Asthma

TL;DR. Asthma is a chronic inflammatory disease of the airways that makes them twitchy. The muscle wrapped around each small airway contracts too readily, the lining is swollen and produces excess mucus, and the combination narrows the tubes so that breathing out becomes difficult. The narrowing is reversible, which is what distinguishes asthma from COPD, and the reversibility is why a puff of a bronchodilator can transform someone in minutes. The most important thing to understand about treatment is a mismatch that kills people: the blue reliever inhaler makes you feel better and does nothing about the underlying inflammation, while the preventer inhaler makes you feel nothing and is the drug that keeps you alive.

Key takeaways

• About 260 million people have asthma, and it causes over 400,000 deaths a year, most of them in low- and middle-income countries and most of them preventable.
• The two problems are bronchoconstriction (fast, reversible) and airway inflammation (slow, and the actual disease).
• Most asthma deaths follow a pattern: over-reliance on the reliever inhaler, under-use of the preventer, and failure to recognise deterioration. National reviews find most deaths had identifiable, avoidable factors.
• Guidance has changed fundamentally: reliever-only treatment is no longer recommended for adults, because using a short-acting bronchodilator alone is associated with worse outcomes.
• Asthma is not one disease. Type 2 high asthma (allergic and eosinophilic) responds to steroids and to the new biologic drugs; other phenotypes respond less well.
• A quiet chest in a severe attack is an emergency sign, not reassurance. It means too little air is moving to make a wheeze.

What it is

In short: Twitchy airways that narrow reversibly, which is the feature separating asthma from COPD, and diagnosis needs objective proof of that variability.

An airway is a tube with a smooth muscle ring around it and a moist lining inside. In asthma, three things go wrong together:

1. Bronchoconstriction: the smooth muscle contracts, narrowing the tube.
2. Inflammation: the lining is swollen, infiltrated with immune cells, further narrowing the lumen.
3. Mucus: excess secretion, sometimes forming plugs.

The result is variable, reversible airflow obstruction. Symptoms are wheeze, breathlessness, chest tightness, and cough, characteristically worse at night and in the early morning, and provoked by triggers.

Diagnosis requires both symptoms and objective evidence of variable obstruction, because neither alone is enough:

Asthma is over-diagnosed in some settings (labels applied to any wheeze in childhood, many of which resolve) and under-diagnosed in others, and objective testing is the corrective for both.

Don't be confused: asthma and COPD both cause airflow obstruction, and they are different diseases. Asthma is typically variable and largely reversible, usually starts in childhood, and is driven by eosinophilic allergic inflammation. COPD (Chapter 45) is largely fixed and progressive, usually starts after decades of smoking or smoke exposure, and is driven by neutrophilic inflammation and tissue destruction. They can coexist, and the treatments overlap without being interchangeable: inhaled steroids are the foundation of asthma treatment and are used far more selectively in COPD.

The history

In short: Two separate epidemics of asthma deaths, decades apart, both caused by drugs that relieved symptoms without treating the inflammation.

Asthma appears in Egyptian, Chinese, and Greek texts; the word is Greek for panting. Treatment was symptomatic for millennia: stramonium cigarettes (containing anticholinergic alkaloids, which genuinely dilate airways) were sold well into the twentieth century, alongside coffee, which contains a relative of theophylline.

That history contains the same lesson twice: treating the symptom without the inflammation kills people, and both death epidemics were caused by drugs that made patients feel better.

What actually goes wrong

In short: An allergen cross-links antibodies on mast cells, which degranulate within minutes, and a slower inflammatory phase follows hours later.

Type 2 inflammation, the dominant pattern, particularly in allergic asthma. An inhaled allergen (house dust mite faeces, cat dander, pollen, mould) is picked up by dendritic cells in the airway lining and presented to T helper 2 cells. Those cells release interleukin-4, 5, and 13, which drive:

• B cells to produce IgE antibodies specific to the allergen.
• IgE to coat mast cells in the airway wall.
• Eosinophils to be recruited and to survive longer in the tissue.

On re-exposure, allergen cross-links IgE on mast cells, which degranulate within minutes, releasing histamine, leukotrienes, and prostaglandins. Smooth muscle contracts, vessels leak, and mucus is secreted. That is the early phase, minutes to an hour. A late phase follows 4 to 12 hours later as eosinophils and T cells arrive and produce more persistent inflammation, which is why an attack can seem to settle and then return overnight.

Chronic remodelling. Repeated inflammation thickens the basement membrane, increases smooth muscle mass, and increases mucus gland size. Over years, this converts some of the reversible obstruction into fixed obstruction, which is the argument for treating inflammation early rather than waiting for symptoms to become frequent.

Non-type-2 asthma exists and is important because it responds poorly to steroids: neutrophilic asthma, obesity-associated asthma (where mechanical and inflammatory factors combine), and occupational asthma from irritants. Roughly half of adult asthma is not driven by type 2 inflammation.

Triggers are individual and worth identifying:

What it does to the body

In short: Well-controlled asthma produces nothing at all, and an attack escalates through warning signs of which the most dangerous are the quietest.

Between attacks, well-controlled asthma may produce no symptoms at all. Poorly controlled asthma produces nocturnal waking, exercise limitation, school and work absence, and, over years, fixed airflow loss.

An acute attack escalates predictably, and knowing the sequence matters because the late stages are the dangerous ones:

The counterintuitive signs are the important ones. A patient who stops wheezing and looks calmer may be improving, or may be moving no air. A normal blood carbon dioxide in someone who should be hyperventilating is an ominous sign, not reassurance.

Is it deadly?

Yes, and disproportionately where care is weakest.

• Over 400,000 deaths a year globally, most in low- and middle-income countries where inhaled corticosteroids are unavailable or unaffordable.
• Asthma mortality has fallen substantially in high-income countries since inhaled steroids became standard.
• The UK's National Review of Asthma Deaths (2014) examined every asthma death in a year and found potentially avoidable factors in the majority: excessive reliever prescriptions (many patients had been issued more than 12 reliever inhalers in the previous year), under-prescribed preventers, no personal asthma action plan, no follow-up after previous attacks, and under-recognition of severity by patients and clinicians.
• Prior severe attacks predict future ones. Anyone who has needed hospital admission or oral steroids should be treated as higher risk indefinitely.

Is it contagious?

No. Asthma cannot be transmitted.

The confusion arises because respiratory viruses, which are contagious, are the most common trigger of asthma attacks. Catching a cold from someone can precipitate your attack; you did not catch the asthma.

Who gets it

In short: 260 million people, with rates that rose sharply in rich countries and are now rising in urbanising poorer ones, tracking housing, pollution, and early-life exposures.

• Prevalence: roughly 260 million people. Rates rose sharply in high-income countries from the 1960s to the 1990s and have plateaued or fallen since, while rising in urbanising low- and middle-income countries.
• Age and sex: more common in boys in childhood, and more common in women after puberty. Roughly half of childhood asthma improves substantially in adolescence, though airway abnormality often persists.
• Genetics: heritable and polygenic. Family history of asthma, eczema, or hay fever raises risk. The 17q21 locus is the strongest childhood asthma association.
• The atopic march: eczema in infancy, then food allergy, then asthma and allergic rhinitis, a sequence common enough to have a name.
• Environment: air pollution (both traffic-related and household solid fuel), damp and mouldy housing, tobacco smoke including in pregnancy, obesity, and occupational exposures. Occupational asthma accounts for roughly 10 to 15 percent of adult-onset asthma and is important because removing the exposure early can cure it.
• The hygiene hypothesis in its modern form: early-life microbial exposure appears protective. Children raised on traditional farms with regular exposure to livestock and unprocessed milk have markedly lower rates of asthma and allergy, a finding replicated across several European cohorts. The mechanism appears to involve early immune education toward regulatory rather than allergic responses. This does not license avoiding vaccines or hygiene, and the specific protective exposures are still being identified.
• Inequality: asthma outcomes track deprivation strongly in most countries, through housing quality, air pollution exposure, and access to preventive care.

Treatment, and how it works

In short: Treat the inflammation continuously and relieve symptoms with something that also treats inflammation, which is why reliever-only treatment has been abandoned.

The whole logic of asthma treatment is: treat the inflammation continuously, and relieve symptoms as needed, using something that also treats inflammation.

The change that matters most. Global asthma guidance (GINA) now recommends that adults and adolescents should not be treated with a short-acting reliever alone. Instead, the reliever should be a combination of inhaled corticosteroid plus formoterol, so that every time symptoms prompt a puff, an anti-inflammatory dose is delivered along with the bronchodilation. This approach, used both as needed and as maintenance-and-reliever therapy, reduces severe attacks compared with the older strategy. It directly addresses the central failure mode: people take the drug that makes them feel better and skip the one that prevents attacks, so the fix is to put them in the same inhaler.

Severe asthma biologics, matched to phenotype by blood eosinophil count, IgE level, and FeNO:

These reduce attacks by roughly half or more in selected patients and allow many to come off oral steroids, which is their most valuable effect.

Inhaler technique is a treatment variable, not a detail. Studies consistently find that a large proportion of patients use their inhalers incorrectly, delivering little drug to the airways. Spacers substantially improve delivery from metered-dose inhalers and should be used routinely in children and commonly in adults.

Acute attack treatment: high-dose inhaled bronchodilator (via spacer or nebuliser), ipratropium, systemic corticosteroids (which take hours to work and are still given immediately), controlled oxygen, and magnesium sulphate in severe cases, with escalation to ventilation if needed. Every attack requiring oral steroids should trigger a review, because it marks someone at higher risk of the next one.

What treatment costs

In short: Inhaled steroid side effects are mostly preventable and far smaller than the risk of untreated asthma, and fear of them causes real harm.

• Inhaled corticosteroids: oral thrush and hoarse voice (both largely preventable by rinsing the mouth after use and by using a spacer), a small effect on growth velocity in children (roughly half a centimetre in the first year, without meaningful effect on final adult height), and at high doses, adrenal suppression, bone loss, cataract, and glaucoma. These risks are far smaller than the risks of untreated asthma, and worry about them is a common cause of harmful under-treatment.
• Beta agonists: tremor, palpitations, low potassium at high doses.
• Montelukast: neuropsychiatric effects including sleep disturbance, nightmares, agitation, and mood change, prompting regulatory warnings. Worth asking about specifically.
• Oral corticosteroids, if used repeatedly or long term: weight gain, diabetes, osteoporosis, cataract, thin skin, infection risk, adrenal suppression, and mood disturbance. This is the cost that biologics are designed to avoid.
• Biologics: injection site reactions, rare anaphylaxis with omalizumab, transient blood eosinophilia with dupilumab, and high cost.

What the person can do

In short: Take the preventer daily when you feel well, count your reliever use, get a written action plan, and have your inhaler technique checked.

• Take the preventer daily, including when you feel well. This is the single most important behaviour in the chapter, and the hardest to sustain precisely because it produces no sensation.
• Count your reliever use. Needing a reliever more than twice a week, or getting through more than about two or three reliever inhalers a year, means the asthma is not controlled, whatever it feels like.
• Get a written asthma action plan specifying what to do as symptoms or peak flow change and when to seek help. Having one is associated with fewer hospital admissions, and most patients do not have one.
• Learn and check your inhaler technique, and use a spacer.
• Do not smoke, and do not let anyone smoke around a person with asthma. Smoking also makes inhaled steroids less effective.
• Get the annual influenza vaccine, plus COVID-19 and pneumococcal vaccines as recommended.
• Identify and reduce your triggers: dust mite measures where allergy is confirmed, address damp and mould in housing (a landlord obligation in many jurisdictions), and manage occupational exposures. Occupational asthma should be reported and investigated early, since continued exposure makes it permanent.
• Exercise. Well-controlled asthma should not limit sport. Pre-treatment before exercise and proper preventive therapy allow it, and many elite athletes have asthma.
• Treat hay fever and reflux, both of which worsen asthma control.
• Seek urgent help if the reliever is not lasting four hours, if you cannot complete a sentence, or if peak flow falls below half your best. Do not wait to see if it settles.

Living with it

Asthma is a disease of invisible risk, which shapes its psychology. People minimise it because they feel well most of the time, and severity is systematically under-recognised by both patients and clinicians. The people who die are frequently those who had learned to live with symptoms and had stopped regarding them as abnormal.

At the same time, over-restriction is a real harm, particularly for children who are excluded from sport and activity because of asthma that could be controlled. The goal of treatment is a completely normal life, and anything less should prompt a treatment review rather than an adjustment of expectations.

What's next

• Anti-inflammatory reliever therapy becoming standard everywhere, including in the low-income settings where most asthma deaths occur.
• Biologics earlier in the disease, and the open question of whether treating severe asthma aggressively early prevents the airway remodelling that becomes irreversible.
• Better treatment for non-type-2 asthma, the phenotype current drugs serve worst.
• Access. The most consequential single fact in this chapter is that inhaled corticosteroids, which have transformed asthma mortality in rich countries, remain unaffordable or unavailable in many low-income countries. WHO added them to the Essential Medicines List for this reason, and supply remains the binding constraint.

Sources and notes

Prevalence (about 260 million in 2021) and mortality figures are from Global Burden of Disease analyses and WHO. GINA (Global Initiative for Asthma) strategy reports, 2019 onward, for the change away from SABA-only treatment and for severity and treatment step definitions. UK National Review of Asthma Deaths, Royal College of Physicians, 2014. Beta agonist death epidemics: New Zealand fenoterol studies (Crane et al., The Lancet, 1989) and the earlier 1960s isoprenaline epidemic. LABA monotherapy safety: SMART trial and subsequent FDA analyses. Farm exposure and allergy protection: PARSIFAL and GABRIELA studies, and Stein et al., NEJM, 2016 (Amish and Hutterite comparison). Inhaled corticosteroid growth effects: CAMP study long-term follow-up, NEJM, 2012. Biologic efficacy: individual trial programmes for each agent. Montelukast neuropsychiatric warning: FDA boxed warning, 2020.

Open questions. Why asthma prevalence rose so sharply in the late twentieth century and then plateaued is not fully explained. Whether early aggressive treatment prevents airway remodelling is unproven. Effective treatment for neutrophilic asthma does not exist.

Next: the airway disease that does not reverse. 👉