Allergies Explained: Causes, Testing and Treatment

An allergy is the immune system attacking something harmless. Pollen, cat dander, peanut protein and penicillin are not threats, yet in a sensitised person the body responds to them with the same machinery it would use against a parasite — and the resulting inflammation produces everything from a blocked nose to a life-threatening collapse.

Somewhere between a quarter and forty per cent of people worldwide have some allergic condition, and the figure has risen steadily for decades. This guide covers what actually happens during a reaction, which tests are worth having and which are worthless, how the treatments compare, and the areas where advice has reversed completely in recent years.

🔬 What happens during a reaction

Allergy develops in two stages, and the first is silent.

Sensitisation occurs on an early encounter with the substance. The immune system misclassifies it as a threat and produces immunoglobulin E antibodies specific to it. These antibodies attach to the surface of mast cells scattered throughout the skin, airways and gut, and to basophils in the blood. Nothing is felt at this stage. The person is now primed.

The reaction occurs on a later encounter. The allergen binds the antibodies already sitting on the mast cells, which cross-link and trigger the cell to degranulate — releasing histamine, tryptase, leukotrienes, prostaglandins and cytokines within minutes.

Those mediators produce the familiar effects directly. Histamine dilates small blood vessels and makes them leaky, producing swelling, redness and a running nose; it stimulates nerve endings, producing itch and sneezing; and it contracts smooth muscle, producing wheeze and cramping. Leukotrienes drive more sustained airway narrowing and mucus.

Several hours later, a late-phase response can follow as other immune cells arrive at the site. This is why nasal congestion often persists long after sneezing has stopped, and why treating only histamine deals with half the problem.

📈 Why allergies keep increasing

The rise is real and not simply better recognition, and no single explanation accounts for it. Several plausible contributors have emerged.

The hygiene hypothesis, now usually refined as the old friends hypothesis, holds that the developing immune system requires exposure to a diverse range of microbes to calibrate itself, and that modern environments provide too little. Evidence supporting it includes the consistently lower rates of allergy in children raised on farms with livestock, and in larger households.

The microbiome appears to matter, with early antibiotic exposure, caesarean delivery and dietary patterns all associated with allergy risk, though causation remains uncertain.

The dual-allergen exposure hypothesis proposes that sensitisation happens through inflamed skin while tolerance develops through the gut — which would explain why eczema in infancy so strongly predicts food allergy, and why early oral introduction protects.

Air pollution, dietary change, vitamin D status and reduced physical activity have all been implicated to varying degrees. The honest summary is that this is an area of active research rather than settled knowledge.

🗂️ The allergic conditions

The same underlying mechanism produces different diseases depending on where it operates, and they cluster together in the same individuals and families — a tendency called atopy.

The sequence in which they appear in childhood is consistent enough to have a name — the atopic march — typically starting with eczema and food allergy in infancy, followed by asthma and then allergic rhinitis. Recognising it matters because early management of eczema may influence what follows.

🚨 Anaphylaxis

Any discussion of allergy that omits this is incomplete, and the older article this replaces did omit it.

Anaphylaxis is a severe, rapid, systemic reaction involving more than one body system, and it can kill within minutes. It typically begins within seconds to an hour of exposure, most often to food, insect venom or medication.

🧪 Testing that works

Allergy testing exists to confirm what the history already suggests. Used that way it is valuable; used as a fishing expedition it produces misleading results, because sensitisation without clinical allergy is extremely common — a positive test in someone who eats the food without any problem means the person is sensitised, not allergic.

❌ Testing that does not work

A substantial commercial industry sells allergy tests with no diagnostic validity, and the harm is not just financial — people eliminate large numbers of foods on the basis of these results, sometimes to the point of nutritional deficiency, and children are affected most.

• IgG or IgG4 food panels — IgG to food indicates exposure and normal tolerance, not allergy. Professional allergy societies across several continents have issued statements against their use
• Hair analysis — hair contains no information about immune responses
• Applied kinesiology, in which muscle strength is tested while holding a substance
• Electrodermal and VEGA testing, measuring skin electrical resistance
• Cytotoxic and leukocyte activation tests in their commercial forms
• Iridology and pulse testing

If a test result leads to eliminating a long list of ordinary foods, that is a strong signal the test was not valid. Genuine food allergy usually involves a small number of specific foods with clear, reproducible, rapid reactions.

💊 Antihistamines

Antihistamines block the histamine receptor, which addresses itch, sneezing, running nose and hives well, and nasal blockage poorly. They divide into two generations that differ considerably in safety.

The distinction matters practically. First-generation agents cross into the brain, causing drowsiness and impairing driving and concentration — sometimes the following morning, and sometimes without the person realising. They also have anticholinergic effects that make them poorly suited to older adults. Where they retain value is in specific situations: severe itch disturbing sleep, chronic urticaria where sedation at night is useful, and non-allergy indications such as nausea.

Among the second-generation drugs, differences are modest. Cetirizine is generally the most potent and causes mild drowsiness in a minority; fexofenadine and bilastine are the least sedating and suit people who drive or operate machinery; loratadine and desloratadine sit in between. In chronic urticaria, guidelines allow the dose to be increased several-fold above the standard, which is effective and should be done under medical direction rather than independently.

👎 What actually works best for a blocked nose

This is the most useful practical point in the article, because the common assumption is wrong.

Intranasal corticosteroids — fluticasone, ciclesonide, mometasone, budesonide — are more effective than oral antihistamines for allergic rhinitis overall, and considerably more effective for congestion specifically, because they suppress the whole inflammatory process rather than blocking one mediator. They are the first-line treatment for anything beyond mild intermittent symptoms.

Two things determine whether they work:

• Regular use. Full benefit takes days to build. Used only on bad days, they underperform
• Correct technique. Aim the spray outward toward the ear on the same side, not toward the septum in the middle. Aiming at the septum causes irritation and nosebleeds and delivers the drug to the wrong place. Do not sniff hard afterwards

Available options include fluticasone and ciclesonide. Intranasal azelastine is an antihistamine spray that acts faster than a steroid spray and is useful for breakthrough symptoms or in combination.

Decongestant sprays deserve a specific warning. They work impressively for a few days, then cause rebound congestion that is worse than the original problem and drives continued use. They should not be used beyond about three to five consecutive days.

Saline rinsing is cheap, safe and genuinely helpful, clearing allergen and mucus and improving the effect of medicated sprays used afterwards.

Leukotriene receptor antagonists such as montelukast address the mediators antihistamines do not, and are used mainly where asthma and rhinitis coexist. Awareness has grown of neuropsychiatric effects including mood change, sleep disturbance and vivid dreams, particularly in children, so the benefit needs to justify the trial.

💉 Immunotherapy

Everything above controls symptoms. Immunotherapy is the only treatment that changes the underlying allergy.

It works by administering gradually increasing amounts of the allergen — by injection, or as tablets or drops under the tongue — over a period of three to five years. The immune system shifts toward tolerance, producing blocking antibodies and regulatory responses that persist after treatment ends.

It is well established for allergic rhinitis caused by pollen, house dust mite and animal dander, and it is highly effective for insect venom allergy, where it converts a potentially fatal allergy into a manageable one. In children with allergic rhinitis it may reduce the likelihood of going on to develop asthma. Oral immunotherapy for food allergy, particularly peanut, is now available in specialist centres, though it raises tolerance to accidental exposure rather than allowing free eating.

The requirements are real: a long commitment, an accurate diagnosis of which allergen matters, and administration under supervision because reactions can occur. It is not a treatment to start casually, and it is worth considering seriously for anyone whose symptoms persist despite proper medication.

🧬 Biologic treatments

For severe allergic disease not controlled by conventional therapy, antibody treatments targeting specific parts of the allergic pathway have transformed outcomes over the last fifteen years.

Omalizumab binds IgE itself and is used in severe allergic asthma and chronic urticaria. Dupilumab blocks a shared signalling pathway and is used in atopic dermatitis, asthma and nasal polyps, often with dramatic effect in people who had exhausted other options. Several others target individual cytokines in severe asthma.

They are expensive, given by injection, and restricted to specialist services with defined severity criteria. Mentioning them matters because someone whose eczema or asthma has been unmanageable for years may not know these exist.

🏠 Avoidance, honestly assessed

Avoidance is the logical first step and its effectiveness varies enormously depending on the allergen.

👶 What changed in prevention

Advice on preventing food allergy in children reversed completely, and this is worth stating clearly because the old guidance is still repeated.

For years, parents were told to delay introducing peanut, egg and other allergenic foods, on the theory that early exposure caused allergy. Rates rose anyway. A landmark trial then tested the opposite approach in high-risk infants, introducing peanut early rather than avoiding it, and found a large reduction in peanut allergy by age five.

Current guidance therefore recommends introducing allergenic foods early, from around four to six months alongside other solids, and continuing them regularly rather than sporadically. Infants with severe eczema or existing food allergy should be assessed first, but for the general population early introduction is now the recommendation.

Alongside this, treating infant eczema properly matters more than was appreciated, because sensitisation appears to occur through inflamed skin. Consistent emollient use and prompt treatment of flares is not merely about comfort.

📋 Building a plan that works

For most people with allergic disease, a workable approach has four parts.

Identify the trigger properly, using history first and testing to confirm, rather than testing broadly and reacting to whatever comes back positive.

Reduce exposure where it is practical, accepting that for pollen this achieves relatively little and medication will do the work.

Treat consistently rather than reactively. The commonest reason allergic rhinitis remains uncontrolled is intermittent use of a treatment that requires regular use. Starting a nasal steroid a couple of weeks before a known pollen season, rather than after symptoms begin, changes the whole season.

Escalate when control is inadequate. Persistent symptoms on proper treatment are a reason to review the diagnosis, add a second agent, or consider immunotherapy — not a reason to accept the situation. Poorly controlled allergic rhinitis worsens asthma, disturbs sleep and measurably affects work and school performance, and the burden is routinely underestimated by everyone involved.

Oral and intranasal treatments are stocked in the allergy category, with Zyrtec (cetirizine) among the most widely used second-generation antihistamines.

❓ Frequently asked questions

📑 Sources and editorial

• ARIA guidelines for allergic rhinitis and its impact on asthma
• EAACI and AAAAI position statements on allergy diagnostic testing, including statements against IgG food panels
• Du Toit G et al. — Learning Early About Peanut Allergy trial and subsequent guidance on early allergenic food introduction
• International consensus guidance on anaphylaxis recognition and adrenaline use
• Evidence reviews on allergen immunotherapy for rhinitis, asthma and venom allergy
• FDA prescribing information for cetirizine, fexofenadine, loratadine, azelastine and fluticasone
• Related products: allergy medications category
• RXshop Editorial Team — reviewed by Emily Chen, MD, MPH, Internal Medicine