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Identifying Asthmatic Triggers

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Asthma, a chronic respiratory disease that affects 4% of the US population,1 is responsible for considerable global morbidity and healthcare costs2 and is one of the leading non-communicable diseases worldwide.3 In the 1990s and early 2000s, substantial global progress was made on key outcomes such as allergy-related hospital admission and mortality, but little improvement has been observed in these areas over the past 10 years.4 Asthma symptoms, exacerbations, and triggers are often associated with lower quality of life, including fatigue, activity limitation, negative effects on social life and relationships, and reduced productivity.3

What is the functional medicine approach to treating asthma? In the following video, IFM educator Shilpa P. Saxena, MD, talks about getting at the root cause of the disease by identifying the asthma trigger:

The prevalence of asthma is increasing in many countries, especially among children.5 Interestingly, the incidence of childhood asthma varies among countries, with typically higher prevalence in “Westernized” nations.6 A 2019 study found that a child’s risk of developing asthma is lower the more the microbiota of the child’s home resembles that of a farm house.7 The study analyzed microbiota from 400 Finnish and 1,000 German homes and found that the microbiota in homes that seem to be protective from asthma contained bacteria typical of the outdoor environment, including bacteria in soil. The results call into question whether asthma could be prevented in the future by modifying children’s early microbial exposures.7

A study published in 2019 of 714 Parisian children as part of an ongoing prospective study, called Pollution and Asthma Risk: an Infant Study (PARIS) birth cohort, found that children strongly sensitized to house dust mites at ages eight and nine had the highest risk of asthma and allergic rhinitis.8 Another similar cohort study in Taiwanese children found that asymptomatic toddlers with early house dust mite sensitization had higher risks of developing asthma, allergic rhinitis, atopic dermatitis, and abnormal lung functions at seven years of age.9 A 2020 study evaluating the connection between air pollution and childhood asthma found that children exposed to NO2—a major traffic-related air pollutant—are more than twice as likely to have early-onset asthma.10 This risk is higher even when NO2 levels are within World Health Organization guidelines, the study says.10

During childhood, chronic rhinosinusitis with nasal polyps and severe respiratory infections such as pneumonia were identified as risk factors for the development of severe adult-onset asthma according to a 2021 Finnish population study.11 Early life covariates increasing this risk include growing up in environments where exposure to biologic allergens is more frequent and having parental history of asthma, allergy, and smoking.11 A cross-sectional study published in the Journal of Respiratory Medicine suggested that the immunopathology of childhood-onset asthma is more likely correlated to allergic phenotype and viral respiratory infection, while adult-onset asthma is non-atopic in nature and generally characterized by T2 inflammation.12 Obesity and metabolic syndrome are comorbid factors associated with onset-adult asthma but interestingly not with childhood-onset asthma.12 While studies have not found a causal connection between metabolic disorders and the development of asthma, increasing evidence suggests that low-grade inflammation and pro-inflammatory cytokine status in adipose tissue is implicated in its pathology.12,13

Asthma may also be rooted in changes in both innate and adaptive immunity.14 An imbalance of the immune microenvironment may be a possible cause of asthma pathogenesis, in which T cells and macrophages engage in crosstalk. This crosstalk transmits either anti-inflammatory or pro-inflammatory signals, and recent studies have highlighted that an imbalance of T cells or macrophage dysfunction contributes to the progression of asthma. In a 2020 article, researchers proposed a theoretical basis for this, putting forth the hypothesis of a connection between the cytokine storm and severe asthma. They believe that studying the role of and the crosstalk between T cells and macrophages may contribute to the development of new, personalized treatments.14

In adults, comorbidities are more prevalent in severe asthma than in patients with mild-to-moderate disease.15 Pulmonary comorbidities include upper respiratory tract disorders (obstructive sleep apnea, allergic and nonallergic rhinitis, chronic rhinosinusitis, nasal polyposis) and middle/lower respiratory tract disorders (chronic obstructive pulmonary disease, allergic bronchopulmonary aspergillosis and fungal sensitization, bronchiectasis, dysfunctional breathing). Extrapulmonary comorbidities include anxiety, depression, gastroesophageal reflux disease, obesity, and cardiovascular and metabolic diseases.15 In the elderly population, asthmatics are at a higher risk for morbidity and mortality from their asthma than younger patients.16 Evidence also suggests that elderly asthmatics are more likely to be underdiagnosed and undertreated.16

For patients with asthma, young and old, intervening in the allergic march,17 as Dr. Saxena describes, can have a powerful, long-lasting impact on health. The functional medicine model helps clinicians get to the root cause of asthma and develop individual treatment protocols, including dietary changes and other lifestyle modifications to both prevent and ease symptoms. More information:

Learn More About Immune Imbalance

Dust, Allergies, and Asthma in Children

Improving Pediatric Asthma Care

A PROACTIVE APPROACH TO PEDIATRIC ATOPY, RHINITIS, AND ASTHMA

References

  1. National Health Interview Survey, January – March 2017. National Center for Health Statistics. US Department of Health and Human Services, Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/data/nhis/earlyrelease/insur201708.pdf. Published August 2017. Accessed December 6, 2021.
  2. Pavord ID, Beasley R, Agusti A, et al. After asthma: redefining airways diseases. Lancet. 2018;391(10118):350-400. doi:10.1016/S0140-6736(17)30879-6.
  3. Stanescu S, Kirby SE, Thomas M, Yardley L, Ainsworth B. A systematic review of psychological, physical health factors, and quality of life in adult asthma. NPJ Prim Care Respir Med. 2019;29(1):37. doi:10.1038/s41533-019-0149-3.
  4. Ebmeier S, Thayabaran D, Braithwaite I, Bénamara C, Weatherall M, Beasley R. Trends in international asthma mortality: analysis of data from the WHO Mortality Database from 46 countries (1993–2012). Lancet. 2017;390(10098):935-945. doi:10.1016/S0140-6736(17)31448-4.
  5. Global Initiative for Asthma. Global strategy for asthma management and prevention. Global Initiative for Asthma. https://ginasthma.org/wp-content/uploads/2019/04/wmsGINA-2017-main-report-final_V2.pdf. Published 2017. Accessed December 6, 2021.
  6. Lawson JA, Brozek G, Shpakou A, et al. An international comparison of asthma, wheeze, and breathing medication use among children. Respir Med. 2017;133:22-28. doi:10.1016/j.rmed.2017.11.001.
  7. Kirjavainen PV, Karvonen AM, Adams RI, et al. Farm-like indoor microbiota in non-farm homes protects children from asthma development. Nat Med. 2019;25(7):1089-1095. doi:10.1038/s41591-019-0469-4.
  8. Gabet A, Rancière F, Just J, et al. Asthma and allergic rhinitis risk depends on house dust mite specific IgE levels in PARIS birth cohort children. World Allergy Organ J. 2019;12(9):100057. doi:10.1016/j.waojou.2019.100057.
  9. Su KW, Chiu CY, Tsai MH, et al. Asymptomatic toddlers with house dust mite sensitization at risk of asthma and abnormal lung functions at age 7 years. World Allergy Organ J. 2019;12(9):100056. doi:10.1016/j.waojou.2019.100056.
  10. Lau N, Smith MJ, Sarkar A, Gao Z. Effects of low exposure to traffic related air pollution on childhood asthma onset by age 10 years. Environ Res. 2020;191:110174. doi:10.1016/j.envres.2020.110174.
  11.  Toppila-Salmi S, Lemmetyinen R, Chanoine S, et al. Risk factors for severe adult-onset asthma: a multi-factor approach. BMC Pulm Med. 2021;21(1):214. doi:10.1186/s12890-021-01578-4.
  12.  de Boer GM, Tramper-Stranders GA, Houweling L, et al. Adult but not childhood onset asthma is associated with the metabolic syndrome, independent from body mass index. Respir Med. 2021;188:106603. doi:10.1016/j.rmed.2021.106603.
  13.  Aydin M, Koca C, Ozol D, et al. Interaction of metabolic syndrome with asthma in postmenopausal women: role of adipokines. Inflammation. 2013;36(6):1232-1238. doi:10.1007/s10753-013-9660-9.
  14.  Zhu X, Cui J, Yi L, et al. The role of T cells and macrophages in asthma pathogenesis: a new perspective on mutual crosstalk. Mediators Inflamm. 2020;2020:7835284. doi:10.1155/2020/7835284.
  15.  Rogliani P, Sforza M, Calzetta L. The impact of comorbidities on severe asthma. Curr Opin Pulm Med. 2020;26(1):47-55. doi:10.1097/MCP.0000000000000640.
  16.  Dunn RM, Busse PJ, Wechsler ME. Asthma in the elderly and late?onset adult asthma. Allergy. 2018;73(2):284-294. doi:10.1111/all.13258.
  17.  Bantz SK, Zhu Z, Zheng T. The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma. J Clin Cell Immunol. 2014;5(2):202. doi:10.4172/2155-9899.1000202.

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