Examination of Witnesses (Questions 433-439)
MS MANDY
EAST, PROFESSOR
GIDEON LACK,
DR RICHARD
PUMPHREY AND
MRS HAZEL
GOWLAND
31 JANUARY 2007
Q433Chairman: Can I welcome you all here today
and thank you for coming. The individual members of the Committee
will not be declaring their interests as we go round because that
has all been noted in a separate document. I wonder if I could
start off by asking you to introduce yourselves and then we will
go into questions.
Mrs Gowland: I am Hazel Gowland. The reason
why I am here primarily is because I have a severe, potentially
life-threatening allergy to nuts and peanuts. I have a number
of hats. You have called me today as Allergy Action. Allergy Action
is basically me; I am self-employed. I have a sole trader business
but I also work for the Anaphylaxis Campaign. As Ian mentioned
I am the person who has been delivering all this training. I have
a number of roles to play. I give free information to anybody
who is allergic who ever asks me for help. I have a formal role
as the food adviser for the Anaphylaxis Campaign which is varied.
It has involved liaising with Sue and the FSA team on all the
policy documents and these pieces of guidance and so on. I also
work with Dr Pumphrey on analysis of where people get caught out
with allergic reactions so I have a research role from the practical,
human point of view. I am delivering the training for the Food
Standards Agency and for the project in Northern Ireland and across
the border for the environmental health officers. Independently
I also made a training DVD which I think I sent you. I do not
know whether you have seen it, but it is an accessible training
pack for caterers. I train caterers and other food handlers including
schools, nurseries, childcare, chefs, et cetera who call me on
a commercial basis.
Q434 Chairman: Thank you. Dr Pumphrey?
Dr Pumphrey: I am Richard Pumphrey. I have many
years' experience in allergy clinics and in running a Health Service
laboratory that undertakes allergy investigation of patients.
My particular expertise here is that I have made a special study
of everyone in the country who has died from an acute allergic
reaction to food and that has produced a lot of new insights into
what the problems are.
Professor Lack: I am Gideon Lack. I am a consultant
in paediatric allergy. I work at King's College London and St
Thomas' Hospital. I have been practising paediatric allergy for
the past 15 years; my particular area of interest is systemic
allergic disease or complex allergic disease in young children.
I am mainly interested in the rise in food allergies and what
may be the causes behind them and how to prevent them, particularly
the relationship between early diet in the first year of life
and subsequent development of allergies. My other particular area
of interest is severe or difficult asthma in childhood and the
role of allergies in contributing towards this.
Ms East: My name is Mandy East. I am the national
co-ordinator for the Anaphylaxis Campaign which is a national
support organisation for those living with the most severe of
allergies that could lead to anaphylaxis. I also represent the
Anaphylaxis Campaign to the National Allergy Strategy Group which
is the coming together of many patient support groups and medical
professionals set up to improve allergy services.
Q435 Chairman: Thank you. I think
it would be helpful if I could ask you to start off by explaining
to us the difference between food allergy, food intolerance and
food anaphylaxis. Dr Pumphrey, would you like to start?
Dr Pumphrey: People can obviously react adversely
to food in a number of different ways. At one end you have toxic
reactions where nearly everybody would react to that food with
an adverse response. Then there are different types of hypersensitivity
reaction where most people can tolerate the food but for particular
individuals that food will cause a problem. Those are now divided
into those who have an allergic basis (that means anything that
is immunological) and those which are due to other mechanisms.
So you have non-allergic hypersensitivity or you have allergic
hypersensitivity. Allergic hypersensitivity is now also divided
into that which is IgE-mediated and that which is not (IgE is
the allergic kind of antibodies that we can measure in a laboratory,
which you get measured if you have an allergy test for example).
Those are the principal different types of adverse response that
you can have to a food.
Q436 Chairman: Could I just ask you,
is so-called oral allergy syndrome a true allergy?
Dr Pumphrey: Yes. Oral allergy syndrome is generally
caused by an IgE-mediated response. The allergic antibodies are
key to the oral allergy syndrome. The reason it is only oral allergy
is that the things you are allergic to in the food are very labile,
they are destroyed by acid in the stomach and so the allergy does
not spread beyond the mouth. It also needs to be something that
is absorbed through the membranes in the mouth to cause a local
response there.
Q437 Lord Taverne: Could you remind
me about the non-IgE allergic response basis for that?
Dr Pumphrey: An allergic but non-IgE response
typically would be something like gluten sensitivity where there
is an immunological process underlying this in that you have IgA
antibodies against one of the components of the food but also
you have auto-immune response involvement as well and the lymphocytes
are involved in the response, so you get a local destructive response
in the lining of the gut, for example, as a result of eating food
that contains gluten. That has an immunological basis to it but
it is not IgE-mediated.
Professor Lack: Dr Pumphrey made some very important
distinctions and in clinical practice we see these different sorts
of reactions being manifested to the same foods. Part of the confusion
can be in disentangling these diagnoses, sometimes they may even
co-exist. To give an example, I may see a six-month old baby who
comes in with eczema who has tasted milk formula for the first
time. The face immediately swells up, there is vomiting, there
are breathing difficulties; that is an immunological reaction;
therefore it is an allergic reaction. It is quick on-set; it is
IgE mediated and you can test for this easily. In contrast a different
child could come in at six months of age with severe eczema, diarrhoea,
poor weight gain and has delayed on-set reaction to milk. Very
often this child will have inflammation in the gut; there are
T lymphocytes in the gut that are responsible for this. While
this is also an immunological response to a food and therefore
represents an allergic reaction, it is a delayed non-IgE mediated
type of reaction. We are discovering a lot more about these delayed
onset allergic diseases in children and in adults. The third type
of clinical presentation to cow's milk would be a child who has
been drinking milk, who has had gastroenteritis, often due to
a viral infection, and then the gut stops producing the enzyme
lactase. This child has a metabolic deficiency—has a deficiency
in the enzyme lactase—and therefore cannot break down lactose
(which is the sugar present in milk) and consequently has diarrhoea
and other symptoms. This is not immunologically-mediated, and
therefore is not an allergic reaction. It is often short-lived,
but in some people who are genetically pre-disposed it may continue
into adulthood. The same child may manifest all three types of
allergies to cow's milk at different times in childhood.
Q438 Lord Colwyn: This is a question
I should know the answer to, but when does a severe food allergy
become anaphylaxis? I was under the impression that anaphylaxis
was when respiration becomes impossible and the patient could
die without medical intervention.
Professor Lack: The term anaphylaxis is used
to a certain extent differently by different people and in some
ways is viewed differently by our North American colleagues. Everyone
is in agreement that a life-threatening food allergy represents
anaphylaxis; so one that causes compromise of the respiratory
system or compromise of the cardiovascular system (drop in blood
pressure); is considered life threatening and therefore anaphylaxis.
Some people also call a systemic allergic reaction—one which
manifests all over the body or on different parts of the body—anaphylaxis.
In children who have a food allergic reaction of the rapid onset
IgE type (the face swelling, for example), some 30 to 40 per cent
of children at some point in their lives will have respiratory
compromise as a result of these reactions and will need to seek
medical assistance or need to use an asthma pump because of difficulty
breathing.
Q439 Lord Rea: From what has just
been said it is not surprising that the Institute of Food Research
has said that estimates of the number of people suffering from
food allergy are imprecise. Our attention was drawn to the BMJ
article of 2 September where experts Professor Colver and Professor
Hourihane give different estimates of the prevalence. How could
studies be improved to more effectively monitor the prevalence
of food allergy, intolerance and anaphylaxis?
Dr Pumphrey: The key problem here is the distribution
of severity. You have a lot of people who have a very mild allergy
and a few people who have very severe allergies. It is a continuous
distribution so you have to make a choice as to where to put the
cut-off point and a small change in your criteria could produce
a 30-fold change in the numbers of people you are counting. I
do not think that technically you are ever going to come up with
an accurate, precise figure. You can say that three per cent of
the population have food allergies providing you define what you
mean by it. Or you could say that one per cent of the population
have food anaphylaxis and you might get agreement with people.
You can quite accurately say that only five to 15 people each
year die from food allergies; you do have a cut-off there.
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