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ASTHMA

ASTHMA. THE FACTS. Important changes in the prevalence of asthma have been noted over the past 20–30 years . During the 1980s and early 1990s there was a substantial worldwide increase in the prevalence , particularly in children.

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ASTHMA

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  1. ASTHMA

  2. THE FACTS • Important changes in the prevalence of asthma have been noted over the past 20–30 years. • During the 1980s and early 1990s there was a substantial worldwide increase in the prevalence, particularly in children. • However, in recent years this trend appears to have plateaued and may even have reversed in children.

  3. Among those aged under 35 years, the prevalence of asthma fell significantly from 14.0% to 11.4% between 2001 and 2004–05. • However, in the same period, there was no change in the prevalence of asthma among people aged 35 years and over. • Based on more recent self-reported data from the NHS, an estimated 10.0% of the Australian population had current asthma in 2007–08.

  4. Among those aged under 15 years, the prevalence of asthma is higher for males than females but, among those aged 15 years and over, the reverse is true. • Overall, females had a significantly higher prevalence of current asthma (10.9%) than males (8.9%) in 2007–08, although the highest prevalence occurred in males aged 5–9 years (15.1%). • See chart on following slide

  5. DEATHS • Asthma death rates in Australia are high by international standards, although asthma is not a leading cause of mortality. • In 2007, asthma was certified as the underlying cause of 385 deaths. This corresponds to an asthma mortality rate of 1.67 per 100,000 population, representing 0.28% of all deaths.

  6. Since the peak in deaths from asthma in the late 1980s, the mortality rate has fallen by about 70%. Overall, the rate is higher in females than males. • Since the mid- to late 1980s, there has been a substantial decline in deaths attributed to asthma in 5–34 year olds—in fact, the death rates have fallen by more than 85%. • Refer to the following slide

  7. Burden of disease • It is estimated that, in 2010, asthma will be the 10th leading contributor to the overall burden of disease in Australia, accounting for 2.3% of the total number of DALYs. • In that year, 66,000 years of healthy life are estimated to be lost due to asthma. The great majority (92%) of DALYs due to asthma arise from YLD caused by the condition.

  8. Asthma is estimated to be the leading cause of burden of disease among children aged 0 to 14 years in 2010, contributing 37,700 DALYs (18.4% of total DALYs in that age group). • Furthermore, chronic respiratory disease, which includes asthma, was the fourth leading contributor to the Indigenous health gap in the burden of non-communicable conditions during 2003.

  9. It accounted for 9% of the gap, behind CVD (23%), diabetes (12%) and mental disorders (12%). • Overall, it is predicted that asthma will continue to rank as one of the major causes of disease burden in Australia for the next two decades, particularly among females.

  10. GP encounters

  11. Hospitalisations

  12. What is asthma? • Asthma is a chronic inflammatory airway disease, either intrinsic or extrinsic (allergic), which can be triggered by an allergy to specific antigens, a hypersensitivity reaction to bacteria or viruses causing an immunoglobulin E (IgE) response or a combination of the above (Porth 2002 pp.639-641) • Like autoimmune disease it is a chronic disturbance of immunological function. (Bone 2005) • Therefore, asthma is not just the attacks, these are the ‘tip of the iceberg’. (Bone 2005)

  13. TRIGGERS • Refer to the booklet: Asthma – the Basic Facts page 3.

  14. It has been suggested that Th2 cytokines, both directly and indirectly, are responsible for most of the aspects of the allergic inflammation of asthma.(Romagnani, S. 2000, ‘T-cell subsets’., Annals of Allergy, Asthma and Immunology., vol. 85, pp. 9-18) These Th2 cells may also play a pathogenic role even in intrinsic asthma. • This was confirmed by Stirling & Chung(2000. European Respiratory Journal, vol.16, iss. 6, pp. 1158-74) who discussed that a treatment approach for asthma would include the inhibition of Th2 derived cytokine expression and the blockade of these cytokines in IgE and eosinophils.

  15. Further research by Wei et al (2005, ‘Involvement of human natural killer cells in asthma pathogenesis: natural killer 2 cells in type 2 cytokine predominance’, Journal of Allergy and Clinical Immunology, vol.115, no.4, pp.841-7 World Scientific, Singapore.) provided additional confirmation when they stated that Th2 cells play a pivotal role in the pathogenesis of asthma.

  16. Up to 20% of the asthmatic population is sensitive to aspirin and present with a combination of sinusitis, rhinitis and asthma when exposed to the drug. (Babu, KS & Salvi, SS. 2000, ‘Aspirin and asthma’, Chest, vol.118, no. 5, pp. 1470-6) • The condition known as aspirin-exacerbated respiratory disease (AERD) has been described by Fahrenholz(Fahrenholz, JM. 2003, ‘Natural history and clinical features of aspirin-exacerbated respiratory disease’, Clinical Review of Allergy and Immunology, vol.24, no.2, pp.113-24)as one where persistent asthma develops in the third or fourth decade after multiple unsuccessful sinus operations and subsequent treatment with aspirin and corticosteroids to deal with the respiratory mucosal inflammatory processes.

  17. In patients with sinusitis and asthma, the sinusitis precedes the asthma in more than 90% of cases. Of these more than half were aspirin sensitive and more than 90% were prescribed steroids. (Bone 2005)

  18. A list of allergens associated with extrinsic asthma that can be responsible for a Type 1 Hypersensitivity response, has been drawn up by Vardaxis(1995 p. 153-4) and includes various pollens, various drugs and foods. • Vally& Thompson (2003, ‘Allergic and asthmatic reactions to alcoholic drinks’, Addiction Biology, vol. 8, no. 1, pp. 3-11) reported that over 40% of asthmatics found that alcoholic drinks can trigger an allergic reaction, in particular the amines and sulphite additives in wine and specific components of beer, spirits and distilled liquors.

  19. Wheat has been shown to cause severe IgE mediated reactions (Daengsuwan, T., Palosuo, K., et al 2005, ‘IgEantibodiesto w-5 gliadin in children with wheat-induced anaphylaxis’, Allergy, vol. 60, no.4, p. 506).

  20. The impact of alcohol on lung airway functions is dependent on the concentration, duration and route of exposure. Brief exposure to mild concentrations of alcohol may enhance mucociliary clearance, stimulates bronchodilation and probably attenuates the airway inflammation and injury observed in asthma. Prolonged and heavy exposure to alcohol impairs mucociliary clearance, may complicate asthma management and likely worsens outcomes. (Sisson J, 2007, ‘Alcohol and Airways Function in Health and Disease’, Alcohol, vol.41, no.5, pp.293-307)

  21. Intervention studies have demonstrated the effect that intestinal worms (geohelminths) have on either atopy or asthma (Cooper, PJ. 2004, ‘Intestinal worms and human allergy’, Parasite Immunology, vol. 26, no. 11-12, p. 455). • In a study by Caress & Steinemann(Caress, SM & Steinemann, AC. 2005, ‘National prevalence of asthma and chemical hypersensitivity: an examination of potential overlap’, Journal of Occupational & Environmental Medicine, vol. 47, no. 5, pp. 518-22)of 1057 people, 42% of asthmatics reported the existence of multiple chemical sensitivities. As well, 29.7% of asthmatics exhibited breathing difficulties when exposed to air fresheners and 32% to scented products.

  22. Corticosteroids can be responsible for the suppression of immune response with an increased risk of more chronic disease due to acute infection with various opportunistic microbes (Breakspear, I. 2003, ‘Steroids & Herbs: a long & complicated relationship’ at a seminar given by Phytomedicine). • This has been confirmed by Anzueto & Niederman(2003, ‘Diagnosis and Treatment of Rhinovirus Respiratory Infections’, Chest, vol. 123, pp. 1664-1672)who established that rhinoviruses, members of the Picornaviridae family, were associated with exacerbations of asthma and sinusitis.

  23. They reported that contributing factors to the hypersensitivity reaction caused by these viruses include vagally mediated reflex bronchoconstriction, activation of inflammatory cells and the induction of IgE switching. • While the symptomatic treatment of these viruses can involve using corticosteroids, they warned that the steroids may actually increase the viral replication.

  24. A further concern was discussed by Just et al (2005, ‘Immediate allergy to oral corticosteroids’, La Review de Medecine Interne, vol. 26, no.4, pp.331-4) when he warned that while corticosteroid allergy is rare it can be fatal and that people with an existing intolerance to aspirin and sulfites, who are also asthmatic, need to be vigilant. • They have also been found to be ineffective in altering the Th2 response to allergens (Hussain, Iftikhar & Kline, JN. 2004, ‘DNA, the Immune System and Atopic Disease’, Journal of Investigative Dermatology Symposium Proceedings, vol. 9, no.1, p.23).

  25. Gastro-oesophageal reflux (GOR) has a proven relationship with bronchial reactivity in asthma (Vincent, D., Cohen-Jonathan, AM., Leport, J et al 1997, ‘Gastro-oesophageal reflux prevalence and relationship with bronchial reactivity in asthma’, European Respiratory Journal, vol.10, pp. 2255-2259) with this study showing a 32% prevalence of GOR in a nonselected population of 4432 asthmatics attending a hospital outpatients clinic. They also found an association between Irritable Bowel Syndrome (IBS), GOR and asthma.

  26. This was further recognized by Avidan et al (2001, ‘Temporal associations between coughing or wheezing and acid reflux in asthmatics’, Gut, vol.49, no. 6, pp. 767-73) when they found that GOR was common in asthmatic patients with two possible causes: • microaspiration of gastric reflux into the gut causing a mucosal reaction; • vagally medicated oesophageal – tracheobronchial reflex resulting in bronchospasm.

  27. They referred to the perpetuating feedback cycle between the cough of asthma and GOR. • A further complication associated with GOR is that many of the current asthma medications actually promote the development of the condition (Meletis, CD & Barker, J. 2004, ‘State-of-the-art complementary therapeutics for asthma’, Alternative & Complementary Therapies, June: 105-110).

  28. Results have shown a deleterious role of cleaning agents on asthma, and a high risk of asthma in cleaners in both private homes and offices. The use of industrial cleaning agents was also found to have a deleterious effect on both asthma and lung function. (Moual N, Kennedy S & Kauffmann F. 2004, ‘Occupational exposures and asthma in 14,000 adults from the general population ‘, American Journal of Epidemiology, vol.160, no.11, pp.1108-1116)

  29. This study showed attributable risk of exposure to dusts, gases, and fumes with results showing 5 to 13% for occupation or exposure known to cause occupational asthma and from 14 to 36% for more general exposure to dusts, gases, and fumes. (Moual N, Kennedy S & Kauffmann F. 2004, ‘Occupational exposures and asthma in 14,000 adults from the general population ‘, American Journal of Epidemiology, vol.160, no.11, pp.1108-1116)

  30. Smoking • parental history of asthma and allergy is most strongly associated with early onset persistent asthma and suggest that among genetically predisposed children, early in life smoking exposure, maternal smoking during pregnancy, favours the development of early onset asthma that persists into later early childhood. (London S, Gauderman W, Avol E et al. 2001, ‘Family history and the risk of early onset persistent, early onset transient and late onset asthma’ Epidemniology, vol.12, no.5, pp.577-583)

  31. Smokers with asthma have been shown to suffer exacerbation of asthma symptoms and to have a higher risk for developing chronic obstructive pulmonary disease (COPD) compared to people with asthma who do not smoke. (Zundert R, Engels R, Kleinjan M & Eijnden R. 2008, ‘An Integration of Parents’ and Best Friends’ Smoking, Smoking-Specific Cognitions, and Nicotine Dependence in Relation to Readiness to Quit Smoking: A Comparison between Adolescents with and without Asthma’, Journal of Paediatric Psychology, vol.33, no.8, pp.821-832)

  32. Viral infections • Respiratory viral infections are the most common cause of asthma exacerbations in both adults and children. Rhinovirus is the most common virus associated with the common cold and is also the most common virus implicated in asthma exacerbations. (Powell H, Smart J, Wood L et al. 2008, Validity of the Common Cold Questionnaire (CCQ) in Asthma Exacerbations’, PLoS One, vol.3, no.3)

  33. Stress: (Chen E & Miller G. 2007, ‘Stress and Inflammation in Exacerbations of Asthma’ Brain Behaviour Immunology, vol.21, no.8, pp.993-999) • Stress is seen as a process that accentuates the airway inflammatory response to environmental triggers and, in doing so, increases the frequency, duration, and severity of patients' symptoms. • How? The theory is that the body views stress as an external demand from an individual's social environment where the external stressor is appraised as being threatening and unmanageable.

  34. These emotional and cognitive processes sensitize the Th-2 pathway, such that upon exposure to a trigger, there is a more pronounced inflammatory response, leading to increased frequency, duration, and severity of symptoms.

  35. ASTHMA AND THE ATHLETE (McKenzie D & Boulet L. 2008, ‘Asthma, outdoor air quality and the Olympic Games’ CMAJ. Vol.179, no.6, pp.543–548). • The relation between air quality and respiratory health problems is substantial. • The primary air pollutants are ozone, sulfur dioxide, nitrogen dioxide and particulate matter. • Carbon monoxide is also of interest to the athlete because of its ability to compete for oxygen on hemoglobin. • Power generating plants, road transport and industry are the primary sources of these compounds.

  36. Ozone is not emitted directly from any industrial source in significant quantities. At ground level, it is primarily generated by a series of chemical reactions driven by sunlight. Particulate matter is associated with a range of effects on health, including the respiratory and cardiovascular systems. People with existing lung and heart disease are at risk of death from exposure to high levels of particulate matter. • In athletes with asthma, the diameters of the large and small airways are likely compromised during exercise, and even small changes will have negative effects on the work of breathing and gas exchange. Consequently, exercise induced arterial hypoxemia is prevalent among athletes with asthma during high-intensity exercise.

  37. With exposure to an environment that has poor air quality, air pollutants may trigger asthma symptoms, usually in a dose dependent manner. A well designed, randomized crossover study, showed that exhaust emissions from motor vehicles with diesel engines exacerbated asthma and increased the severity of asthma symptoms and medication use. • Air pollutants may also enhance allergen-induced airway responses, as has been shown in animal models. With the high minute ventilation seen during exercise, the effects of exposure to these pollutants are more noticeable in athletes than in non-athletes and likely more evident in people with asthma than in those without asthma.

  38. Because poor air quality may exacerbate asthma, increase symptoms and result in poor performance, optimal control of this condition is essential to allow highly trained athletes to compete.

  39. DIETARY IMPLICATIONS • Go off dairy foods for the next 3 weeks • Try to remove any wheat based products for the next 3 weeks and replace with either Oats or Rice based products. • Include garlic in the diet • Include the antioxidant berries and vegetables in the diet • Include oily fish and nuts in the diet as a means of increasing the omega fatty acids to suppress the production of pro-inflammatory cytokines • Include regular gentle exercise

  40. Reference list: Australia’s Health 2010, a publication by the Australian Institute of Health and Welfare, Canberra Jamison,J (2003) Clinical Guide to Nutrition and Dietary Supplements in Disease Management, Churchill Livingstone McGuire,K & Beerman,K, (2007) Nutritional Sciences: From Fundamentals to Food, Thomson Rolfe,S, Pinna,K & Whitney,E (2009) Understanding Normal and Clinical Nutrition 8th Edition, Cengage Whitney,E, Rolfes,S, Crowe,T, Cameron-Smith,D & Walsh,A (2011) Understanding Nutrition, Cengage www.aihw.gov.au

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