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The Asthma Epidemic Ioana AGACHE

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The Asthma Epidemic Ioana AGACHE

  1. 1. The asthma epidemic: How did we come to worldwide 300 Million patients? Ioana Agache Transylvania University Brasov Romania
  2. 2. Disclosure In relation to my presentation, I declare no conflict of interest
  3. 3. Current situation – asthma prevalence 2008- 2010 : 334 millions Global Burden of Disease Study 2000- 2002: 235 millions
  4. 4. Asthma affects both affluent and poor countries Prevalence of asthma symptoms among 13-14 years old (ISAAC) Lai CKW, et al. Thorax 2009
  5. 5. Uncontrolled asthma Prevalence of asthma symptoms in the last 12 months among 18-45 years old in 70 countries (World Health Survey) To T, et al. BMC Public Health 2012
  6. 6. Severe asthma Prevalence of severe asthma among 13-16 years old (ISAAC) Lai CKW, et al. Thorax 2009
  7. 7. Asthma deaths WHO Detailed Mortality Database, updated Feb 2014
  8. 8. The Burden of Asthma (YLDs) YLD = years lived with disability Vos T et al. Lancet 2015; 386:743-800
  9. 9. Current situation - summary no available therapeutic regimens can cure asthma rates of deaths due to asthma worldwide have reduced greatly over the past 25 years, however they are still high in low income countries the burden of asthma will continue to be driven by increasing prevalence
  10. 10. Q1. What are the risk factors for asthma
  11. 11. Global Burden of Disease Study 2013 (data from 188 countries, comprehensive methodology for risk factors) Incomplete methodological approach Murray C, et al. Lancet published online Sep 11, 2015
  12. 12. Global Burden of Disease Study - methodology Murray C, et al. Lancet published online Sep 11, 2015
  13. 13. Global Burden of Disease Study – risk factors Murray C, et al. Lancet published online Sep 11, 2015
  14. 14. Global Burden of Disease Study – risk factors Murray C, et al. Lancet published online Sep 11, 2015
  15. 15. Incomplete methodological approach Associations are reported between a wide range of risk factors and childhood asthma in observational studies which cannot substantiate causality Few risk factors have been assessed in primary prevention studies and these failed because of bulk selection of patients
  16. 16. Incomplete methodological approach There is no single exposure which seems likely to cause asthma Single exposures are invariably contaminated by other exposures.
  17. 17. Risk factors associated with asthma The hygiene hypothesis (mainly related to atopy) Obesity/diet/lifestyle Genetic background Environmental tobacco smoke and other pollutants Atopy Occupational exposure Pet ownership
  18. 18. The hygiene hypothesis is not new
  19. 19. The hygiene hypothesis – the farm effect
  20. 20. The hygiene hypothesis – the farm effect den Dekker HT, et al. Chest. 2015;148(3):607-17.
  21. 21. The hygiene hypothesis – the farm effect
  22. 22. What is the protective factor?
  23. 23. What is the protective factor?
  24. 24. What is the protective factor? Smit LA et al, Clin Exp Allergy. 2007;37(11):1602-8.
  25. 25. What is the protective factor?
  26. 26. Personal and home cleanliness Weber J, et al. AJRCCM. 2015;191:522-529 Perinatale Asthma Umwelt Langzeit Allergie Studie (PAULA) birth cohort
  27. 27. Smoking increases the risk of asthma by 1.6 King M.E, Mannino D.M, Holguin F. Panminerva Medica 2004; 46: 97-110
  28. 28. Postnatal parental smoking increases the risk of asthma with 20% Burke H et al. Pediatrics. 2012;129(4):735-44
  29. 29. Maternal smoking Continued maternal smoking during pregnancy was associated with increased risks of early and persistent wheezing (OR: 1.24) and asthma (OR:1.65) den Dekker HT, et al. Chest. 2015;148(3):607-17. prospective cohort study among 6,007 children paternal and maternal smoking during pregnancy (never, first trimester only, continued) secondhand tobacco smoke exposure during childhood
  30. 30. Maternal smoking – transgenerational effect Li YF, et al. Chest. 2005;127(4):1232-41 In utero exposure to maternal smoking was associated with increased risk for asthma diagnosed in the first 5 years of life, and for persistent asthma (OR 1.5) Grandmaternal smoking during the mother's fetal period was associated with increased asthma risk in her grandchildren (OR 2.1)
  31. 31. Outdoor pollution increases asthma incidence in adults Jacquemin B et al. Environ Health Perspect. 2015;123(6):613-216
  32. 32. Obesity and asthma Weinmayr G, et al. Plos One 2014; 9(12):e113996
  33. 33. Obesity and asthma Weinmayr G, et al. Plos One 2014; 9(12):e113996
  34. 34. A dietary basis for inflammatory diseases interactions between dietary or bacterial metabolites and immune cells and pathways for gut homeostasis. Thorburn AN, et al. Immunity 2014;40:834-842.
  35. 35. A dietary basis for inflammatory diseases Palmer DJ, et al. Immunol Allergy Clin N Am 2014;40:825-837.
  36. 36. Emerging risk factors Inference from other preventive strategies The indoor environment (dampness, ventilation) Maternal fatty acid status and low vitamin D during pregnancy Prenatal exposures to persistent organic pollutants or stress Climate change
  37. 37. Climate change
  38. 38. Kunzli N, et al. Am J Respir Crit Care Med. 2006;174(11):1221-8
  39. 39. Inference from other preventive strategies folic acid supplementation in the first trimester only or first trimester and later had increased relative odds of asthma retrospective cohort study of 104,428 children, born 1996-2005 the association folic acid supplementation and childhood asthma at ages 4.5-6 years. folic acid supplementation around conception helps prevent neural tube defects Veeranki SP, et al. Epidemiology. 2015 Sep 10. [Epub ahead of print]
  40. 40. Q2. When do these risk factors intercede
  41. 41. Asthma risk factors journey Genetic factors Epigenetic factors Early window of risk (the prenatal environment) Acquired risk factors (obesity/diet, pets, indoor and outdoor pollution/occupational) The cumulated risk of severe asthma complex interactions of lung structure and function genes with environmental exposures
  42. 42. Douwes J at el. Eur Respir J. 2008 ;32(3):603-11 Early window of opportunity and persistent exposure
  43. 43. Saskatchewan Rural Cohort Study Group • 30.6% - early farm living (first year of life) only • 34.4% - both early and current farm living • 17.4% had never lived on a farm • women had a decreased risk for both asthma and hay fever with an early farm exposure only • men currently living on a farm without an early farm exposure had an increased risk for ever asthma Early window of opportunity and gender Rennie DC et al. J Asthma. 2015 Sep 17:1-9. [Epub ahead of print]
  44. 44. Q3. What can we do to prevent asthma 2. Address specific risk factors (atopy) Allergen immunotherapy (AIT) 3.Promote excellence in care 4.Raise awareness at a societal and political level 1. Focus on measures with potential to improve lung and general health
  45. 45. 1. Focus on measures with potential to improve lung and general health Reduce smoking and ETS Reduce indoor and outdoor air pollution and occupational exposures Improve feto-maternal health Community level Reduce social inequalities Educational level Reduce childhood obesity; encourage a diet high in vegetables and fruit Promote breastfeeding Reduce smoking and ETS
  46. 46. AIT in allergic rhinitis prevents asthma The PAT study Long term efficacy of AIT The German real life study 2. Address specific risk factors
  47. 47. AIT in allergic rhinitis prevents asthma The PAT study Jacobsen L et al. Allergy. 2007;62(8):943-8.
  48. 48. AIT in allergic rhinitis prevents asthma The German real life study data from German National Health Insurance cohort of 118,754 patients with AR and without asthma who had not received AIT in 2005 risk of incident asthma from 2007 to 2012 Schmitt J et al. J Allergy Clin Immunol. 2015 Sep 11. pii: S0091-6749(15)01101-X. doi: 10.1016/j.jaci.2015.07.038. [Epub ahead of print])
  49. 49. The German real life study only 2.1% received AIT Schmitt J et al. J Allergy Clin Immunol. 2015 Sep 11. pii: S0091-6749(15)01101-X. doi: 10.1016/j.jaci.2015.07.038. [Epub ahead of print]) the preventive effect was demonstrated only for the SC route and was stronger for AIT > 3 years the risk of incident asthma was significantly less in patients exposed to AIT (RR = 0.60)
  50. 50. 3. Promote excellence in care High quality guidelines for clinical practice National Asthma Strategies in countries responding to the Global Asthma Network Survey
  51. 51. 4. Increase awareness
  52. 52. Take home messages A better understanding of the factors that cause asthma is urgently needed This knowledge needs to be translated into public health and primary prevention measures effective worldwide. Think outside the box: WHO: relevant risk factors for the causation of asthma WHAT: types of novel primary prevention strategies developed HOW: research methods used to provide the evidence base for their implementation

Hinweis der Redaktion

  • In the GI tract, dietary fiber is primarily digested by
    commensal bacteria in the colon, which produces
    high concentrations of SCFAs, such as acetate,
    propionate, and butyrate. Other metabolites, such
    as u-3 fatty acids, succinate, or kynurenic acid,
    are directly consumed and absorbed throughout
    the GI tract. In addition, metabolites can be
    directly absorbed in the small intestine. SCFAs
    (mainly acetate) are transported from the gut to the
    blood, where they can influence bone marrow and
    many cell types throughout the body. Another
    major point of intersection is the transfer of metabolites
    to the developing fetus. SCFAs are able
    to cross the placenta or be delivered via breast
    milk, where they can influence gene expression
    and the development of the immune system.
  • Adult Canadian population
  • Adult Canadian population

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