In Part 1 of this series we looked at the evidence for whether food allergy is genuinely on the rise. The answer was yes, with real caveats about the exact numbers. In this post, we look at why. What has changed in the modern environment to make food allergy more common? And if you are living with a food allergy, what does this tell you about the condition you are managing?
The answer comes down to how your immune system learned during early life — and what happens when that learning is disrupted.
Your immune system needed to be taught
Your immune system was not born knowing what to attack and what to leave alone. It had to learn. In your first months and years of life, it was exposed to bacteria, food proteins, pollen, and countless other things from the environment. Each exposure was a lesson. The immune system used these lessons to calibrate itself — to build up a picture of what was a genuine threat and what was safe to ignore.
When that early environment is rich and varied, the immune system tends to calibrate well. When it is more limited — fewer bacteria, less environmental diversity — the calibration can go wrong. One result of poor calibration is an immune system that treats harmless things as threats: pollen, animal hair, food proteins. This is the central idea behind what scientists call the hygiene hypothesis [1].
The name is misleading. It sounds like it means dirty conditions protect against allergy. That is not quite right. The more accurate version is this: diverse early-life exposure to environmental microbes — bacteria, fungi, and other tiny organisms in our surroundings — appears to train the immune system's regulatory circuits, the parts that keep responses measured and proportionate. Without enough of that diversity, those circuits may not develop as well [1,2].
What the evidence shows
The hygiene hypothesis has been debated and refined over decades, and the science is genuinely complicated. A 2023 study by researchers at the Karolinska Institute Institutet in Sweden raised laboratory mice in conditions designed to mimic a natural, microbe-rich environment from birth — and found they still developed allergic responses about as strongly as mice raised in clean conditions [3]. That finding challenged the simple version of the hypothesis and showed the relationship between microbial exposure and allergy is more nuanced than it first appeared.
What the evidence does consistently support is a more specific pattern: certain types of early-life exposure — particularly to diverse gut bacteria in the first year of life — appear to reduce the risk of developing allergic disease. It is not about being generally exposed to more germs. It is about whether the gut microbiome — the community of bacteria in your digestive system — developed with enough diversity during a critical early window [1,2].
Several things that are common in modern life appear to reduce that diversity. Birth by caesarean section means a newborn does not pass through the birth canal, one of the main ways babies first acquire gut bacteria. Early or frequent antibiotics disrupt the developing microbiome at the moment it matters most. Living in urban environments reduces exposure to the range of microbes found in more natural settings. None of these factors alone explains the rise in food allergy, and the science is honest about the fact that the full picture is not yet clear [2,4].
The peanut story — and what it changed
The clearest piece of evidence about how early immune learning shapes food allergy comes from a trial that overturned decades of medical advice.
For many years, doctors told parents of high-risk babies — those with severe eczema or egg allergy — to avoid giving them peanut products. The reasoning seemed sensible: if peanut can cause a severe allergy, avoid it early to reduce the risk.
That advice was wrong.
The LEAP trial (Learning Early About Peanut) tested this directly. It enrolled 640 high-risk infants aged four to eleven months and split them into two groups. One group ate peanut products regularly until age five. The other avoided peanut entirely. At age five, 17% of the avoidance group had developed peanut allergy. Only 3% of the consumption group had. Early, regular peanut consumption cut peanut allergy by 80% in high-risk infants [5].
A follow-up confirmed the protection lasted even after a year of stopping peanut consumption [6]. And a 2024 study following the original LEAP participants into adolescence found the protection still held — peanut allergy in 4.4% of the early-consumption group versus 15.4% in the avoidance group [7].
The mechanism is called oral tolerance, which we cover in detail in Part 4. When a young infant's immune system encounters a food protein through the gut, in the right conditions, it learns to treat that protein as safe. Avoidance denied the immune system that lesson. The peanuts were not the problem. The absence of peanuts during the critical early window was.
What this means for your condition
These findings are directly relevant to you if you are a young adult living with a food allergy.
A generation of infants was raised under advice to avoid peanut and other allergenic foods. Many of those children are now adults in their twenties and thirties. Some developed allergies that the science now suggests may have been preventable. If you are one of them, that is not your fault. It is the result of medical guidance that was later shown to be wrong.
Current clinical advice has reversed completely. Organisations now recommend introducing allergenic foods early for most infants, including those at moderate risk [4]. The next generation may see different rates. But you carry the condition now, and understanding where it came from does not make it go away — it does, however, help you make sense of it.
The UK FSA estimates that around 6% of UK adults have a clinically confirmed food allergy [8]. That number reflects the current reality. It is not going to shrink quickly. Your need for clear, written, specific allergen information when you eat out is not a passing trend. It is a long-term fact of life — and understanding the biology behind it is one more tool you have for managing your condition well.
Coming in Part 3: coeliac disease — the autoimmune condition that could explain your symptoms, what it actually does to your body, and why it needs a different approach from other gluten-related conditions.
References
Kelly MS, Bunyavanich S, Phipatanakul W, Lai PS. The environmental microbiome, allergic disease and asthma. J Allergy Clin Immunol Pract. 2022;10(9):2206–2217. DOI: 10.1016/j.jaip.2022.06.006
Augustine T, Kumar M, Al Khodor S, van Panhuys N. Microbial dysbiosis tunes the immune response towards allergic disease outcomes. Clin Rev Allergy Immunol. 2023;65(1):43–71. DOI: 10.1007/s12016-022-08939-9
Ma J, Urgard E, Runge S, Classon CH, Mathä L, Stark JM, et al. Laboratory mice with a wild microbiota generate strong allergic immune responses. Sci Immunol. 2023;8(87):eadf7702. DOI: 10.1126/sciimmunol.adf7702
Chan Ng PP, Tham EH, Lee BW. Primary prevention of allergy — is it feasible? Allergy Asthma Immunol Res. 2023;15(4):419–436. DOI: 10.4168/aair.2023.15.4.419
Du Toit G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803–813. DOI: 10.1056/NEJMoa1414850
Du Toit G, Sayre PH, Roberts G, Sever ML, Lawson K, Bahnson HT, et al. Effect of avoidance on peanut allergy after early peanut consumption. N Engl J Med. 2016;374(15):1435–1443. DOI: 10.1056/NEJMoa1514209
Du Toit G, Huffaker MF, Radulovic S, et al. Follow-up to adolescence after early peanut introduction for allergy prevention. NEJM Evid. 2024;3(6):EVIDoa2300311. DOI: 10.1056/EVIDoa2300311
University of Manchester, Manchester University NHS Foundation Trust, University of Southampton, Amsterdam University Medical Centre, Isle of Wight NHS Trust. Patterns and Prevalence of Adult Food Allergy (PAFA). London: UK Food Standards Agency; 2024. DOI: 10.46756/sci.fsa.ehu454
