You might have thought that health specialists would closely monitor the prevalence of allergies in the population, especially when they are far more common than they used to be. In fact, it happens less than you would think. For asthma, for example, the government publishes statistics on the numbers of people that are admitted to hospital or die from the condition, but it does not publish a running total of how many people are affected overall.
The University of Aberdeen is one of very places that does regularly publish data on childhood asthma, eczema and hay fever, going back as far as 1964. Though we only survey what is happening in the city, the figures are closely watched because they have a very good record of predicting the incidence of these allergies across the rest of western Europe.
When we published our five-yearly report on July 29, it showed that childhood prevalence of asthma had fallen by a third to around 20% following a long rise over decades. Reasons are likely to include improved air quality, reduced smoking, changing diets and improved diagnosis.
The figures showed something else very interesting too. Since our study began, in line with most other research into the prevalence of allergies, rises and falls in the rate of asthma have been broadly followed by those for eczema and hay fever. Not on this occasion, though. The latter two complaints stayed around their previous levels as asthma rates fell on their own.
The allergy debate
Specialists have for many years debated the nature of allergy. We know that allergies are associated with the immune system producing an antibody called immunoglobin E (IgE), which binds itself to common things in our environment such as grass pollen and house dust mites when they come in contact with the body. The classic view was that allergic people overproduced this antibody, which in turn produced substances that caused the inflammation and irritation in complaints such as asthma or eczema. In short, asthma, eczema and hay fever were thought to be caused by being allergic.
There’s a flaw in this argument, though. If an organism is going to become allergic to something outside it, it must be exposed through a crack in the skin. For this reason, some specialists began arguing from the early 1990s that you became allergic to something because there was a problem with, in the case of asthma, the cells lining the lungs. In this scenario the primary “abnormality” is in these lung cells, which leads to asthma and also does not provide an effective barrier against environmental exposures. The immune system is fundamentally normal and is just doing what it is meant to do and responding to exposures which “leak” through into the body. The immune response then adds to the problem caused by the lung-cell abnormality.
Public opinion can be hard to change (and medical opinion harder still) but we are now at a point where most medical people would accept that it is not the allergy that causes asthma – though some certainly still believe it. What we don’t have yet is proof, though we will hopefully produce some over the next few years at this university and with colleagues across the UK through our studies into the lung cells of small children.
In the meantime, this is where the divergence in our stats comes in. If being allergic caused allergies, you would expect the rates of asthma, hay fever and eczema across the population to roughly move in unison. In other words, for many years our stats and those from other sources supported the old theory.
At the same time, though, supporters of that theory had to contend with the fact that having one of these allergies has never meant you would have all of them – a correlation you would also expect if the theory were true. In our most recent figures, for instance, only 55% of children with asthma had hay fever, and only 64% of them had eczema. This weakish correlation has always supported the newer theory – and the divergence now backs this up. It adds to the probability that we misunderstood the nature of allergy for a long time. It does leave the mystery of why the allergy rates moved in unison for so long, but that is a matter for another day.
This doesn’t have a huge bearing on our ability to treat asthma. It is more about knowing that we understand a process correctly and this is important to preventing asthma. In terms of treatment, the general view is that asthma can’t be cured. But there is mounting evidence that it can be prevented by exposing babies who are genetically predisposed to the condition to the right environment while they are in the womb and then for the first couple of years of their life. What we still don’t know is what the right environment is, but modifying exposures to cats, dogs, mould, smoking, breastfeeding and weaning diet are likely to be important.
I can see us reaching a point in ten or 15 years where pregnant mothers with at-risk unborn children will be offered a course of “environmental modification” treatment, possibly as simple as a pill. Ensuring that the immune system of children at increased risk for asthma is flooded by exposed to allergens at a sufficiently early stage will switch off any later IgE production. Although they may still have the lung-cell abnormality, at least they don’t get the added hit of an allergic immune system. In this sense at least, a cure for asthma may not be far away.