Allergy prevention – reality or not?

Abstract

While the epidemic of respiratory allergy (asthma and rhinitis) which began 50–60 years ago has begun to taper off in some parts of the world, most notably in affluent countries, a second wave involving food allergy and atopic dermatitis is in full swing. Once established allergic diseases, while episodic with changing manifestations over time, last for decades and are often lifelong. The number of lives affected and the quality of life implications mandates investigation of interventions to mitigate these conditions which together constitute the commonest long-term disorders to affect young people. The health economic burden of allergic diseases is considerable and as new biological therapies are approved this will only increase. The search for a cure has hitherto been fruitless but there is the hope that by understanding basic mechanisms it will eventually be possible to design targeted biological therapies to switch off the allergic process. However, this is an expensive enterprise and the costs of curative treatment may well be prohibitive. Prevention has become a focus for many long-term conditions and allergic disease must be included given the potential that strategies will confer considerable health/economic benefits. Health promotion which emphasises avoidance of environmental tobacco smoke, alcohol, pollution and obesity with promotion of exercise, and a nutritious diet has implications for allergic disease as well as the usual focus on cardio-vascular disease, cancer and metabolic syndrome. There are four potential ‘windows of opportunity’ in early life which impact on the genetic potential to develop allergy in young children. They are in line with the developmental origins of health and disease hypothesis often now known as the first 1 000 days from conception to the second birthday. Published studies of factors influencing the ontogeny and prevention of allergy have shown very different outcomes which makes careful attention to design and methodology critical. Most publications conflate diverse phenotypes each of which are associated with different gene/environment interactions. Allergic sensitisation must be considered separately from allergic disease. Atopic dermatitis/eczema, asthma, rhinitis, food, drug and insect venom allergy all have separate genetic and environmental influences. Many studies are underpowered to account for all the likely confounding factors. Some focus only on so-called ‘high-risk families’ with parental allergic disease, whereas others study whole populations. Notwithstanding these concerns, it is our firm belief that by combining interventions we should be able to offer a basket of ‘allergy-prevention’ strategies both for high-risk families and whole populations. The interventions will confer benefits for many long-term conditions.