Asthma is a chronic obstruction of the lumen of the small airways in the lung. The bronchioles are lined with smooth muscle and as the muscle contracts, the lumen becomes smaller. This inflammation stimulates certain cascades and causes smooth muscle constriction. As a result, the inflammation causes the lumen to shrink until the obstruction causes wheezing. Patients afflicted cannot expel air through these small airways, causing the pulmonary flow rate in the small airways to decrease during an asthma attack. In such case, patients have a reversible airway inflammation, which is the opposite of irreversible as in the case of COPD (Chronic Obstructive Pulmonary Disorder).
First descriptions of Asthma
“The first modern descriptions come from Sir John Floyer’s treatise on asthma from 1698. (Figure 1). Floyer, who had asthma, described the still predominant Hippocratic humoral pathology, but also described bronchial constriction as a cause for wheezing. He discussed his own asthma flares, providing some of the first descriptions of uncontrolled asthma. He also described his association of symptoms with regions and triggers, which was later identified as allergic asthma.”1
Prevalence of Asthma
“According to the Centers for Disease Control and Prevention, the prevalence of asthma among U.S. children increased from 3.6% in 1980 to 5.8% in 2003. Asthma is the third leading cause of hospitalization among persons under 18 years of age in the United States, exceeded only by pneumonia and injuries. Increases in the prevalence of asthma of similar or even greater magnitude were reported from other countries during the second half of the 20th century. For example, in 1964, 19% of Australian children were reported by their parents to have had asthma or wheezing at some time during their first 7 years of life; in 1990, such symptoms were reported for 46% of children. For many countries, there are no data on temporal changes in the prevalence of asthma before the 1990s. After the 1990s, estimates of temporal trends in the prevalence of asthma in several European and Asian countries are conflicting. In some populations, the prevalence of diagnosed asthma is still rising, whereas in others it appears to be stable or decreasing slightly. There are no clear differences in trends in prevalence between children and adults, between severe and mild asthma, or between developed and developing countries; however, there are few studies from developing countries.”3
Characteristics of Asthma and Related Terminology
Asthma is characterized by inflammation that causes constriction of small airways. IgEe, an immunoglobulin E, might trigger this inflammation, which releases histamine and causes swelling. In turn, this also shrinks the constricting airway.
Two types of nerves (and their corresponding receptors) affect smooth muscle. The first one is the beta receptor. So, when the nerve releases its compound into the beta receptor, it causes relaxation. The other one is the muscarinic receptor, which causes constriction. To achieve muscle relaxation pharmacologically, use an anti-muscarinic while favoring beta agonists. Inflammation causes restriction, so also use anti-inflammatories.
“Asthma identifies a spectrum of respiratory-related symptoms, typically with a link to reversible airflow limitation. Like the terms arthritis or anemia, the term asthma does not identify any specific underlying pathobiology, but is a broad, umbrella-like term that covers multiple groupings of patient characteristics or phenotypes. While the term asthma has been traditionally used to describe a childhood onset disease associated with atopic/allergic responses, asthma can develop later in life, with minimal link to allergy. Although mild to severe disease has been identified across the spectrum of asthma, many studies now show that ‘severe asthma’ is not a phenotype, but rather a description of a group of patients with high medical needs, whose pathobiologic and clinical characteristics vary widely. This heterogeneity has made the study of the underlying pathobiologies of severe asthma problematic. Therefore, to move the understanding of severe asthma forward, several factors deserve attention, including (a) a unified clinical definition of the umbrella-term asthma, (b) biased and unbiased approaches for the identification of clinical and (ideally) matched molecular phenotypes, (c) animal models to address the importance of specific molecular pathways, and (d) targeted treatment approaches in humans that confirm the relevance of particular molecular pathways to defined clinical molecular phenotypes. Linking these steps should enable identification of precisely treatable endotypes of severe asthma.”4
“Clinical diagnosis of asthma can be made if recurrent respiratory symptoms especially current wheeze or wheeze in the last 12 months are present. Presence of a trigger, other allergic diseases, personal or family history of asthma; clinical improvement and increase in the peak flow and forced expiratory volume in one second of ≥12% after salbutamol administration increases the likelihood of asthma. At diagnosis severity grading, patient education, removal or reduction of the trigger should be done. Follow up 2–6 weeks and assessment of control during therapy is essential. Therapy should be adjusted up or down depending on control levels. Patients should be instructed to increase the frequency of their bronchodilators and/or steroids therapy when they start to experience worsening symptoms.”5
Events that can trigger problems in our airways
- Quality of air we breath
- Acid reflux can irritate the airway. GERD can cause symptoms of asthma
- Post nasal drip may also cause asthmatic symptoms.
- Cotton dust
- Wood dust
- Samters Triad (aspirin sensitivity, asthma, nasal polyps)
- Cold air
- Food allergies
- Dust mites
Epidemiology and others implications in asthma
“There is evidence that, in some areas of the Western world, the prevalence of asthma may have plateaued. The environmental factors causally driving the temporal changes remain largely unknown. Therefore, there are few truly justified recommendations for the prevention of asthma. Avoidance of passive and active exposure to smoke is warranted for many other health reasons and also for asthma prevention, because the epidemiologic evidence strongly suggests a causal link between exposure to smoke and the onset of asthma. By contrast, many other proposed avoidance strategies, such as reducing allergen levels, implementing changes in diet, withholding vaccinations or treatment with antibiotic and antipyretic agents, administering probiotics, or even exposing children to pets early in life, are either ineffective or unverified as primary prevention measures.”6
Symptoms of Asthma include
- Chest tightness (encountering resistance during inhaling and exhaling)
Asthma and Diet
“Systemic and airway effects of dietary patterns on asthma. The Western diet promotes a pro-inflammatory environment and causes an increase in airway inflammation. Fruit and vegetable consumption has systemic anti-inflammatory properties, with a decrease of pro-inflammatory cytokines in plasma. Fruit and vegetables are also associated with lower airway inflammation and a reduction of neutrophils in asthmatics. Gut microbiota plays a role in immune response to diet in asthma. Metabolites such as short-chain fatty acids (SCFA) (including ω-3 fatty acids) that have immunomodulatory effects are produced in high amounts after fruit and vegetable intake. The western diet altered microbiota composition and potentiate inflammation.”9
Foods that contribute to asthma
“Chronic inflammation of the airways is a key component of asthma, which may be modulated by dietary intake. High fat intake, a characteristic of the Western diet, can cause an increase in airway inflammation. Consumption of a high-fat mixed meal has been shown to increase sputum neutrophils 4 h post-meal in patients with asthma, as well as activation of a number of genes in sputum involved in “immune system processes”, such as TLR4, indicating an increase in airway inflammation. Reduction of dietary saturated fat intake was associated with a reduction in neutrophilic airway inflammation in asthmatics. In adults with severe asthma, higher fat and lower fiber intakes have been associated with increased eosinophilic airway inflammation”10
How to Treat Asthma
Since asthma is a reactive disease, patients must to find out what causes their asthmatic episodes. Some medicines have side effects, patients should not use a drug that they do not require. Find things you can control, like pets, pillows full of allergens, postnasal drip, and GERD, among others. Uncontrollable factors are pollen in air and weather temperature, to name a few.
Temperature factors apply to almost any asthmatic that has exercised in cool weather, especially during a strenuous activity like jogging, basketball or soccer. The cold air does not have time to warm and thus irritates our bronchioles, triggering or exacerbating an asthma episode.
Most common medications to treat asthma attacks are SABA (short-acting beta-agonists) such as albuterol or Levalbuterol. Other medications such as Ventolin act as bronchodilators, and prophylactic medications such as Flixotide prevent attacks.
Ideally, patients should know what causes or triggers their asthma so that doctors customize and plan their treatment individually. While asthma is reversible, this disease can affect the patients’ quality of life, so they should adjust accordingly.
“Recent reports continue to shed light on methods to understand factors that influence the course of asthma, methods to assess and communicate levels of control, and new targets for intervention as well as new immunomodulators. It will now be important to carefully assess risk factors for the development of asthma as well as the risk for asthma exacerbations and to improve the way we communicate this information in the health care system. This will allow parents, primary care physicians, specialists and provider systems to more effectively intervene in altering the course of asthma and to further reduce asthma morbidity and mortality.”11
“Significant advances have been made in the past 10 years in defining asthma control as well as individuals at risk for asthma exacerbations. We now recognize the limitations of our available treatments and seek new strategies for intervention that will fill those gaps in disease management. Some of those medications, such as the monoclonal antibody immunomodulators, will be expensive at least upon initial approval. Therefore, there will be resistance to their utilization unless cost-effectiveness can be demonstrated. In this era of cost containment, while moving to strategies of prevention, it will be important to organize health care systems in order to identify patients who are inadequately controlled as indicated by frequent exacerbations, increased medication requirements or loss of pulmonary function over time. A patient profile that combines clinical features along with reliable predictors of beneficial effects to certain treatments will be useful in individualizing treatment plans. These treatment effects may differ in adults and children. Enhanced communication systems will be necessary among parents, clinicians, health care providers, and the pharmaceutical industry so that we continue the pathway of understanding the disease and developing new treatments that address the unmet needs of patients who are at risk for severe consequences of unchecked disease persistence or progression.”12
Current treatment and therapies come from the evolution of the concept of asthma. “Our understanding of asthma has evolved over time from a singular disease to a complex of various phenotypes, with varied natural histories, physiologies, and responses to treatment. Early therapies treated most patients with asthma similarly, with bronchodilators and corticosteroids, but these therapies had varying degrees of success. Similarly, despite initial studies that identified an underlying type 2 inflammation in the airways of patients with asthma, biologic therapies targeted toward these type 2 pathways were unsuccessful in all patients. These observations led to increased interest in phenotyping asthma. Clinical approaches, both biased and later unbiased/statistical approaches to large asthma patient cohorts, identified a variety of patient characteristics, but they also consistently identified the importance of age of onset of disease and the presence of eosinophils in determining clinically relevant phenotypes. These paralleled molecular approaches to phenotyping that developed an understanding that not all patients share a type 2 inflammatory pattern. Using biomarkers to select patients with type 2 inflammation, repeated trials of biologics directed toward type 2 cytokine pathways saw newfound success, confirming the importance of phenotyping in asthma. Further research is needed to clarify additional clinical and molecular phenotypes, validate predictive biomarkers, and identify new areas for possible interventions.”13
Consult with a specialist if you suspect to have asthma. Do not take medications without a diagnosis, remember that the treatment will depend on individual factors.
(1, 2, 13) Evolving Concepts of Asthma. Gauthier, M., Ray, A. & Wenzel, S.E. American Journal of Respiratory and Critical Care Medicine. 2015. https://www.atsjournals.org/doi/10.1164/rccm.201504-0763PP
(3, 6, 7) The Asthma Epidemic. Eder, W., Ege, MJ. & von Mutius, E. The New England Journal of Medicine. 2006. https://www.nejm.org/doi/full/10.1056/NEJMra054308?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed
(4) Current concepts of severe asthma. Ray, A., Raundhal, M., Oriss, T.B., Ray, P. & Wenzel, S.E. JCI The Journal of Clinical Investigation. 2016. https://www.jci.org/articles/view/84144
(5) Guidance on the diagnosis and management of asthma among adults in resource-limited settings. Kirenga, B.J., Schwartz, J., de Jong, C., van der Molen, T. & Okot-Nwang, M. African Health Science. 2015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4765426/
(8, 9, 10) Diet and Asthma: Is It Time to Adapt Our Message? Guilleminault, L., Williams, E.J., Scott, H.A., Berthon, B.S., Jensen, M. & Wood, L.G. Nutrients. 2017. https://www.mdpi.com/2072-6643/9/11/1227
(11, 12) Advances in Pediatric Asthma in 2013: Coordinating Asthma Care. Stanley J. Szefler. The Journal of Allergy and Clinical Immunological. 2014. https://www.jacionline.org/article/S0091-6749(14)00114-6/fulltext