise plan with your physician to ensure the program is appropriate for your particular circumstance.
The point is – whatever exercise program you follow – start one and keep it going. Next to smoking cessation, it’s the very best thing you can do on your own to improve how you feel and breathe no matter what age you are!
Friday, October 8, 2010
New study shows 51% of COPD patients likely have Osteoporosis
Osteoporosis is a degenerative bone disease that results in low bone density which weakens bones and ultimately leads to frequent bone fractures. It has long been considered a condition that is often found in COPD patients. A new Dutch study published online ahead of print reveals that the prevalence of osteoporosis in COPD patients is likely much higher than previously reported – as high as 1 of every 2 COPD patients!
Why? According to the research team, “Most studies in COPD patients use dual energy absorptiometry (DXA) scan only to determine osteoporosis, therefore microarchitectural changes without a low BMD are missed. Aim of the current study was to determine the prevalence and correlates of osteoporosis in COPD patients based on DXA-scan, X-ray of the spine (X-spine) and the combination thereof.” (Graat-Verboom L, et al. Osteoporosis in COPD outpatients based on bone mineral density and vertebral fractures. Journal of Bone and Mineral Research. 2010 Sep 27. [Epub ahead of print])
In other words, in previous studies only one testing method (dual energy absorptiometry) has been typically used to make a diagnosis of osteoporosis in COPD patients and the researchers desired to know whether there would be an increase in diagnosed cases of osteoporosis in COPD patients by utilizing an alternative method (X-ray of the spine to identify vertebral fractures), and then by using both methods.
The study team discovered that dual energy absorpitometry only identified osteoporosis in 24% of the 255 COPD patients participating in the study, while spine X-rays identified osteoporosis in 37% of study subjects. When both methods were used in combination, the diagnosis of osteoporosis among the COPD patients in the study rose to 51%. As an interesting but frightening side note, 93 of the COPD patients in the study had spine fractures detected by X-Ray, but only 8 of these patients were aware prior to the X-Ray that they had fractured vertebrae.
Even more stunning was their discovery that the percentage of osteoporosis diagnosis was relatively consistent across the spectrum of mild, moderate, severe and very severe COPD patients – implying that osteoporosis is present early on in the development of COPD.
What leads to osteoporosis in COPD patients? Ironically, many of the same factors that tend to worsen shortness of breath…the combination of prolonged exposure to cigarette smoke, a sedentary lifestyle, inadequate exposure to sunlight, and low body weight due to poor/low nutritional intake.
As case in point, the researchers discovered that Vitamin D deficiency was present in over 86% of COPD patients in the study (when using the same deficiency cut-off level employed in diagnosing osteoporosis in post-menopausal women)! Vitamin D, as regular readers of our blog and e-letters well know, is typically produced in the body by skin-cell receptors that utilize UV-B rays from direct sunlight as a catalyst. Vitamin D is essential for the production and maintenance of healthy bones. Many COPD patients lead sedentary, indoor lifestyles and therefore do not get adequate exposure to sunlight. In addition, cigarette smoke has been shown to leach Vitamin D from the body. For COPD patients who don’t get adequate exposure to sunlight, a double whammy happens – it increases airway inflammation and leads to bone density loss. Click here to see our recent article about Vitamin D deficiency and airway inflammation.
Further, many COPD patients are physically inactive. Not only does this weaken the cardiovascular function and muscle strength/function, it also significantly weakens bones. You see, bone strength is reinforced by engaging in weight bearing tasks (walking and lifting weights for example). Because many COPD patients do not regularly exercise and instead spend significant portions of each day sitting/lying down, bone loss from lack of direct sunlight is compounded by lack of physical activity.
Further still, many COPD patients are significantly underweight. This is most often due to the combination of depressed appetite caused by the body’s chemical reaction to cigarette smoke, poor dietary caloric intake of protein & vital nutrients (including Vitamin D fortified foods), and a higher-than-normal metabolism due to the fact that COPD patients burn significantly more calories to take in/expel each breath – even at rest. Low body weight is highly correlated with osteoporosis – again because it means that less weight/load is placed on bones in the body.
So what can you do if you are concerned about the possibility that you might have osteoporosis? Well, first, it’s a good idea to ask your doctor to order both of the above mentioned diagnostic tests to determine if you have osteoporosis or osteopenia (a term doctors apply to low bone density that isn’t quite bad enough to call osteoporosis yet) – especially given the prevalence of previously undetected fractured vertebrae discovered in the Dutch study.
There are prescription drugs available that purportedly increase bone mass but they come with some significant and unpleasant side effects (as a side note, approximately 87% of the Dutch study subjects were NOT taking prescribed bone medication). In our opinion, your first best defenses to improve bone density are the same recommendations we make for improving shortness of breath in our Breathe Better for Life guide/CD, www.breathebetterforlife.com.
1. Start and maintain a regular exercise program that includes both cardiovascular training and strength training. Our Breathe Better for Life guide/CD provides a specific exercise program regimen formulated specifically for COPD patients and smokers based on the principles and practices of the COPD treatment pulmonary rehabilitation. Even a simple walking program that involves 20-40 minutes of walking 3-5 days each week will provide some protective value for both COPD symptoms and osteoporosis.
2. Increase your exposure to direct sunlight (without sunscreen lotion on that blocks UV-B rays)…meaning get outside with multiple parts of your body exposed to direct sunlight for 20-30 minutes a day (combine that with your walking program and you’re knocking off two important steps in one action!)
3. Supplement your diet with foods rich in Vitamin D (and/or fortified with Vitamin D). For a good listing of Vitamin D rich foods, click here.
4. Consider adding a Vitamin D3 dietary supplement to your daily routine – we recommend 2,000 IU daily dosage (make sure your Vitamin D3 comes in the form of cholecalciferol).
5. Increase protein sources to your daily diet – three particularly good sources that have been shown in previous studies to be associated with better respiratory function are soy isoflavones (soy bean sprouts, tofu, soy beans), fish and dairy products (both dairy products and fish are also rich sources of Vitamin D).
Why? According to the research team, “Most studies in COPD patients use dual energy absorptiometry (DXA) scan only to determine osteoporosis, therefore microarchitectural changes without a low BMD are missed. Aim of the current study was to determine the prevalence and correlates of osteoporosis in COPD patients based on DXA-scan, X-ray of the spine (X-spine) and the combination thereof.” (Graat-Verboom L, et al. Osteoporosis in COPD outpatients based on bone mineral density and vertebral fractures. Journal of Bone and Mineral Research. 2010 Sep 27. [Epub ahead of print])
In other words, in previous studies only one testing method (dual energy absorptiometry) has been typically used to make a diagnosis of osteoporosis in COPD patients and the researchers desired to know whether there would be an increase in diagnosed cases of osteoporosis in COPD patients by utilizing an alternative method (X-ray of the spine to identify vertebral fractures), and then by using both methods.
The study team discovered that dual energy absorpitometry only identified osteoporosis in 24% of the 255 COPD patients participating in the study, while spine X-rays identified osteoporosis in 37% of study subjects. When both methods were used in combination, the diagnosis of osteoporosis among the COPD patients in the study rose to 51%. As an interesting but frightening side note, 93 of the COPD patients in the study had spine fractures detected by X-Ray, but only 8 of these patients were aware prior to the X-Ray that they had fractured vertebrae.
Even more stunning was their discovery that the percentage of osteoporosis diagnosis was relatively consistent across the spectrum of mild, moderate, severe and very severe COPD patients – implying that osteoporosis is present early on in the development of COPD.
What leads to osteoporosis in COPD patients? Ironically, many of the same factors that tend to worsen shortness of breath…the combination of prolonged exposure to cigarette smoke, a sedentary lifestyle, inadequate exposure to sunlight, and low body weight due to poor/low nutritional intake.
As case in point, the researchers discovered that Vitamin D deficiency was present in over 86% of COPD patients in the study (when using the same deficiency cut-off level employed in diagnosing osteoporosis in post-menopausal women)! Vitamin D, as regular readers of our blog and e-letters well know, is typically produced in the body by skin-cell receptors that utilize UV-B rays from direct sunlight as a catalyst. Vitamin D is essential for the production and maintenance of healthy bones. Many COPD patients lead sedentary, indoor lifestyles and therefore do not get adequate exposure to sunlight. In addition, cigarette smoke has been shown to leach Vitamin D from the body. For COPD patients who don’t get adequate exposure to sunlight, a double whammy happens – it increases airway inflammation and leads to bone density loss. Click here to see our recent article about Vitamin D deficiency and airway inflammation.
Further, many COPD patients are physically inactive. Not only does this weaken the cardiovascular function and muscle strength/function, it also significantly weakens bones. You see, bone strength is reinforced by engaging in weight bearing tasks (walking and lifting weights for example). Because many COPD patients do not regularly exercise and instead spend significant portions of each day sitting/lying down, bone loss from lack of direct sunlight is compounded by lack of physical activity.
Further still, many COPD patients are significantly underweight. This is most often due to the combination of depressed appetite caused by the body’s chemical reaction to cigarette smoke, poor dietary caloric intake of protein & vital nutrients (including Vitamin D fortified foods), and a higher-than-normal metabolism due to the fact that COPD patients burn significantly more calories to take in/expel each breath – even at rest. Low body weight is highly correlated with osteoporosis – again because it means that less weight/load is placed on bones in the body.
So what can you do if you are concerned about the possibility that you might have osteoporosis? Well, first, it’s a good idea to ask your doctor to order both of the above mentioned diagnostic tests to determine if you have osteoporosis or osteopenia (a term doctors apply to low bone density that isn’t quite bad enough to call osteoporosis yet) – especially given the prevalence of previously undetected fractured vertebrae discovered in the Dutch study.
There are prescription drugs available that purportedly increase bone mass but they come with some significant and unpleasant side effects (as a side note, approximately 87% of the Dutch study subjects were NOT taking prescribed bone medication). In our opinion, your first best defenses to improve bone density are the same recommendations we make for improving shortness of breath in our Breathe Better for Life guide/CD, www.breathebetterforlife.com.
1. Start and maintain a regular exercise program that includes both cardiovascular training and strength training. Our Breathe Better for Life guide/CD provides a specific exercise program regimen formulated specifically for COPD patients and smokers based on the principles and practices of the COPD treatment pulmonary rehabilitation. Even a simple walking program that involves 20-40 minutes of walking 3-5 days each week will provide some protective value for both COPD symptoms and osteoporosis.
2. Increase your exposure to direct sunlight (without sunscreen lotion on that blocks UV-B rays)…meaning get outside with multiple parts of your body exposed to direct sunlight for 20-30 minutes a day (combine that with your walking program and you’re knocking off two important steps in one action!)
3. Supplement your diet with foods rich in Vitamin D (and/or fortified with Vitamin D). For a good listing of Vitamin D rich foods, click here.
4. Consider adding a Vitamin D3 dietary supplement to your daily routine – we recommend 2,000 IU daily dosage (make sure your Vitamin D3 comes in the form of cholecalciferol).
5. Increase protein sources to your daily diet – three particularly good sources that have been shown in previous studies to be associated with better respiratory function are soy isoflavones (soy bean sprouts, tofu, soy beans), fish and dairy products (both dairy products and fish are also rich sources of Vitamin D).
Monday, October 4, 2010
Zinc reduces inflammation due to cigarette smoke
A new study published in late August showed that laboratory mice fed a diet high in zinc had 50-60% lower markers of inflammation in lung tissue samples than mice fed a diet low in zinc. The study authors suggest that supplementing zinc in COPD patients, asthmatics and smokers may be helpful in reducing inflammation associated with airway diseases (inflammation is believed to be a leading cause of breathlessness in COPD patients).
According to the study authors, “Zinc is a dietary trace metal that has been clinically and physiologically linked to airway inflammatory diseases, such as asthma and COPD. Patients with COPD have lower serum, plasma and hair zinc levels than healthy subjects. In addition, there is a negative correlation between plasma zinc and wheezing. Zinc supplementation had favorable effects on oxidant–antioxidant balance in patients with COPD.” (Lang CJ, et al. Dietary zinc mediates inflammation and protects against wasting and metabolic derangement caused by sustained cigarette smoke exposure in mice. Biometals. Published online ahead of print, August 29, 2010. (doi:10.1007/s10534-010-9370-9))
In other words, zinc seems to act as an antioxidant in lung tissue, particularly in cells of the lining of the lungs known as epithelial cells. According to the research team, zinc is naturally abundant in epithelial cells, but the effects of a diet that is low in zinc content combined with prolonged exposure to cigarette smoke depresses levels of this important nutrient and thus contributes to airway inflammation. By supplementing dietary zinc in laboratory mice exposed to cigarette smoke, the researchers hypothesized that signs of inflammation would be reduced.
As regular readers of our e-letters and blog know well, there are a host of antioxidants that have been studied (and continue to be studied) in relation to airway inflammation. You see, it’s clear from blood plasma samples that smokers and COPD patients are significantly deficient in antioxidant counts compared to healthy non-smoking adults. Scientists theorize that the pro-oxidative nature of cigarette smoke overwhelms the body’s supply of antioxidants consumed through diet or produced in the body creating a condition referred to as “oxidative stress”. Oxidative stress in simple terms is an imbalance of pro-oxidative molecules (too much of a bad thing) and anti-oxidative molecules (too little of a good thing) in the body. As a result of the imbalance, more pro-oxidative molecules get through to lung tissues and damage them, creating inflammation, which in turn leads to persistent shortness of breath.
Therefore, researchers seeking for ways to alleviate inflammation have been testing a variety of antioxidants to boost blood plasma levels of these protective nutrients to judge whether doing so has a positive effect on airway inflammation. In this particular zinc study (and in a growing number of other studies on other antioxidants) the answer appears to be yes.
But a word of reason – from the scores of studies we’ve reviewed on antioxidants and airway inflammation, it is clear that there is no single magic antioxidant. The human body absorbs, processes and produces a wide range of antioxidants and so the best advice is to eat a diet rich in foods that contain high levels of antioxidants (most often colorful fruits and vegetables) and if you desire to add additional antioxidants through dietary supplements, favor products that give you a broad base of different antioxidants rather than massive doses of a single antioxidant.
In the Biometals zinc study itself, the research team divided the laboratory mice into three groups. One group was fed a diet of whey protein that is low in zinc content, one group was fed the same whey protein supplemented by additional zinc sulfate, and a third group received the same basic diet but with a much higher level of supplemented zinc.
Then the mice were exposed to smoke from 2 cigarettes for 15 minutes, 3 times a day, 5 days a week for 8 weeks. Then the mice were euthanized and their lung tissues sampled and examined for a variety of measures.
One of the measures the researchers looked at were the number of macrophages (white blood cells) present in alveolar (lung) tissue samples – one outcome of the inflammation process is the production of white blood cells (in fact the body over-produces white blood cells because the inflammation process makes the body think there is a massive infection occurring). Here the researchers found that cigarette exposed mice who were fed the diet supplemented with high zinc content had 50-60% fewer macrophages – thus demonstrating a significant reduction in the inflammatory response to cigarette smoke.
As the study authors noted, “The 50–60% reduction in alveolar macrophages in Zn-supplemented mice supports our evolving hypothesis that Zn is an important anti-inflammatory mediator of airway inflammation. Restoring airway Zn levels through dietary supplementation may lessen the severity of lung inflammation when Zn intake is low.”
Now, unfortunately, there is no specific guidance in the study on how much supplemental zinc is beneficial for smokers/COPD patients for reducing airway inflammation, and it is not a matter of simply translating the amount fed to the mice per unit of body weight and multiplying it by your own body weight.
That said the odds are high that you have a zinc deficiency if you smoke and/or have COPD, but before you go crazy adding massive amounts of zinc to your diet, we would recommend you ask your doctor to order a blood or hair sample test to determine whether you have a deficiency and how severe your deficiency is. From there, you and your doctor can determine a supplemental zinc dosage level appropriate for your particular circumstance.
In the meantime, for a good listing of foods high in zinc content published by the National Institutes of Health’s Office of Dietary Supplements that you can access by clicking here. This same web page provides additional information about the daily recommended intake of zinc from food/dietary supplements and provides guidance on how much is too much.
According to the study authors, “Zinc is a dietary trace metal that has been clinically and physiologically linked to airway inflammatory diseases, such as asthma and COPD. Patients with COPD have lower serum, plasma and hair zinc levels than healthy subjects. In addition, there is a negative correlation between plasma zinc and wheezing. Zinc supplementation had favorable effects on oxidant–antioxidant balance in patients with COPD.” (Lang CJ, et al. Dietary zinc mediates inflammation and protects against wasting and metabolic derangement caused by sustained cigarette smoke exposure in mice. Biometals. Published online ahead of print, August 29, 2010. (doi:10.1007/s10534-010-9370-9))
In other words, zinc seems to act as an antioxidant in lung tissue, particularly in cells of the lining of the lungs known as epithelial cells. According to the research team, zinc is naturally abundant in epithelial cells, but the effects of a diet that is low in zinc content combined with prolonged exposure to cigarette smoke depresses levels of this important nutrient and thus contributes to airway inflammation. By supplementing dietary zinc in laboratory mice exposed to cigarette smoke, the researchers hypothesized that signs of inflammation would be reduced.
As regular readers of our e-letters and blog know well, there are a host of antioxidants that have been studied (and continue to be studied) in relation to airway inflammation. You see, it’s clear from blood plasma samples that smokers and COPD patients are significantly deficient in antioxidant counts compared to healthy non-smoking adults. Scientists theorize that the pro-oxidative nature of cigarette smoke overwhelms the body’s supply of antioxidants consumed through diet or produced in the body creating a condition referred to as “oxidative stress”. Oxidative stress in simple terms is an imbalance of pro-oxidative molecules (too much of a bad thing) and anti-oxidative molecules (too little of a good thing) in the body. As a result of the imbalance, more pro-oxidative molecules get through to lung tissues and damage them, creating inflammation, which in turn leads to persistent shortness of breath.
Therefore, researchers seeking for ways to alleviate inflammation have been testing a variety of antioxidants to boost blood plasma levels of these protective nutrients to judge whether doing so has a positive effect on airway inflammation. In this particular zinc study (and in a growing number of other studies on other antioxidants) the answer appears to be yes.
But a word of reason – from the scores of studies we’ve reviewed on antioxidants and airway inflammation, it is clear that there is no single magic antioxidant. The human body absorbs, processes and produces a wide range of antioxidants and so the best advice is to eat a diet rich in foods that contain high levels of antioxidants (most often colorful fruits and vegetables) and if you desire to add additional antioxidants through dietary supplements, favor products that give you a broad base of different antioxidants rather than massive doses of a single antioxidant.
In the Biometals zinc study itself, the research team divided the laboratory mice into three groups. One group was fed a diet of whey protein that is low in zinc content, one group was fed the same whey protein supplemented by additional zinc sulfate, and a third group received the same basic diet but with a much higher level of supplemented zinc.
Then the mice were exposed to smoke from 2 cigarettes for 15 minutes, 3 times a day, 5 days a week for 8 weeks. Then the mice were euthanized and their lung tissues sampled and examined for a variety of measures.
One of the measures the researchers looked at were the number of macrophages (white blood cells) present in alveolar (lung) tissue samples – one outcome of the inflammation process is the production of white blood cells (in fact the body over-produces white blood cells because the inflammation process makes the body think there is a massive infection occurring). Here the researchers found that cigarette exposed mice who were fed the diet supplemented with high zinc content had 50-60% fewer macrophages – thus demonstrating a significant reduction in the inflammatory response to cigarette smoke.
As the study authors noted, “The 50–60% reduction in alveolar macrophages in Zn-supplemented mice supports our evolving hypothesis that Zn is an important anti-inflammatory mediator of airway inflammation. Restoring airway Zn levels through dietary supplementation may lessen the severity of lung inflammation when Zn intake is low.”
Now, unfortunately, there is no specific guidance in the study on how much supplemental zinc is beneficial for smokers/COPD patients for reducing airway inflammation, and it is not a matter of simply translating the amount fed to the mice per unit of body weight and multiplying it by your own body weight.
That said the odds are high that you have a zinc deficiency if you smoke and/or have COPD, but before you go crazy adding massive amounts of zinc to your diet, we would recommend you ask your doctor to order a blood or hair sample test to determine whether you have a deficiency and how severe your deficiency is. From there, you and your doctor can determine a supplemental zinc dosage level appropriate for your particular circumstance.
In the meantime, for a good listing of foods high in zinc content published by the National Institutes of Health’s Office of Dietary Supplements that you can access by clicking here. This same web page provides additional information about the daily recommended intake of zinc from food/dietary supplements and provides guidance on how much is too much.
Subscribe to:
Posts (Atom)