Select Committee on Science and Technology Minutes of Evidence

Examination of Witnesses (Questions 91-99)

Professor Peter Burney, Professor Aziz Sheikh, Dr Graham Devereux and Professor John Warner


  Q91Chairman: Can I start by welcoming you here today? Thank you for coming to give evidence to us as a committee. We have a members' note of our declared interests so we will not be going round declaring our individual interests as a committee today. We will ask you questions and there may be supplementary questions to the main questions as we go through. I wonder if you would like to start by introducing yourselves.

  Professor Burney: I am Peter Burney. I am Professor of Respiratory Epidemiology and Public Health at Imperial College.

  Professor Sheikh: I am Aziz Sheikh, Professor of Primary Care Research & Development at the University of Edinburgh.

  Dr Devereux: I am Graham Devereux. I am Clinical Senior Lecturer at the University of Aberdeen, and I am a respiratory physician at Aberdeen Royal Infirmary.

  Professor Warner: I am John Warner. I am Professor of Paediatrics at Imperial College, having moved from Southampton only four months ago where I was Professor of Child Health. My special area of interest and expertise is in early life origins of allergy.

  Q92  Chairman: I wonder if I might start with a question to all of you. In written evidence we have had described the progression from eczema and food allergy in infancy to asthma in the pre-teen years as the "allergic march". I wonder if you could explain to us what are the mechanisms of the allergic march and how we can halt it.

  Professor Warner: It is a clinical observation that many infants who develop food allergy and eczema go on subsequently to have asthma and allergic rhinitis and there appears to be a progression from one disease to another which has been termed the "allergic march". Whether having eczema per se makes you more likely to go on to have asthma I think is not clear because it is more probable that there are common underlying factors that predispose you to both conditions, but for some people they only inherit and are exposed to environmental factors that predispose to one and not the other. At the moment we are still unclear about all the mechanisms that are involved in the generation of the individual diseases within that allergic march, but one thing we can say for certain is that if an infant starts with evidence of allergy there is a very high probability that they are going to show one or more problem associated with that.

  Q93  Chairman: You suggested in your answer that there are certain unknowns about the origin and progression of allergic disease. I wonder if you could highlight where you feel the main unknowns are and how we could find out about them.

  Professor Warner: I think we have got a long way in identifying the genetic components. What we do not know is how genetic factors interact with environmental factors in individuals, to lead to disease, so it is focusing on how the geno-type is influenced by the environment to create the clinical manifestations.

  Q94  Chairman: Do people suffering from allergic disease ever lose their sensitisation?

  Professor Burney: Not once people have become adult. People tend to accumulate their sensitisation during childhood and early life. One of the things that is noted in cross-sectional surveys is that older people have less allergy, but the important thing is that if you follow the same people as they get older they do not generally lose their allergies. The explanation for the lower prevalence of allergies in older people is that people who were born towards the beginning of the 20th century tended to get less allergy during their early years, so they are people who never became very allergic rather than people who have lost their allergies. The importance of this is that it helps us to predict what will happen to the allergic epidemic that we have at the moment and how soon it will start to subside.

  Q95  Lord Taverne: Just following that up, you mention in your paper that 80 per cent of asthmatics tend to lose their allergy during puberty and then start recovering some of it again. Have you any idea why that might be?

  Professor Burney: I do not think that I said that. That might be from someone else's paper. Maybe.

  Professor Warner: Perhaps I can add a bit to that. There are infants who show various food allergies who lose their allergies once they get to four, five, six years of age. However, once they have reached about seven to eight years of age, if they retained the allergies then in general they persist for evermore and they might actually increase the range of allergies. However, even amongst those who lose sensitivity, say, to egg or to milk, which is very common in infancy and less common in older children, they are still at higher risk of developing new allergies to inhalants like house mites and pollens. As far as adolescence is concerned, yes, there is no doubt that particularly boys tend to improve their asthma and many of them lose their symptoms, although the majority, if you do sophisticated lung function tests, still show an abnormality and many of those come back in their late twenties with a recurrence of problems. We think part of that is physiological in that the lungs are at their best in early adulthood and, as they begin to lose some of their elastic recoil with age the problem shows itself again.

  Q96  Lord Taverne: The suggestion seems to be that there is still a net decrease after puberty. Only some then develop the allergies again. Is that right?

  Professor Warner: It is always very difficult. The problem is that paediatricians lose sight of their patients. I think it has been said that they are more likely to outgrow their paediatricians than their asthma. From the longitudinal studies a pretty high per centage, even of milder asthmatics who lose their symptoms in adolescence, by 30 have had a recurrence of symptoms, not necessarily as severe as they were in childhood but certainly they are wheezing again and they are requiring some treatment for their asthma.

  Q97  Chairman: Are there any specific measures you feel should be recommended routinely for children to prevent the development of asthma and eczema?

  Professor Warner: I would love to be able to say that there were measures right now that one could recommend but there is none other than saying, "Do not smoke in pregnancy", and, well, "Do not ever smoke", not only because of the adverse effect it has on the child's health but also because of the bad example it sets for the children who then take up smoking themselves, which in turn increases the risk of relapse of asthma if it has improved. Other reasonable recommendations are "Sustain a good diet", and, "Breast feed if at all possible". I think beyond that at the moment we do not have enough evidence to make any other statements.

  Q98  Lord May of Oxford: Can I ask a question in this context for which one of the data points is myself? When I was 12 I missed half the school year with asthma and since the age of 18 I have essentially never had it, and I know other people like that, so may it not be that the word "asthma" embraces quite a wide range of things? It is not something like measles. There will be some that are allergy based and some that have other bases, so it is difficult to make generalisations. Is that true?

  Professor Burney: I would agree with that. One of the confusing issues, particularly in childhood, is that there are a lot of other conditions that are probably not allergic which make people wheeze. The view generally is that these are very common in infancy and in very young children, but I suspect that they actually continue for a bit longer than that so that throughout childhood you have probably got a mixture of people with other conditions, just as in older life you get people who get rather different wheezy conditions which can be confused with asthma, so I think your distinction between those that have an allergic basis and those that do not may well be a good distinction. One other thing which I think is sometimes missed, at least in relation to more severe disease, is that asthma gets worse among women during the child-bearing years so that from puberty up to the menopause women probably have a worse deal during that time of their life than at other times of their life.

  Professor Sheikh: As the Committee may be aware, The Lancet recently published a very provocative editorial saying that the term "asthma" has outlived its usefulness; it is far too crude a term, so I think in due course we will have a more refined understanding and a more refined range of terminology because it is very much a catch-all at the moment. In relation to primary prevention strategies, which you were asking about, to try and stop the initiation or halt the progression of the allergic march, as Professor Warner has said, the key recommendations that we would suggest are suitable at a population level,—that is, taking all-comers,—are minimising exposure to tobacco smoke and breast feeding wherever possible. However, we do have some clearly high risk families and in these families there are some interventions which appear to be promising. One in mothers who are unable to breast feed, for whatever reason, is the use of hydrolysed formula milk preparation. What is happening there is that the cows' milk protein is being broken down. There is evidence now from a few randomised control trials to show that this can halt the progression of allergic problems and the other area that seems quite interesting and promising is looking at the role of pro-biotics. This involves giving particular forms of lactobacillus and bacteria in early life, perhaps in combination with other approaches, and again there is early evidence that these may be promising interventions, but overall as we are advocating intervening in healthy individuals at the moment before they have developed any disease in early life the burden of evidence for intervening is very high if we are advocating primary prevention strategies. What underlies this is that we are at the early stages in terms of our understanding of which interventions work and there needs to be far more work done in building on those early trials.

  Professor Warner: This is a very difficult area. Recently there has been a meta-analysis of all studies of using hydrolysed milk formulae in allergy prevention and, whilst there are clearly some trials which have shown an impact, at the moment the conclusion is that more work is required. It is a promising area, but before making recommendations in particular groups there is a lot more research to do; likewise with pro-biotics but now the more exciting area looks to be pre-biotics, that is, just creating the right environment in the gut for organisms to grow normally, and there are one or two trials in process at the moment and one has just been published with what looks like very good results.

  Q99  Lord Colwyn: You covered the point about smoking and breast feeding. I pulled something out of The Telegraph a month ago saying that there is evidence that maternal diet and maternal exercise are important in the development of the child's in uterus lungs. Is that correct? Are you aware of that?

  Professor Warner: Yes. Dr Devereux has done a lot of work in that area as well, but that is nutrition rather than trying to avoid food allergens. There are lots of nutrients that may be important. Dissecting out which are important is what is difficult, but Dr Devereux can answer that question better.

  Dr Devereux: The work we have been doing in collaboration with people in America is that it looks quite promising that maternal diet during pregnancy is influencing the development of asthma in children. I am not talking about maternal ingestion of allergens; I am talking about maternal ingestion of nutrients, particularly vitamin E, possibly vitamin D and even zinc. There are now two studies showing associations that low maternal intake of vitamin E during pregnancy is associated with the increased risk of children having wheeze, asthma, reduced lung function and increased markers of lung inflammation. The $64,000 question is what happens if you intervene to change women's diet in pregnancy, and that is a study that needs to be done.

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