Memorandum by the Institute of Food Research
(IFR)
The Institute of Food Research (IFR) is an independent
research organisation, with charitable status, sponsored by the
Biotechnology and Biological Sciences Research Council (BBSRC).
IFR's mission is to undertake international-quality scientific
research relevant to food and human health, and to work in partnership
with others to provide underpinning science for consumers, policy
makers, the food industry and academia. IFR has two research programmes
relating to the subject of this inquiry, and this response was
written by Dr Clare Mills who is the Programme Leader on one of
these. IFR welcomes the opportunity to respond to this Inquiry.
Reference is made in the text to EuroPrevall.
This is a European-funded Framework 6 Intellectual Property project
which is aiming to define the prevalence and cost and basis of
food allergy across Europe.
DEFINING THE
PROBLEM
1. Allergies are a disease state which results
from malfunctioning of the immune system. They can involve either
cellular of humoral (antibody) based reactions. With regards to
food allergies, the European Academy of Allergy and Clinical Immunology[1]
classifies them in the context of many adverse reactions to foods,
including IgE-mediated allergies (sometimes also referred to as
type-I hypersensitivity reactions) and non-IgE mediated allergies.
Coeliac disease is the best characterised on the non-IgE mediated
allergies; there may be others which have not been clearly defined
involving the humoral and/or cellular immune system. In the EAACI
classification immune-mediated allergies are distinguished from
non-immune mediated food intolerances which include lactose intolerance
and other undefined but reproducible reactions to foods. The evidence
given below is focussed on food allergies rather than respiratory
or other types of allergies, although the diseases are often connected.
2. IgE-mediated food allergies, like other
allergies, involve a sensitisation phase, where an IgE response
is generated towards an environmental agent (pollen, dust, food)
in a susceptible individual. Predisposition towards developing
IgE is associated with a polarisation of T-cell responses towards
a Th-2 phenotype. However, the mechanism whereby one individual,
and not another, begins to develop IgE towards an agent is not
clearly understood. It may be that during early life the immune
system is plastic and that interaction with microbes and infections
may play a role in avoiding the development of an atopic phenotype.
Much of the ideas surrounding this are presented in the "Hygiene
Hypothesis".[2]
There is also an emerging issue with regards to nutritional status
and development of allergy. The development of the allergic phenotype
has a clear genetic element and efforts are underway to identify
genetic markers related to development of allergy although this
is very much in its infancy with regards food allergy.
3. Following sensitisation of an individual
an allergic reaction may be elicited on subsequent exposure to
an allergenic agent. The mechanisms whereby this occurs are generally
well understood. However, the mechanisms underlying interactions
with other factors, such as those in exercise-induced anaphylaxis
(a symptom which can be associated with food allergies) are less
clear. In addition the food allergies of some individuals (especially
young infants) resolve whilst for others there can be a rapid
progression from mild to severe reactions. The mechanisms underlying
the evolution of allergies responses in this way is not understood
and is hard to predict, presenting a problem regarding management
of food allergies for the individuals concerned.
Why is the incidence of allergy and allergic diseases
rising? Why does the UK in particular have such high prevalence
of allergy?
4. Estimates of the prevalence of food allergy
are generally imprecise. Many studies have not used unselected
populations and none have employed the "gold standard"
for diagnosis of food allergy, double blind placebo controlled
food challenge (DBPCFC)[3]
as there are many shortcomings with current serological approaches
to diagnosing food allergies.[4]
Such a diagnosis is necessary since serological analysis for food-specific
IgE is not an effective predictor of actual food allergy—many
have food specific IgE in their blood without suffering any allergic
reactions associated with consumption of a particular food. Best
estimates of reactions are 5-7 per cent of infants and 1-2 per
cent of adults. There has been no study to determine effectively
the overall rate of food allergy outside the UK. In the UK the
most effective study has been undertaken for peanut in the Isle
of Wight, which was undertaken at two time points several years
apart for one food (peanut) in young children. It showed an increase
in the sensitisation to peanuts, although there was insufficient
statistical power to determine changes in the prevalence of DBPCFC
symptoms. It has been generally assumed that food allergies are
following other types of allergic disease (the "atopic march")
but studies (EuroPrevall) have only just begun to define the incidence
of food allergy in several countries, including the UK. It may
be that exposure to environmental factors (eg indoor environments
affecting exposure to dust mite allergens, tree and crop pollens,
and pollution) together with infections in early life all play
a role in the apparent increases in allergic disease in general.
However, a cohesive explanation is currently lacking due to our
not having an adequate mechanistic explanation as to why some
individuals, and not others, develop allergies.
What gaps exist in establishing the overall disease
burden for all types of allergy and what are the barriers to filling
these gaps?
5. Lack of funding for epidemiology studies
of sufficient size to define the incidence of food allergies and
linking them with other types of allergic disease means we are
missing vital objective information on the size of the food allergy
problem. Research to provide this information needs to be undertaken
in young children, school-age children and adults and backed up
with effective objective diagnosis of allergy with DBPCFC for
food allergies.
6. There are no data on the socioeconomic
impact of food allergies as the instruments are only just being
developed to do this (see above). All that is available is anecdotal
information.[5]
There have been no instruments for assessing the economic impact
of food allergies. These are being developed in EuroPrevall but
will not be applied in the UK. In order to ascertain the burden
of allergic disease the population studies need to be linked to
the socioeconomic instruments developed for measuring the disease
burden which are available for allergic asthma and other allergies,
and now becoming available for food allergies.
TREATMENT AND
MANAGEMENT
7. Treatments for inhalant allergies include
immunotherapy which is much more widely used in mainland Europe
than the UK. This involves administering increasing doses of an
allergen and requires considerable commitment from the patient
to receive the treatment on a weekly to monthly basis with repeat
visits to the clinic. In some instances immunotherapy for inhalant
allergies associated with food allergies may affect the latter.
8. There are currently no effective treatments
for food allergies. Patients with severe symptoms are given emergency
medication (adrenaline) and told to avoid problem foods. There
may not be adequate resources in hospitals to allow re-testing
of individuals to assess if the allergy has resolved, which is
especially relevant in children. Without this becoming more routine
it is likely that individuals are living with mitigation strategies
which are no longer necessary, with all the socioeconomic burden
that carries to practice food avoidance.
9. There are potential avenues of research
ongoing which may lead to development of effective preventive
measures. Since funding is limited their development is slow.
The application of recombinant immunotherapy using proteins resembling
allergenic molecules, but with the major IgE-epitopes to de-sensitise
individuals, is showing promise for food allergy, including putting
in novel delivery vehicles including bacteria. These may, for
those individuals with severe reactions, need to be coupled with
anti-IgE therapy to avoid adverse reactions to the immunotherapy.
There are also potential therapies emerging using parasites, since
individuals with parasitic infections do not appear to manifest
allergic reactions. Probiotic and prebiotic approaches may act
as a preventive by helping to establish a gut micflora that promotes
a non-allergic phenotype. These require more effective intervention
studies which also take account of the timing of the intervention.
For example, is it only effective if given in the first months
of life when the gut microflora becomes established?
Is the level of UK research into allergy and allergic
disease adequate?
10. With regards to food allergy research,
the majority of the UK research portfolio is funded by the UK
FSA in support of food allergen management. However, FSA does
not fund the fundamental mechanistic studies that will be required
to develop more effective diagnostics, therapies and preventive
strategies. There is no clear avenue to allow funding of multidisciplinary
research regarding the socioeconomic burden of food allergy and
to join it up to population studies with individuals with clearly
defined food allergies.
GOVERNMENT POLICIES
11. The information and advice given by
governments in general can be confusing and conflicting. This
reflects the fact that scientific opinion is not clear and the
fact that the research and knowledge that is required to form
opinion is currently lacking in two areas: defining the size of
the allergy problem (from the number of people with allergies
to the cost and burden to society of this disease) and the mechanisms
underlying what makes some people become allergic and what makes
some substances more allergenic than others.
How effectively are food policy and food labelling
regulations responding to the rise in food allergies?
12. The lack of knowledge about food allergies
is resulting in policies being implemented which aim to protect
the consumer which have not been thought through and are not founded
in fact but on assumption. For example, soya has to be labelled
as a food allergen and yet studies on soya allergy are difficult
to undertake because of a lack of patients that can be recruited
with a defined soya allergy. There is a need also to address how
information about food allergies is conveyed to consumers—this
has yet to be done. There is a real danger that consumers are
being deluged with information but that this is not provided in
a targeted and useful way.[6]
Providing information is not communication. There is a clear need
to target information to particular at-risk groups such as young
men, who are at greater risk of not managing their food allergies
adequately resulting in severe or even fatal reactions. This reflects
the risky behaviours this age group may adopt with regard to other
health problems. Food allergic teenagers may not carry their adrenaline
and read labels in the same way that teenage diabetics do not
manage their blood sugar levels. With regard to the industry,
allergic consumers are at greatest risk from suffering an allergic
reaction whilst eating in a restaurant. These risks would be reduced
if there was more support for the development of the tools and
materials necessary to promote adequate training on food allergen
management in the catering sector.
13. We are not in a position to comment
on the two questions posed below.
Are current regulatory arrangements, for example,
those governing private clinics offering diagnostic and therapeutic
services and the sale of over the counter allergy tests, satisfactory?
Do housing policy and regulations governing the
indoor environment pay enough attention to allergy?
6 October 2006
1 EAACI; Johansson SG, Bieber T, Dahl R, Friedmann
PS, Lanier BQ, Lockey RF, Motala C, Ortega Martell JA, Platts-Mills
TA, Ring J, Thien F, Van Cauwenberge P, Williams HC. Revised nomenclature
for allergy for global use: Report of the Nomenclature Review
Committee of the World Allergy Organisation, October 2003 ALLERGY(2001),
56:813-824. Back
2
see Bloomfield SF, Stanwell-Smith R, Crevel RW, Pickup J Clin
Exp Allergy. 2006; 36 (4):402-25 for a recent review. Back
3
DBPCFC; Standardization of Food Challenges in Patients with Immediate
Reactions to Foods. C Bindslev-Jensen, BK Ballmer-Weber, U Bengtsson,
C Blanco, C Ebner, J Hourihane, AC Knulst, DA Moneret-Vautrin,
K Nekam, B Niggemann, M Osterballe, . Ortolani, J Ring, C Schnopp,
T Werfel. ALLERGY (2004), 59:690-697. Back
4
IgE-mediated food allergy diagnosis: current status and new perspectives
Asero R, Ballmer-Weber BK, Beyer K, Conti A, Dubakiene R, Fernandez-Rivas
M, Hoffmann-Sommergruber K, Lidholm J, Mustakov T, Elberink O,
Pumphrey RSH, Stahl Skov P, van Ree R, Vlieg-Boerstra, BJ, Hiller
RO. Hourihane J, Kowalski M, Papadopoulos NG, Wal J.-M, Mills
ENC, Vieths S, Molecular Nutrition and Food Research 2006 in press. Back
5
Miles S, Fordham R, Mills ENC & Mugford M. 2005 A framework
for measuring costs to society of IgE-mediated food allergy. Allergy
60 996-1003. Back
6
Mills ENC Valovirta E Madsen C Taylor SL Vieths S Anklam E Baumgartner
S Koch P Crevel RWR & Frewer L 2004 Information provision
for allergic consumers: where are we going with food allergen
labelling? Allergy 59 1262-1268. Back
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