I searched the forum and didn't see a thread dedicated to Chronic Obstructive Pulmonary Disease, COPD, and since I just recently started hearing more about it I decided to look into it and post what I found.
COPD is a chronic inflammatory condition in the lungs. The mucus membranes become inflamed and the result is a choking of the airways, a decrease in the ability to breathe and move, leading up to death. Approximately 16 million individuals are affected by it within the United States. It is supposedly the 4th largest killer in the world and continues to rise against the other leading three. If one of those other three is the Secret Team then I'd say COPD has its work cut out for it
.
The culprit has been identified as smoking. Whereas I'm inclined to believe that the particulate matter in the average pesticide-loaded cigarette could be very dangerous, well we all know better. The following is research showing the nature of both the disease itself, the causes, possible ways to combat it (including of course the very effective ketogenic diet) and the standard market-driven approach to singling out cigarette smoke and maximizing pharmaceutical profits.
To begin with I wanted to look at mucus in general, just to refresh my mind on its importance in health.
Following that I stumbled across this article that shows the vulture mindset that moves us constantly towards a dead planet.
_http://online.wsj.com/article/PR-CO-20130418-906159.html?mod=googlenews_wsj
Following that I got a refresher on the toxic nature of the cities we live in, and how important it is to maintain our "nutritional defenses" while keeping in mind the dangers of iron overload. I also wonder how conservative these numbers are from the WHO:
_http://www.who.int/phe/health_topics/outdoorair/databases/burden_disease/en/index.html
Cigarette smoke could certainly contribute to the invasion of toxins into the lungs, but it is far more complex:
_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706597/
And, since I kept reading about bronchitis and its relation to COPD I decided to refresh my mind on what it was all about. Since it is viral in origin, I wonder if the rise in COPD might not be related to an invasion from the skies?
And various therapies:
Angelica, from Wikipedia:
Rhemannia, from Wikipedia:
I do not think that pollution accounts for all of the increase in COPD, but that our crowded skies, our genetically modified food, and our meals void of nutrition are definitely coming together to create the perfect storm. And this is just one of the waves. Anyways, I hope this is helpful.
COPD is a chronic inflammatory condition in the lungs. The mucus membranes become inflamed and the result is a choking of the airways, a decrease in the ability to breathe and move, leading up to death. Approximately 16 million individuals are affected by it within the United States. It is supposedly the 4th largest killer in the world and continues to rise against the other leading three. If one of those other three is the Secret Team then I'd say COPD has its work cut out for it
. The culprit has been identified as smoking. Whereas I'm inclined to believe that the particulate matter in the average pesticide-loaded cigarette could be very dangerous, well we all know better. The following is research showing the nature of both the disease itself, the causes, possible ways to combat it (including of course the very effective ketogenic diet) and the standard market-driven approach to singling out cigarette smoke and maximizing pharmaceutical profits.
To begin with I wanted to look at mucus in general, just to refresh my mind on its importance in health.
Airway mucus: its components and function.
Lillehoj ER, Kim KC.
Source
Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, Maryland 21201, USA.
Abstract
The airway surface liquid (ASL), often referred to as mucus, is a thin layer of fluid covering the luminal surface of the airway. The major function of mucus is to protect the lung through mucociliary clearance against foreign particles and chemicals entering the lung. The mucus is comprised of water, ions, and various kinds of macromolecules some of which possess the protective functions such as anti-microbial, anti-protease, and anti-oxidant activity. Mucus glycoproteins or mucins are mainly responsible for the viscoelastic property of mucus, which is crucial for the effective mucociliary clearance. There are at least eight mucin genes identified in the human airways, which will potentially generate various kinds of mucin molecules. At present, neither the exact structures of mucin proteins nor their regulation are understood although it seems likely that different types of mucins are involved in different functions and might also be associated with certain airway diseases. The fact that mucins are tightly associated with various macromolecules present in ASL seems to suggest that the defensive role of ASL is determined not only by these individual components but rather by a combination of these components. Collectively, mucins in ASL may be compared to aircraft carriers carrying various types of weapons in defense of airbome enemies.
Following that I stumbled across this article that shows the vulture mindset that moves us constantly towards a dead planet.
_http://online.wsj.com/article/PR-CO-20130418-906159.html?mod=googlenews_wsj
It is widely recognized that the global social and economic burden of COPD is high; affecting an estimated 64 million people worldwide. However, the availability of accurate data for COPD prevalence is hampered by variability in study methodology and both under-diagnosis and misdiagnosis of the disease. While 12 million Americans are diagnosed with COPD, it is estimated that an additional 12 million remain undiagnosed. The economic burden of COPD is tremendous. This creates a tremendous opportunity for substantial economic gains by pharmaceutical companies that can bring novel products to market. In Europe the annual economic burden of respiratory diseases is estimated to be approximately 102 billion, with COPD responsible for over half of the burden.
Following that I got a refresher on the toxic nature of the cities we live in, and how important it is to maintain our "nutritional defenses" while keeping in mind the dangers of iron overload. I also wonder how conservative these numbers are from the WHO:
_http://www.who.int/phe/health_topics/outdoorair/databases/burden_disease/en/index.html
Burden of disease associated with urban outdoor air pollution for 2008
For 2008, the number of premature deaths attributable to urban outdoor air pollution is estimated to amount to 1.34 million worldwide. Of these, 1.09 million deaths could be avoided if the mean annual Air Quality Guideline values of PM10=20μg/m3 and PM2.5=10μg/m3 were implemented.
The number of total deaths attributable to outdoor air pollution presents an increase of 16% as compared to the previous figure of 1.15 million deaths for the year 2004. This increase is linked to recent increases in both air pollution concentrations and the total population affected as cities grow.
COPD in Helsinki, Finland: socioeconomic status based on occupation has an important impact on prevalence
Abstract
Objectives: Chronic obstructive pulmonary disease (COPD) is globally a major, but often undiagnosed, cause of morbidity and mortality. The aims of this study were to assess the prevalence of COPD in Helsinki, Finland, with international diagnostic criteria and to analyse risk factors including socioeconomic status, and disease severity. Methods: A general population sample of 628 adults (368 women) completed flow-volume spirometry with bronchodilation test and a structured interview. Post-bronchodilation spirometry was assessed both using the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria and relative to the fifth percentile of the reference value (lower limit of normal, LLN). Results: According to GOLD criteria, 37 (5.9%), and by using the LLN criteria, 43 subjects (6.8%) had airway obstruction consistent with COPD. Using the GOLD criteria, four subjects or 0.6% of the population had severe, 3.0% moderate, and 2.2% mild COPD. Of those with post-bronchodilator obstruction, 49% had no previous diagnosis of obstructive airways disease and did not use medication for any respiratory disease. The prevalence of undiagnosed COPD defined by GOLD was 2.9% (LLN 3.3%). In addition to age, smoking history, and prior history of asthma, socioeconomic status based on occupation was significantly related to COPD in the population. Manual workers in industry (GOLD 10.0%, LLN 11.7%) and non-manual assistant employees (10.2%, 10.2%) had a significantly higher prevalence of COPD than professionals (2.8%, 2.3%). Conclusions: Although smoking is the main modifiable risk factor for COPD, the disease was significantly related to manual workers and non-manual assistant employees, i.e. socioeconomic groups reflecting occupation.
Cigarette smoke could certainly contribute to the invasion of toxins into the lungs, but it is far more complex:
_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706597/
The pathogenesis of pulmonary hypertension in COPD and its treatment also remain a huge challenge (Higgenbottom 2005). We need to learn much more about the molecular genetics of COPD (Sanford et al 1997). Why do only 15%–20% of smokers develop airflow obstruction (Sanford et al 1997)?
The initial report of outcome showed that 22% of patients who received special care stopped smoking as part of the study, compared with 5% in the usual care group. Patients who succeeded in stopping had a small improvement in FEV1 initially, followed by a slow decline up to five years of follow-up (Figure 4). Ipratropium did not improve baseline lung function, but did increase airflow on each day that it was tested over the course of the study.
And, since I kept reading about bronchitis and its relation to COPD I decided to refresh my mind on what it was all about. Since it is viral in origin, I wonder if the rise in COPD might not be related to an invasion from the skies?
What Causes Bronchitis?
Acute bronchitis is generally caused by lung infections, 90% of which are viral in origin. Repeated attacks of acute bronchitis, which weaken and irritate bronchial airways over time, can result in chronic bronchitis.
Industrial pollution is another culprit. Chronic bronchitis is found in higher-than-normal rates among coal miners, grain handlers, metal molders, and other people who are continually exposed to dust and fumes. But the chief cause is heavy, long-term cigarette smoking, which irritates the bronchial tubes and causes them to produce excess mucus. The symptoms of chronic bronchitis are also worsened by high concentrations of sulfur dioxide and other pollutants in the atmosphere.
And various therapies:
Nonpharmacological therapies
Rehabilitation
Rehabilitation with exercise training as a core component is an essential part of the treatment of COPD. It is safe, and improves symptoms and quality of life [102]. There might even be a mortality benefit, but studies have been underpowered to show conclusively a lower mortality with rehabilitation [103]. Patients of all disease stages and ages profit from rehabilitation programmes [104], and even starting rehabilitation during an exacerbation seems to be safe and feasible [105]. Rehabilitation should include education about COPD and treatment options, exercise training, nutritional intervention and psychosocial support. Effectiveness has been well documented for in-patient, out-patient and home-based programmes [103].
Oxygen therapy and noninvasive ventilation
The administration of oxygen >15 hours per day improves survival in COPD patients with chronic respiratory failure and severe resting hypoxaemia [106]. In patients without resting hypoxaemia a clear benefit has not been shown for oxygen supplementation and it is currently not recommended [107].
A survival benefit was noted for nocturnal noninvasive ventilation in patients with very severe, oxygen-dependent COPD and daytime hypercapnia. However, this intervention reduced their quality of life [108].
Surgical treatments
Surgical treatments such as lung volume reduction surgery, bronchoscopic lung volume reduction, bullectomy and lung transplantation are treatment options for very selected groups of patients. Patients with severe, predominately upper lobe emphysema and low exercise capacity after rehabilitation show improved survival with lung volume reduction surgery, and patients with high exercise capacity after rehabilitation show improved quality of life and exercise capacity after lung volume reduction surgery [109]. Bronchoscopic lung volume reduction entails the positioning of endobronchial valves. Patients with advanced heterogeneous emphysema profited from endobronchial valves, with increased lung function and exercise capacity. However, this might be at the cost of a higher rate of subsequent exacerbations [110], pneumonia and haemoptysis [110]. As mentioned before, this treatment option only applies to a highly selected group of patients with COPD. Bullectomy in patients with a single giant bulla results in improved quality of life, and improves symptoms and lung function [111].
Lung transplantation in COPD is limited by the availability of donor organs. Carefully selected patients with very severe COPD benefit in terms of better functional capacity and quality of life [112].
Disease management strategies
Self-management education in patients with COPD might be associated with a reduction in hospital admissions, but there is still insufficient evidence to make clear recommendations on the form and content of these programmes [113]. A recent study of a comprehensive care management programme including individual educational sessions, an action plan and proactive telephone calls was stopped early because of excess mortality in the intervention group [114]. Another recent study of self-management interventions in the primary care setting showed no benefit in terms of quality of life, self efficacy or frequency of exacerbations with ongoing telephone support and tailored sessions or routine monitoring compared with usual care [115].
Undernutrition in Patients with COPD and Its Treatment.
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung and whole body caused mainly by tobacco smoking. Patients with advanced COPD are in a state of undernutrition, referred to as pulmonary cachexia; the exercise performance and quality of life (QOL) of these patients are deteriorated, the vital prognosis is unfavorable, and the medico-economic burden posed by poorly nourished COPD patients is high. The mainstays of COPD treatment are pharmacotherapy, mainly with bronchodilators, and non-pharmacotherapeutic approaches such as respiratory rehabilitation and nutrition counseling. Nutritional supplement therapy, consisting primarily of high calorie intake, has been demonstrated to be effective for maintaining and improving the muscle strength and exercise tolerance in poorly nourished COPD patients. The efficacy of intake of various nutrients, besides a high calorie intake, for amelioration of the disease state of COPD has also been reported. The roles of adipokines in the pathophysiology of COPD have begun to receive attention recently, and not only their regulatory effects on appetite and nutritional status, but also their influence on systemic inflammation have been increasingly clarified. We review the papers on COPD and nutrition and discuss the role of nutritional supplement therapy in the treatment of COPD.
Abstract
Recent evidence suggests that inadequate hydration of airway surfaces is a common mechanism in the pathogenesis of airway mucus obstruction. Inhaled hypertonic saline (HS) induces osmotic water flux improving hydration of airway surfaces. However, trials in patients with obstructive lung diseases are limited. The aim of this study was to investigate effects of HS on mucus obstruction and airway inflammation in the prevention and treatment of obstructive lung disease in vivo. We, therefore, used the βENaC-overexpressing mouse as a model of chronic obstructive lung disease and determined effects of preventive and late therapy with 3% HS and 7% HS on pulmonary mortality, airway mucus obstruction and inflammation. We found that preventive treatment with 3% HS and 7% HS improved growth, reduced mortality, and reduced mucus obstruction in neonatal βENaC-overexpressing mice. In adult βENaC-overexpressing mice with chronic lung disease, mucus obstruction was significantly reduced by 7% HS, but not 3% HS. Treatment with HS triggered airway inflammation with elevated KC levels and neutrophils in airways from wild-type mice, but reduced KC in chronic neutrophilic inflammation in adult ENaC-overexpressing mice. Our data demonstrate that airway surface rehydration with HS provides an effective preventive and late therapy of mucus obstruction with no consistent effects on inflammation in chronic lung disease. These results suggest that through mucokinetic effects HS may be beneficial for patients with a spectrum of obstructive lung diseases, and that additional strategies are required for effective treatment of associated airway inflammation.
Abstract Title:
Effect of N-acetylcysteine on air trapping in COPD: a randomized placebo-controlled study.
Abstract Source:
Chest. 2009 Aug;136(2):381-6. Epub 2009 May 15. PMID: 19447919
Abstract Author(s):
David Stav, Meir Raz
Abstract:
BACKGROUND: FEV(1) is used for the classification of disease severity and is a good predictor of COPD mortality. However, it is a poor predictor of clinical symptoms, exercise tolerance, and response to bronchodilators in COPD. Progressive reduction in inspiratory capacity (IC) during exercise reflects dynamic hyperinflation and is a good predictor of decreased exercise ability as well as increased exertional dyspnea. In animal models of COPD, N-acetylcysteine (NAC), an antioxidant/mucous modifier, has been shown to modify small airways, which mainly causes lung hyperinflation. OBJECTIVE: Our goal was to examine the effect of 1,200 mg/d of NAC on lung hyperinflation at rest and after exercise in patients with moderate-to-severe COPD. METHODS: This was a randomized, double-blind, cross-over study that included 24 eligible patients > 40 years of age with a diagnosis of COPD, a FEV(1) < 70% of predicted, FEV(1)/FVC ratio < 0.70, and a functional residual capacity > 120% of predicted normal. Patients were randomized to placebo treatment or NAC treatment twice daily for 6 weeks. This was followed by a 2-week washout period, and then patients were crossed over to alternate therapy for an additional 6 weeks. Evaluation was performed after each 6 weeks of each treatment. RESULTS: IC and FVC were higher especially after exercise after NAC treatment compared with placebo treatment. In addition, the relationship of residual volume to total lung capacity was reduced in a similar pattern. Furthermore, endurance time was longer after NAC treatment compared with placebo treatment. CONCLUSIONS: NAC treatment of patients with stable, moderate-to-severe COPD has a beneficial effect on physical performance, probably due to a reduction in air trapping. Trial registration: Clinicaltrials.gov Identifier: NCT00476736.
Abstract Title:
Effect of supplementing a high-fat, low-carbohydrate enteral formula in COPD patients.
Abstract Source:
Nutrition. 2003 Mar;19(3):229-32. PMID: 12620524
Abstract Author(s):
Baiqiang Cai, Yuanjue Zhu, Y i Ma, Zuojun Xu, Y i Zao, Jinglan Wang, Yaoguang Lin, Gail M Comer
Abstract:
OBJECTIVE: One of the goals in treating patients with chronic obstructive pulmonary disease (COPD) who suffer from hypoxemia, hypercapnia, and malnutrition is to correct the malnutrition without increasing the respiratory quotient and minimize the production of carbon dioxide. This 3-wk study evaluated the efficacy of feeding a high-fat, low-carbohydrate (CHO) nutritional supplement as opposed to a high-carbohydrate diet in COPD patients on parameters of pulmonary function.S METHODS: Sixty COPD patients with low body weight (<90% ideal body weight) were randomized to the control group, which received dietary counseling for a high-CHO diet (15% protein, 20% to 30% fat, and 60% to 70% CHO), or the experimental group, which received two to three cans (237 mL/can) of a high-fat, low-CHO oral supplement (16.7% protein, 55.1% fat, and 28.2% CHO) in the evening as part of the diet. Measurements of lung function (forced expiratory volume in 1 s or volume of air exhaled in 1 s of maximal expiration, minute ventilation, oxygen consumption per unit time, carbon dioxide production in unit time, and respiratory quotient) and blood gases (pH, arterial carbon dioxide tension, and arterial oxygen tension) were taken at baseline and after 3 wk. RESULTS: Lung function measurements decreased significantly and forced expiratory volume increased significantly in the experimental group. CONCLUSION: This study demonstrates that pulmonary function in COPD patients can be significantly improved with a high-fat, low-CHO oral supplement as compared with the traditional high-CHO diet.
Abstract Title:
[Intervention effect of tongfei mixture on nocturnal hypoxia in patients with chronic obstructive pulmonary disease].
Abstract Source:
Phytother Res. 2008 Aug 11. PMID: 15553819
Abstract Author(s):
Zhao-bo Cui, Ya-dong Yuan, Shu-hong Liu, Dongliang Han, Xiuling Gao, Fucun Qi
Abstract:
OBJECTIVE: To study the effect of tongfei mixture (TFM, a Chinese recipe mainly consisted of angelica and rehmannia root) on nocturnal hypoxia in patients with chronic obstructive pulmonary disease (COPD). METHODS: Sixty patients with COPD of remission phase were randomly divided into 3 groups, 20 in each group. Group A was the control group; Group B, the group simply treated with oxygen; Group C, treated with oxygen and TFM. Changes of pulmonary function, diaphragm muscle mobility (DMM), 6 min walk distance (6MWD), morning arterial blood gas, nocturnal lowest oxygen saturation (LSaO2), mean blood oxygen saturation (MSaO2), the percentage of saturation lower than 90% time account for total sleeping time (SLT90%) and ultrasonocardiogram before and after treatment were observed. RESULTS: Levels of LSaO2, MSaO2 and SLT90% in Groups B and C were significantly higher than those in Group A (P<0.05, P<0.01). The lowering of PaCO2 in Group C was more significant than that in Group B (P<0.05). The mPAP level in Group C was lower, FEV1, 6MWD and DMM were improved than those in Group A and B, showing significant difference (P<0.05). CONCLUSION: Combined use of oxygen therapy and TFM could not only improve the nocturnal hypoxia, but also lower PaCO2. TFM is an important supplement of oxygen therapy.
Angelica, from Wikipedia:
Cultivation and uses
Some species are grown as flavoring agents or for their medicinal properties. The most notable of these is garden angelica (A. archangelica), which is commonly known simply as angelica. Natives of Lapland use the fleshy roots as food and the stalks as medicine. Crystallized strips of young angelica stems and midribs are green in colour and are sold as decorative and flavoursome cake decoration material, but may also be enjoyed on their own. The roots and seeds are sometimes used to flavor gin. Its presence accounts for the distinct flavor of many liqueurs, such as Chartreuse.
Among the Sami people of Lapland, the plant is used to make a traditional musical instrument the fadno.
Seacoast angelica (A. lucida) has been eaten as a wild version of celery.
In parts of Japan, especially the Izu Islands, the shoots and leaves of ashitaba (A. keiskei) are eaten as tempura, particularly in the spring.
A. sylvestris and some other species are eaten by the larvae of some Lepidoptera species, including bordered pug, grey pug, lime-speck pug and the V-pug.
A. dawsonii was used by several first nations in North America for ritual purposes.
A. atropurpurea is found in North America from Newfoundland west to Wisconsin and south to Maryland, and was smoked by Missouri tribes for colds and respiratory ailments. This species is very similar in appearance to the poisonous water hemlock.
The boiled roots of angelica were applied internally and externally to wounds by the Aleut people in Alaska to speed healing.
Candied angelica is a popular cake decoration and flavouring.
The herb, also known by the Chinese name, Bai Zhi, and Latin name, Radix Angelicae Dahurica, is used medicinally in Traditional Chinese Medicine. According to a study, Methoxy-8-(2-hydroxy-3-buthoxy-3-methylbutyloxy)-psoralen has been shown to regulate the cyclooxygenase-2 (COX-2)-dependent phase of prostaglandin D(2) generation in bone marrow-derived mast cells (IC50, 23.5 mM). In addition, this compound consistently modulated the production of leukotriene C(4), demonstrating the ability to modulate both cyclooxygenase-2 and 5-lipoxygenase activity. Furthermore, this compound also affected the degranulation reaction (IC50, 4.1 mM).[6]
Rhemannia, from Wikipedia:
Uses
Sometimes known as Chinese Foxglove due to its superficial resemblance to the genus Digitalis, the species of Rehmannia are perennial herbs. The plants have large flowers and are grown as ornamental garden plants in Europe and North America, and are used medicinally in Asia.
Known as dìhuáng (地黄) or gān dìhuáng (干地黄) in Chinese, R. glutinosa is used as a medicinal herb for arthritic conditions within Chinese traditional formulations.[1]
Chemical constituents
Rehmannia contains the vitamins A, B, C, and D,[citation needed] as well as other compounds, such as an iridoid glycoside, catalpol, that has been shown to exert protective effects on dopaminergic neurons in aged rats to help inhibit microglial activation, thereby reducing the production of pro-inflammatory factors.[2]
I do not think that pollution accounts for all of the increase in COPD, but that our crowded skies, our genetically modified food, and our meals void of nutrition are definitely coming together to create the perfect storm. And this is just one of the waves. Anyways, I hope this is helpful.
