Posts Tagged ‘house dust mite’

Few newborns are already capable of mounting an allergic reaction to dust mite. Actual symptoms of allergy may not appear for several months or years, but the essential first

step – making the allergy antibody, IgE, against the mite allergens – seems to have occurred already for some babies.
In situations where IgE does the job it is supposed to do –protecting against worms and other parasites (see p. 13) – this advance programming of the immune system before birth

has definite advantages. A child whose mother is infected with parasites is born with the ability to make IgE against those parasites, even though he or she has had no direct

contact with them before birth. The baby’s immune system has been forewarned of the likely hazards of life in the outside world.
While this is obviously valuable in conditions where parasitic infections are rife, emerging into a carpeted and well-upholstered world with IgE against dust mite already in the

bloodstream is a serious disadvantage, because it can pave the way for rhinitis and asthma. Given the trouble caused by dust-mite allergen, some doctors think that women should

try to reduce their exposure to it during the second half of pregnancy, so that little or none reaches the unborn child. At present it is not known for sure if this can make a

difference to the risk of allergies developing in a child, but it seems plausible.
What is pretty clear, from several previous studies, is that the level of house-dust mite in the home immediately after birth can make a distinct difference as regards the

chance of allergy developing. Minimising a newborn baby’s exposure to dust mite is worthwhile, and the measures needed to achieve this are described on pp. 244-5.
Carrying out these measures will raise the level of dust-mite allergen in the air temporarily, so it makes sense to do the work in the early stages of pregnancy (or – even

better – before conception), rather than expose yourself and the foetus to a tremendous burst of allergen later on in pregnancy. Or, get someone else to do the work, and stay

away while it is done.
There may be other potential allergens which you should try to eliminate from your home before the baby arrives, such as mould allergens (see p. 122).
Pregnancy
First and foremost – don’t smoke while you are pregnant, or afterwards (see box on p. 107). Any other smokers in the household should smoke outdoors.
What about your diet during pregnancy? Certainly you should eat a good balanced diet with plenty of fruit and vegetables. Taking a small supplement of vitamin E, or eating

plenty of sunflower seeds and oil, would be a good idea. Women with a low
intake of vitamin E and antioxidants (see p. 206) during pregnancy run a higher risk of having an allergic child.
Should you also avoid any foods? Food allergens, such as those from cow’s milk, do reach the foetus, passed from the mother’s blood to the baby’s blood via the placenta. And a

few babies are born already capable of making IgE against food allergens. On the basis of these findings, some doctors have suggested that avoiding potentially allergenic foods

(such as eggs, cow’s milk and peanuts) during pregnancy might help to reduce the risk of food allergy. However, evidence from research trials in which pregnant women followed a

restricted diet, and their children were later studied for allergies, does not show any convincing benefit. And in some studies, the women on restricted diets have not gained as

much weight as they should, and the babies have been slightly below average weight at birth. Most doctors now think that dietary restrictions during pregnancy are not worthwhile

– it is more important to eat well and get enough nutrients.
It does seem sensible not to overeat any particular food during pregnancy, although there is no scientific evidence on this point (simply because researchers have not yet looked

for such evidence). In particular, don’t overdo it with milk and milk products. Make sure you get enough calcium, obviously, but don’t force yourself to drink huge amounts of

milk, especially if you have any distaste for it. Talk to your doctor, midwife or health visitor about the possibility of a calcium supplement, if you dislike milk.
Breast-feeding
‘The cornerstone of allergy prevention is breast-feeding,’ according to Dr Erika Isolauri of Tampere University Hospital in Finland.
At one time, this would have been a controversial statement, but there is now a substantial body of scientific evidence to support the ‘breast-is-best’ idea in relation to

allergy prevention. A number of different studies have shown that exclusive breast-feeding, up to at least four months of age, reduces the risk of developing food allergy or

atopic eczema (or both) in the early years of life.
Exclusive means exactly that – no solids at all until after four months (and six months is better), and no supplementary feeds with infant formula, which is made from cow’s

milk, and therefore contains cow’s milk allergens. Unfortunately, it is sometimes far from easy to ensure that formula feeds are not given just after birth, by well-intentioned

nurses on the maternity ward. Given what we now know about the immune system of the newborn, this is the worst possible time to be delivering an onslaught of potentially

allergenic cow’s milk proteins.
Quite apart from the immediate effect of introducing cow’s milk allergens to the baby, a bottle can disrupt the development of a good breast-feeding relationship between mother

and child, and may lead to the early abandonment of breast-feeding.
Why should this happen? Firstly a different technique is needed for sucking on a bottle teat, and your baby may never develop the knack with nipples if given bottles at an early

stage. Secondly, allaying the baby’s hunger with a bottle can also mean that he or she demands less at the next breast-feed – and since the mother’s milk supply is partly

influenced by the level of demand, this can be detrimental. Some experts believe that occasional bottle-feeds can start a downward spiral of ever-diminishing supply from the

mother.
Dr Arne Host of the Department of Paediatrics at Odense University Hospital in Denmark, who has made a special study of breast-feeding, recommends giving a little boiled water

as a supplement during the first 3-4 days of life, if the breast milk supply is inadequate. After that time, the mother’s own supply should increase to meet the needs of her

baby. Introducing bottle-feeds at an early stage can prevent this delicate balance of supply-anddemand from ever being achieved.
Sometimes (though this is rare) despite everything being done just right, a mother’s supply of milk never quite matches her infant’s appetite. When this happens, and the child

concerned is from an allergy-prone family, the breast milk should be supplemented with an ultra-safe formula feed called a hydrolysate (see box on p. 66).
Hydrolysates should also be used for infants at high risk of allergy who, for whatever reason, cannot be breast-fed. Note that there are two categories of hydrolysate –

extensively hydrolysed formula and partially hydrolysed formula. For the purposes of allergy prevention, an extensively hydrolysed formula should always be used because it has

the lowest risk of causing food allergies.
Preparing to breast-feed
Because breast-feeding is natural, many first-time mothers just assume it will come naturally. Sadly, it often doesn’t.
Cracked nipples are a major obstacle. They are the equivalent of chapped hands, and are often caused by the baby not having ‘latched on’ correctly to the nipple. Help from an

expert breast-feeding adviser, right from the start. can avoid this problem.
Because cracked nipples are so sore, breast-feeding can then become a major ordeal rather than a pleasurable experience as it should be. What is more, infectious bacteria can

enter the breast through the cracks in the skin, causing mastitis, which is painful and may require antibiotic treatment: this is not necessarily a good thing for the baby (see

p. 247).
You can minimise the chance of cracked nipples by making the skin on the nipples tougher and more resilient, so that it does
not crack. Start during pregnancy, in about your fourth month. When you have a bath or shower, rub your nipples vigorously with your flannel for a few minutes. After three weeks

of this, graduate to a soft toothbrush, and brush them gently, then more firmly when they feel ready. Progress to a medium, and then a hard toothbrush.
Breast-feeding support groups can be immensely helpful, when you start breast-feeding, or when you feel things are not going right. Some groups have local advisers. all mothers

themselves with first-hand experience of breast-feeding. Having such an adviser with you, watching you breast-feed your new baby and making suggestions, or pointing out where

you are going wrong, can make all the difference. Look for such a group locally, and establish contact with them well before your due date. You may be able to have an adviser

with you at the birth, to help the baby take his or her first feed: this is of enormous value.
Having prepared yourself, you then have to prepare the nursing staff in the hospital where you will give birth, for the fact that you want to breast-feed exclusively. That means

no supplementary feeds from the staff – not even one bottle. The risks of this practice, in sensitising vulnerable babies to cow’s milk, are still not widely known, so you may

need to be persistent and make your feelings very clear. Talk to your midwife about this well before your expected delivery date, and find out what policy the hospital has about

supplementary feeds. Then see the relevant staff at the hospital.
The nurses are most likely to give the baby a bottle because he or she is crying while you are asleep, and they don’t want to wake you. Staff change all the time, so you will

probably need to put a notice on the crib or cot, to be certain that the baby is never bottle-fed while you are sleeping. If this seems ‘over-the-top’, consider the experience

of British researchers investigating allergy prevention who wanted to ensure that a group of newborns were never given supplementary feeds. They put warning stickers on both the

babies’ cots and the mothers’ beds, as well as asking the midwives and mothers to be very vigilant. Despite this effort, several of the babies being studied were given bottles.
Sometimes nurses give a bottle because they believe that the baby is not getting enough milk from the breast. The idea that mothers “don’t have enough milk”, and that this is

quite a common problem, is part of the medical folklore of breastfeeding today. In fact, true milk insufficiency is very rare. Most cases of poor milk supply arise because a

good breastfeeding relationship between mother and child is never established – and supplementary bottle feeds are partly to blame.
It is entirely possible that your milk supply will not be quite adequate in the first few days, but it should increase rapidly. The best thing, if breast- milk supply is

inadequate, is to give boiled water as a supplement during the first 3-4 days of life (see left).
Some preliminary evidence suggests that mastitis may alter the profile of immune cells in the milk, and that this might possibly increase the risk of the child’s own immune

system becoming allergy-prone. A key preventive measure is not to let the breasts become engorged with milk: the build-up of milk can lead on to mastitis. Learning to express

milk (by hand or with a breast pump) will be useful for times when your breasts feel over-full. Talk to a breast-feeding adviser.
Diet during breast-feeding
Pretty much everything you eat works its way into breast milk, though in very tiny amounts.
The food molecules that get through into breast milk can certainly affect babies who are already sensitised to a food. Cow’s milk is the classic example — cow’s milk proteins

get into human milk if the mother consumes any milk, cheese, yoghurt or other milk products. Babies who have already been sensitised to cow’s milk (by a supplementary

bottle-feed, for example, or even in the womb — see p. 241) react badly to the breast milk, unless the mother avoids all dairy products.
What is less certain is whether the traces of allergen in breast milk — cow’s milk allergen or that from any other food — might be capable of starting off allergy or

sensitivity. Are these minute traces enough to sensitise babies with a strong tendency to allergy? If they are, then mothers of high-risk infants might be well advised to avoid

certain allergenic foods while breast-feeding. Some studies do suggest that there is a reduction in food allergy if breast-feeding mothers avoid cow’s milk, eggs, nuts, fish and

soya. But if this restrictive diet makes your life impossible, then it is better to breast-feed your baby and eat what you like, than not to breast-feed at all.
Unfortunately, some babies do get eczema, in spite of being exclusively breast-fed. If this happens with your child, there are a number of steps you can take to deal with the

problem (see box on p. 248).
Treating the gut flora
Taking a probiotic or bacterial replacer (see p. 205) during the later stages of pregnancy, and continuing with this while breast-feeding, may reduce the risk of atopic eczema

in your child.
Weaning — when and how
The key to reducing the allergy risk for babies is to turn that old political jibe ‘too little, too late’ on its head. Research shows that, with weaning, it is ‘too much, too

early’ that increases the chance of allergic reactions developing. Suddenly presenting an infant of three months with a wide variety of solid foods, including potent allergens

such as eggs, peanuts and fish, can increase the likelihood of food allergy and/or eczema developing. Weaning late, with a limited number of safe foods, should be your goal.
At least four months of exclusive breast-feeding, and preferably six months, is now the standard recommendation for allergy prevention, and it is well supported by scientific

evidence.
But how long should breast-feeding continue after weaning begins? There is little concrete evidence here, but there is a strong belief in the medical community that

breast-feeding should go on for several more months, up to or beyond one year of age if possible, allowing the weaning process to be very gradual. The idea is to introduce new

foods one at a time, alongside breast milk.
As well as allowing the baby’s immune system lots of time to adjust to each new food, prolonged breast-feeding may help in another way as well. Recent research shows that breast

milk contains a great many substances which influence the baby’s immune system, nudging it in the right direction — away from any tendency to allergies.
Avoid those expensive little jars of ready-made baby food. Most contain potent allergens such as cow’s milk, wheat or soya. Making your own baby foods is not difficult, and is

the best way to ensure that your child gets only low-risk foods.
Reducing the risk of peanut allergy
Peanut oil, which contains traces of peanut allergen, is an ingredient of some skin creams. Recent research from the United States shows that babies treated with such creams

were seven times more likely to develop peanut allergy later. In the past, concern has focused on traces of peanut allergen that the baby swallows — either in the breast milk

(because the mother has eaten peanuts) or from her nipple cream. What this new research suggests is that peanut allergens absorbed through the baby’s skin are much
more likely to cause sensitisation. Don’t use any skin products if they have ‘Arachis oil’ or ‘Arachis hypogaea’ in the ingredients list — and steer clear of any cream without a

detailed ingredients list. In the same research study, soy formula also emerged as a risk factor: feeding a baby on this doubled the chance of peanut allergy developing later.

Good health is one of the most important things we can give our kids,’ says Martha, now in her sixties with two grown-up children.
`When I see how bad my daughter’s asthma is, and how hard her life is sometimes because of it, I do feel bad about the fact that I smoked when I was pregnant. But we just didn’t

know in those days. Even my doctor smoked. No one thought anything of it.
`I stopped when she was little, because it seemed to me that her wheezing got worse whenever I lit up. I’m sure that stopping then was better than nothing. It must have helped.
`In any case, there’s no point feeling guilty about things now - that won’t change anything. But if I’d known what damage it could do, I would have stopped sooner.’ Martha’s

regrets stem from the discoveries made in the past decade about the effects of smoking on allergies. We now know that smoking during pregnancy increases the amount of IgE (the

allergy antibody) in the blood of a newborn baby - an indication that he or she is at an increased risk of developing allergies. After the birth, exposing a child to cigarette

smoke continues to encourage high levels of IgE in the blood, as well as irritating the airways and making asthma more likely to develop.
The research on smoking is just one part of a worldwide research effort, during the past 20-30 years, into the possible causes of the allergy epidemic. That research can help

parents who are themselves atopic (allergy-prone) to reduce the risk of passing their allergy problems on to their children.
Who should be implementing these preventive measures? Firstly, any prospective parents who have allergies themselves, or had them as children. They are at higher risk (compared

to a non-allergic parent) of producing a child who is susceptible to allergies. The risk is especially high if both parents have or have had them at some point in their lives.
Secondly, these preventive measures could be worthwhile for parents who don’t have allergies themselves, but who come from atopic families (families with a tendency to allergy).

If you or your partner have brothers, sisters or parents with allergies, you are more likely than the average person to produce allergic children.
Finally, if you already have one allergic child - even though you and your partner don’t have allergies yourselves, and no one else in the family does - there is a

higher-than-average chance that subsequent children will have allergies. Your allergic child is a sign that the genes for allergy are there.
Given the important role that genes play in allergy (see p. 8), preventive strategies make a lot of sense for parents-to-be with allergies in the family.
Unfortunately, this is a topic which often generates confusion - some people assume that if a trait is genetic, it will inevitably come out in the child, and that nothing can be

done to prevent this happening. Although that is true for some inherited traits, such as metabolic abnormalities (see upper box on p. 75), it is not at all the case for allergy.
Developing allergic disease is not inevitable unless a child has a very big dose of the genes that favour allergy. Only a few children - generally those whose mother and father

are both badly affected by allergies - will come into this category. Even with these very high-risk children, following the measures described here will probably help to reduce

the severity of their allergic problems.
For most children at risk of allergies, even though they have some pro-allergy genes, there has to be an unfavourable environment to actually produce allergic disease.

‘Environment’ here means everything external that affects the child, including diet, air quality, allergens, diseases and medical treatment. Factors occurring before birth, such

as the mother’s lifestyle during pregnancy, are also part of the child’s environment. It is the interplay between genes and environment that will decide whether your child

develops allergies or escapes them.
This interaction is not a simple one, however, and different aspects of the environment operate in different ways. Firstly, there are some environmental factors that work at the

most fundamental level -conspiring with the pro-allergy genes to make the overall tendency to allergy far stronger. These are factors such as cigarette smoking by the mother

during pregnancy, or excessive hygiene during childhood, which influence the fundamental make-up of the child’s immune system. Secondly, there are environmental factors, such as

early exposure to house-dust mite or grass pollen, which can cause trouble by provoking specific allergic reactions. Note that factors like these will not become important

unless the allergic tendency is already there.
Efforts to reduce the risk of allergy operate on both types of factor.
On the one hand, there are measures such as quitting smoking or easing up on hygiene, which tackle the allergic predisposition itself. These measures are, in effect, trying to

make a Western child’s immune system more like the immune system of a child from a poor rural village in the developing world, whose chance of developing allergy is very low

indeed.
On the other hand, there are measures such as reducing dust-mite levels, that try to stop the development of particular allergic reactions.
Obviously, if measures of the first kind could be truly successful, there would be little or no need for measures of the second kind. But this kind of success is very difficult

to achieve in modern Western society. Although we can certainly improve matters a great deal, and lessen the tendency to allergy, the conditions that would completely reverse it

are beyond our reach at present. So both kinds of preventive measure remain necessary.
In reading the pages that follow, it is important to keep things in perspective, and not feel excessively anxious about your child. Do what you can, but don’t feel guilty if you

can’t manage everything that is suggested here. And if you already have a child with allergies, please don’t feel guilty about things that might have contributed to this. Only

hindsight is perfect, and you no doubt did the best you could, given the information you had at the time, and the many other constraints and difficulties that you faced. That is

the best that any of us can do.

No single factor lies behind the allergy epidemic — the causes are many and various (see p. 20). What this means for parents interested in allergy prevention is that there is no

single measure which will ensure that your children do not develop allergies. Instead there are a great many different things that can be done, each of which reduces the risk to

some extent. The more of these you do, the lower the risk becomes.
Avoiding allergens
Starting before the birth is best, if you want to reduce allergen exposure for your child (see p. 240). But if you have missed the boat with that one, don’t despair – there is

still a lot to be gained by reducing allergen exposure at a later stage.
If you are ridding your home of allergens after the child’s birth, bear in mind that things will get worse before they get better– there will be a temporary surge in airborne

allergen as a result of the clean-up operation, and you will need to protect the child from this. The best strategy is for the child to be away for a few days while the work is

done, especially if you are taking out carpets, furniture or mattresses. Remember to protect yourself as well, if you are allergy-prone (see p. 109).
One of the most important steps you can take to reduce allergen levels is improve the natural ventilation of your home. This lowers the humidity (assuming you don’t live in an

extremely humid climate), which helps combat both moulds and dust mites. Ventilation also flushes out allergens in the air, especially cat, dog and mould allergens. Half the

problem with modern houses is that the airtight seals around doors and windows, introduced to conserve heat and save energy, turn the indoor air into a rich stew of allergens

and irritants.
House-dust mite
Avoiding high levels of house-dust mite in the home is one of the most valuable things you can do to reduce the risk of allergies in your child. Not only is house-dust mite a

powerful allergen in its own right, it may also act as an agent provocateur as far as the immune system is concerned (see p. 12), and may help to initiate allergic reactions to

other potential allergens – such as those from pets or indoor moulds.
Even if you do nothing else to protect your new baby from mite allergen, at least buy a new mattress and pillow for the cot, with ready-fitted allergen-proof covers. Do the same

for the portable crib, if you have one. Choose anti-mite products that are designed for babies and are guaranteed safe – there is a risk of suffocation with some loose covers

sold for older children and adults (see p. 245).
You may want to eliminate house-dust mite from your own bed as well as the baby’s, because there will probably be times when you take the baby into bed with you for a feed or a

cuddle – and times when, as a toddler, he or she just barges in! It is good to know that your child is still breathing air free from dust-mite allergen in these circumstances.
Deal with your own bed as soon as you can. Some doctors believe that lowering your exposure to dust mite during pregnancy may reduce the risk of sensitising your baby before

birth (see p. 241).
When taking anti-mite measures with your own bed, make sure that there is no risk of suffocation to the baby from the allergen-proof materials used. Microporous membranes based

on plastic could, if sucked onto the baby’s face during sleep, cause suffocation. Loose covers on duvets are worrying in this respect. Buy a new duvet with a built-in

allergen-proof cover, for preference, or a duvet that can be laundered at 60°C or above.
All the other measures for combating dust mites, described on pp. 114-17, will help to protect your child. Buy a good anti-allergen vacuum cleaner if you possibly can, and keep

your baby out of the room while vacuuming if you can’t (open the windows too). Make sure the baby only has new soft toys, preferably washable ones (see p. 116).
It is also an excellent idea to reduce dust-mite levels in the carpets and soft furnishings (see p. 117), because children tend to have very close contact with these in their

early years. A crawling baby, motoring enthusiastically around the sitting room floor, is stirring up the stockpile of dust-mite allergen that is found in any carpet, and

inhaling it in full measure. An adult walking around the same room has a far lower exposure, because dust-mite allergen, being relatively heavy, stays near the ground.
The best option is to go for non-carpet flooring, which doesn’t encourage dust mites. Parents tend to worry about the hardness of this, for a baby or toddler. In fact babies are

far more robust than we generally believe, and a hard floor is no problem for a small child who has never known the luxury of carpeting.
If you really hate the idea of your baby having anything other than carpet to play on, the next best option is to get new carpet, so that you start with zero dust mites. You

must then prevent dust-mite numbers from building up too much, by means of good ventilation, or with the use of a powerful dehumidifier (see p. 117).
Although the first year is the most vulnerable time for your baby, you mustn’t let your guard drop too much as time passes. The moment when a toddler moves from a cot to a ‘big

bed’ is sometimes the beginning of allergy symptoms because, after carefully protecting their child from dust mites in infancy, parents then put him or her into a bed with a

used mattress. This sudden exposure to a high dose of
dust-mite allergen can be the start of asthma. Get a new mattress if you can, and put allergen-proof covers on it. Alternatively, put allergen-proof covers on the existing

mattress.
Moulds
Mould spores are another potent allergen, and you should avoid bringing up a vulnerable child in a damp house if you can, because moulds will be growing there in abundance. Some

new research suggests that heavy exposure to mould allergens in childhood makes allergies in general much more likely. Even in a house that is not obviously damp, it is a good

plan to reduce indoor humidity (see p. 119). Carpets and furnishings that are full of mould spores (see p. 122) should be replaced.
Pets
What about pet allergens – should you find another home for your cat or dog when you are expecting a baby? This is a difficult question because the latest research shows that

pets are a double-edged sword as far as allergies are concerned.
A baby with allergic tendencies who is born into a house with a resident cat or dog is more likely to show allergic reactions to cats or dogs some years later. On the other

hand, there is research showing that having a pet in the house reduces the risk of allergies overall, especially for a child with no brothers or sisters. This is probably

because the pet boosts household levels of endotoxin (see p. 21), and generally makes the environment less hygienic for the child, fulfilling the same anti-allergy role as

brothers and sisters would in the early life of a child (see p. 246).
If you are planning to give your child the kind of grubby childhood that seems to protect against allergy (see p. 246), the additional protection provided by a pet is probably

unnecessary. Or, you could view your pet as having both pros and cons, and decide to keep it, while implementing all the other anti-allergy measures described here. If you do

this, ensure that the house is well ventilated (so pet allergens don’t build up to very high levels) and keep the pet out of the child’s bedroom so that he or she is not

breathing huge amounts of pet allergen while asleep. You could also wash the pet regularly (see p. 125) to reduce allergen levels.
If your child begins to show any signs of allergy to the pet, you must then find it another home.
Avoiding irritants
As well as increasing ventilation and eliminating cigarette smoke from the home completely, it may be worth evicting certain specific items that produce irritant gases.
The main ones are:
•    gas cookers (if you can’t afford to switch to an electric cooker, at least improve the ventilation in your kitchen as much as possible)
•    easy-clean plastic wall coverings and flooring
•    materials such as chipboard and MDF, which give off formaldehyde.
The evidence regarding the possible role of these in increasing the risk of allergies and asthma is described on pp. 128-9. In addition, although there is no evidence on this

point, common sense would suggest getting rid of any plastic or lacquered items that have a powerful smell.
Generally speaking, although traffic pollution can act as an irritant, it seems to play a lesser role in causing allergies and asthma than most people imagine. However, it may

sometimes play a part, especially if there are high levels of diesel fumes in the air (see p. 131).
Infections - friend or foe?
A large group of Italian military cadets were recently studied by doctors interested in the causes of allergy. By taking blood samples and testing them for antibodies to common

infections, the doctors could see what diseases the men had been exposed to early in life. At the same time, the young conscripts were assessed for allergies.
Allergies were least frequent among the young men with antibodies against three common infections that are dispersed via food and faeces – Hepatitis A, Toxoplasma gondii and

Helicobacter pylori. Only one in twelve of the cadets in this group had allergies.
Among the men with no antibodies against any of these infections, the rate of allergy was nearly three times as high – one in five of these cadets had allergies.
The doctors who carried out this experiment believe that these three infections are not necessarily important in themselves, but that they identify individuals who were ‘reared

in an environment that provides a higher exposure to many other orofecal or foodborne microbes’. In other words, they grew up in the kind of household where washing your hands

before meals wasn’t considered too important.
This study adds to the growing body of evidence (see p. 21) which shows that an over-clean environment during childhood encourages the development of an allergic disposition.
Those with lower rates of allergy include:
•    children raised on farms with livestock. The more exposure the children have to farm animals, the less the likelihood of them developing allergies.
•    children from homes with high levels of bacterial endotoxin in the household dust (see p. 21)
•    children who have fewer baths, and wash their hands less often (see p. 21)
•    children with brothers and sisters, especially those with older siblings. Some of the protection here may be due to the impact of the mother’s hormones and immune system

on the foetus in the womb: these effects change with successive pregnancies. But close contact with older siblings, and thus exposure to more microbes, probably plays a part.
•    children who go into kindergarten, nursery school or day care with other children at an early age – this is only valuable for children without brothers and sisters
•    children with pets at home – the benefits are much more pronounced for children without brothers and sisters.
The Italian study is especially important because, for the first time, it gives detailed information about the kinds of infections that make a difference in allergy prevention.

The military cadets were also checked for antibodies to measles, mumps, rubella, chickenpox and herpes. None of these infections gives protection against allergies – only

infections carried in food and faeces do.
Exactly what practical use you make of these discoveries is up to you. For most of us, the importance of hygiene was so firmly instilled during our own childhood that it is

quite hard to suddenly become more relaxed about it. But do let your children play in the garden, if you have one, and don’t worry so much about how dirty they get. Encourage

them to do some gardening – medical researchers believe that harmless bacteria in the soil may be particularly important in educating the immune system away from allergies (see

p. 21). Let them play with pets, as long as the animals are not carrying harmful parasitic worms (talk to your vet about whether pets should be treated for parasites). Ease up

or, hand-washing and, if this is your first baby, make sure he or she plays with other children as early in life as possible.
A few chest infections do seem to increase the risk of asthma, notably Respiratory Syncytial Virus (RSV). If this Infects babies, it provokes an IgE-reaction (see box on p. 12)

which may encourage the development of allergies. Unfortunately, there is very little you can do to protect your child from this common virus, but it makes sense not to take the

baby to a hospital for unnecessary trips (visiting relatives, for example) because RSV infections are often picked up in hospital.
Taking care with antibiotics
The possible role of antibiotics in making allergies more likely to develop is an exceedingly controversial topic. Before making any practical decisions in this respect, you

must consult your doctor. Never go against your doctor’s advice, if he or she thinks that antibiotics are necessary.
Several different studies have now produced evidence of a link between antibiotic use before the age of one or two, and the later development of allergies, asthma or both. The

best of these studies was carried out by doctors in Oxford, who followed 1900 children up to the age of sixteen. Among children at risk of allergy (because their mothers had

allergies) taking antibiotics before the age of two was linked with an increase in the rate of allergy from 32% to 54%. The more courses of antibiotics a child received, the

greater the risk.
The type of infection for which the drugs were prescribed was not important, as far as the risk of allergy was concerned, but the type of antibiotic did make a difference.

Broad-spectrum antibiotics, which kill a wide range of bacteria, were more risky –suggesting that the depletion of friendly bacteria in the gut (see p. 204) could be responsible

for increasing the allergy risk. Penicillins seemed less likely to promote allergies than erythromycin or cephalosporins.
This research is not widely known, as yet. And because there is a widespread assumption that giving an antibiotic can do no harm, even if it is unnecessary, antibiotics are

sometimes prescribed when they serve no purpose. In particular, antibiotics are often given for virus infections, especially in childhood, despite the fact that antibiotics are

of no value whatever against viruses. Research shows that doctors are sometimes responding to pressure from anxious parents when they prescribe antibiotics – it is difficult for

some parents to accept that a virus infection cannot easily be treated and just has to ‘run its course’. (Although there are drugs that combat viruses, these are expensive and

produce unpleasant side effects – they are reserved for very serious virus infections such as hepatitis.)
Obviously. when a child needs antibiotics to deal with a serious infection there can be no question about giving them. This is why you should always follow your doctor’s advice.

But it is also worth asking the doctor the following questions before giving antibiotics to your child:
•    are you sure that this is a bacterial infection, and not a virus infection?
•    would it be possible to do tests and check that it is a bacterial infection, before prescribing antibiotics?
•    what is the chance of the child overcoming the infection without antibiotics?
•    would it be dangerous to wait and see if the infection clears up naturally?
Vaccination
The same Oxford research team that investigated antibiotics (see left) also looked at the question of vaccination and allergy. They found a link between vaccination for

pertussis (whooping cough) and increases in asthma, eczema and hayfever. However the increases were not large, and a study from Sweden found that whooping cough vaccination did

not have any effect on rates of allergy and asthma. And researchers in Ethiopia have found that whooping cough vaccination actually reduces the risk of allergy in their country.
This is clearly a complex issue. The contradictory results from different parts of the world suggest that the ‘big picture’ is what counts here – the overall combination of

childhood infections, antibiotic treatment and exposure to harmless bacteria such as those in the soil or from animals. Depending on this big picture, vaccination against

whooping cough may push the allergy risk one way or the other.
There are many other arguments both for and against vaccination and, given our current state of ignorance about the possible effect on allergy, these other considerations are

probably more relevant. Discuss the matter in detail with your doctor before making a decision.

Doctors in Japan recently tried a very simple experiment in allergy prevention. They chose babies suffering from atopic eczema who were allergic to foods, but not allergic to

house-dust mite. Dividing the babies into two groups, the doctors put special allergen-proof covers, designed to protect against house-dust mite (see p. 115), on the mattresses

of all the babies in the first group. Babies in the second group were given ordinary cotton covers.
When the babies were one year old, they were tested again for allergy to house-dust mite. Two out of three children in the second group now gave a positive skin test to

house-dust mite.
By comparison, only one in three of the children from the first group gave a positive skin test. In other words, using the anti-allergy covers for these high-risk children had

cut by half the number who developed an allergic reaction to dust mite.
As this experiment shows, even if a child has already developed allergies, it is not too late to bring protective measures into play. Indeed, an allergy problem in infancy, such

as atopic eczema, can be seen as a warning sign to parents, telling them that they should reduce the child’s exposure to allergens as much as possible.
As well as reducing dust-mite levels, you should minimise your child’s exposure to moulds at home by limiting indoor humidity (see p. 119) and cleaning up any existing mould

growth (see pp. 122-3). This will lessen the chance of mould allergy developing.
Try to avoid staying, even temporarily, in any house that is damp or has old carpets and mattresses. When you are moving house, or carrying out any kind of renovation work,

remember that this will stir up a lot of dust-mite and mould allergens. Protect your child by arranging for a stay away from home.
This pro-active approach should not just apply to airborne
allergens, but also to food, in the opinion of some experts. They
suggest that any child with a true allergy to cow’s milk or egg
should not be given peanuts, tree nuts, fish or shellfish until three
years of age, to avoid sensitisation to these potent food allergens.
Pets are a more difficult issue, with both pros and cons as
regards allergy-prone children (see p. 245). If you decide to keep
your cat or dog, always ventilate the house well, and wash the animal regularly if you can (see p. 125). Be alert for your child developing an allergic reaction to your pet –

don’t turn a blind eye to the symptoms, as parents sometimes do because they are reluctant to accept that the child has become allergic to the family’s much-loved pet. If your

child does develop an allergy to the pet, the best option is to find the animal another home as quickly as possible (see p. 124).
Breast-fed babies with atopic eczema
Although breast-feeding is a good way of protecting children against atopic eczema, it is no guarantee. Sometimes babies become sensitised to food, in spite of being breast-fed,

and then they may react to traces of that same food, eaten by the mother and coming through in her breast milk.
Skin-prick tests (see p. 91) may help to identify the foods responsible for the eczema. Otherwise, a simple elimination diet by the mother, as used for colic (see p. 203), may

pinpoint the offending food. Keeping that food out of the mother’s diet will often clear the baby’s eczema.
Sometimes a breast-fed child’s eczema remains severe, despite the elimination of suspect foods from the mother’s diet. In this case, what should be done? New research from Or

Erika Isolauri – a staunch advocate of breast-feeding – suggests that the best option at this point is to stop breast-feeding promptly. Her research team found that breast-fed

children with persistent eczema had a slower growth rate. If these babies are switched to hypoallergenic formula – either an extensively hydrolysed formula or an artificial

amino-acid formula (see box on p.66) – their eczema symptoms usually subside, and their growth picks up.
Is vaccination safe for those with allergies?
The influenza vaccine and a few others (e.g. yellow fever) are grown in eggs and are not usually given to people with egg allergy. Measles vaccine is grown in cells taken from

eggs and may contain a minute trace of egg allergen, but only those who are extremely sensitive will react: there should be resuscitation equipment available for children who

have had anaphylactic reactions to egg and for those with severe asthma as well as egg allergy. Some vaccines come in vials with latex seals that are designed to be pierced by

the needle of the syringe. A different method should be used for latex-allergic patients. Smallpox vaccine (for bio-terrorism threats) is dangerous for children with atopic

eczema.
Never too late?
The role of modern ultra-clean lifestyles in promoting allergies is now well established (see p. 21). If your child already has allergies, it may seem as if these discoveries

have come too late to help —but that is not the case. Some research suggests that the battle for supremacy between Th1 and Th2 cells (see p. 11) — the unseen power struggle

which decides whether a child will be allergy-prone — is not really settled until some time between the ages of five and seven years. So there is still some potential for

intervening right up to this age. Some studies have suggested that the immune system can be pushed away from an allergic disposition at an even later age, right into adulthood,

by exposure to endotoxin, a bacterial product found around livestock and in `lived-in’ homes.
Several research groups are working on vaccination strategies (for example, using extracts of soil bacteria) that might also be able to achieve this. The initial results are

promising and they suggest that these vaccines can even help adults with allergies. Unfortunately, such treatments will not be available for many years. In the meantime, you can

probably reduce your child’s chance of developing new allergies, and perhaps make the existing ones less severe, by easing up on hygiene (see p. 246).
Fresh air and exercise
With the boom in watching TV and videos, and playing on computer games, some modern children hardly go outdoors at all. As far as allergies and asthma are concerned, there are

two big disadvantages to being a juvenile couch potato. For a start, the couch is also home to dust mites in their millions, and secondly the child is not running about and

using his or her lungs to the full. Airways that are never stretched (because the child never gets out of breath) lose their youthful flexibility in time. Once this has

happened, the airways can never be stretched to their full capacity. Some doctors believe that this may make asthma more likely to develop, or help to make it more severe once

it has developed. Inactivity also encourages obesity, which increases the risk of asthma developing.
Getting outside and running around, or engaging in other vigorous exercise, should be encouraged for any child with allergies. Obviously, you should balance this against the

need to protect the child from pollution peaks and (if your child has hayfever) pollen peaks. Children with exercise-induced asthma should use their reliever inhalers to allow

them to take exercise (see p. 41).
Keep the air at home free from irritants such as nitrogen dioxide (see p. 128), formaldehyde, air fresheners, paint, polish and strong-smelling cleaning fluids. These may

encourage new allergies to develop, and can make existing asthma worse.
Medical treatments
Antihistamines may have a preventive role in very young children with allergies. A study of one- to two-year-olds with atopic eczema found that the antihistamine cetirizine,

taken daily for 18 months, halved the chances of the children developing asthma later.
The children who benefited in this study were those with several risk factors for becoming asthmatic. They had moderate to severe atopic eczema, at least one close relative with

allergies, and allergic sensitisation to pollen or house-dust mite, as shown by skin-prick tests (see p. 91).
The cetirizine was taken at fairly low doses and had no bad effects on the children in this study. What is more, it seemed to benefit their skin as well as reducing the risk of

asthma: those taking the drug had less need of high-strength steroid creams. There is some controversy about the validity of these results, so few children with atopic eczema

are receiving antihistamines at present.
No one yet knows if other antihistamines might have the same effect as claimed for cetirizine. Ketotifen, which is an atypical antihistamine (see p. 159), may do so.
Immunotherapy may also have a protective effect. One study, involving children suffering from nasal allergies, found that those given immunotherapy were less likely to develop

asthma (see p. 165). Another study shows that immunotherapy for children with mite allergy halves the risk of their developing new allergic reactions to other allergens.

Many countries have special schools for children with severe asthma and other allergies. Italian children are sent to one in the Italian Alps, where there is no trace of pollen, house-dust mite, or animal allergens. After nine months these children are a great deal healthier and more active - all their lung function tests are vastly improved. Blood tests show that they are actually less allergic to common allergens than before.
You may not be able to do quite this well at home, but all allergens and irritants can be avoided to some extent. Even if you can’t eliminate them completely, you can certainly reduce your exposure.
Before you start, it is important to be clear about exactly what affects you, otherwise you will be wasting a lot of effort. For example, people who are allergic to dust mite often think that a dusty house will necessarily be worse for them than an apparently clean house, but this is not so (see p. 115). Or they may say ‘Oh, I got asthma on holiday, because the roads were so dusty and I’m allergic to dust,’ forgetting that only house dust contains dust mites. The road dust may have acted as an irritant, and helped to spark the asthma attacks, or it may have contained pollen or mould spores - but it does not contain dust mites or their allergens. Blaming the wrong thing for the asthma attack means that the real culprit is not identified.
If you are not absolutely sure what causes your allergies, skin-prick tests (see p. 91) can identify the allergen. These are especially recommended if your reactions to the presumed allergen are inconsistent, or you don’t respond to the anti-allergen programmes described here. For example, a few people who react to house dust are not allergic to dust mites, but to something else in the dust such as wool fibres or mould spores, or particles from cockroaches, house
flies, carpet beetles or a long-departed cat. Even pollen that has accumulated in house dust can provoke allergic reactions - if you are not an over-keen duster, it can still be there long after the pollen season.
If you have hayfever, knowing which pollens cause your symptoms (and learning to recognise the plants concerned) is useful. You will probably need skin-prick tests to be sure. ‘Hayfever’ can even be a seasonal mould allergy in some people (see p. 27).
Tackling allergens is now big business. There are a lot of people out there competing for your money and false claims are common, especially for anti-mite products. Only a few manufacturers are deliberately misleading, and most false claims probably stem from ignorance or wishful thinking, but be very sure you know the facts about your allergen before you buy.
Air cleaners are a good example. A really good quality air cleaner (which uses a HEPA filter - a High Efficiency Particulate Air filter) is an expensive purchase and, as the advertising tells you, it takes out very small particles with staggering efficiency. But this is entirely irrelevant if the source of those particles is no distance at all from your nose - your mite-infested pillow, for example, or the cat on your lap.
Something else that advertisements for air cleaners rarely mention is that unless you reduce allergen production - tackling mould growth in the house, for example, or keeping the dog outside - the filter can’t help much. In short, air cleaners do have their uses for some allergens, but they can’t work miracles.
The products mentioned here, if not available in your locality, can be bought mail-order from specialist suppliers of anti-allergy products (see p. 255). Note that some offer both very good products and distinctly doubtful products, so judge each item on its individual merits. Ask to see scientific evidence that it works.
Don’t be taken in by vague statements such as anti-allergenic’ - get the facts. This label is often used on pillows with synthetic filling, for example, and people assume that it refers to dust-mite allergy, whereas it simply means that the pillow does not contain feathers. But unless you are allergic to feathers, there is no reason to avoid feather pillows. (In fact, if not covered with mite-proof covers, synthetic pillows collect more dust-mites than feather pillows, because the fabric used for the cover is less tightly woven and the mites and skin particles get in more easily.)
Bad advice is also a hazard. Some of it just wastes your time and effort, but some could actually increase your exposure to the allergen. Advice to vacuum floors daily, or to vacuum beds, is commonplace but this achieves little and it means breathing much more allergen unless you have the right kind of vacuum cleaner. One health magazine even advised its readers with dust-mite allergy to ‘air mattresses by regularly turning them’. This will not affect mite numbers at all, but it will shoot massive amounts of mite allergen out of the mattress and into the nose and lungs.
Ridding your house of allergens and irritants is, in itself, a hazardous procedure because more of the offending substances will be released into the air during the work. If you take up carpets or remove mattresses, dust-mite allergens and mould spores will be churned up in their millions. Just bundling up a duvet will produce invisible clouds of dust mite allergen - and cat allergen, if your pet once slept on the bed.
Ideally, the allergic individual should not do the work, nor be in the house until it is 100% complete and the house has been very thoroughly aired. This is particularly important for those with chronic sinusitis and mould growth in the house, because of the risk of fungal infections in the sinuses (see p. 32).
If you are an allergy sufferer and have absolutely no choice but to do the work yourself, or to be present, then you should get a good quality dust mask and wear it throughout - only take it off when you go outdoors. Those with atopic eczema and sensitivity to airborne allergens should cover their skin carefully -with clothing, not barrier cream.
An ordinary hardware-shop dust mask is not adequate for most allergens - it only takes out really big particles and lets through all the common airborne allergens except pollen. You need a more serious sort of mask, designed for workplace use and conforming to official standards. Before buying one, ask what is the smallest size of particle that it filters out (at 90% efficiency, or better). Compare this with the particle size of your allergen (given in the articles that follow).
You must be able to breathe well through the mask when physically active, and it must fit tightly against your face, forming a seal at all edges. Beards and moustaches tend to prevent this - as does stubble.
Masks that combine an activated carbon filter with a dust filter will take out gases and chemical vapours as well as particles. Cycle shops now sell such masks -or try an industrial supplier. Such a mask can be useful if you are affected by traffic exhaust or industrial pollution as well as an allergen, for example, or if you are exposed temporarily to wet paint or other fumes at home. Activated carbon masks should also filter out the irritant substances from oil-seed rape plants.
Some people who try the anti-allergen programmes feel much better quite fast. But generally these are long-term strategies - you may not reap any benefits for a few weeks, and the improvement may be small at first. Sometimes it takes several months for the full effects to be felt, so be persistent.

Tony had suffered from hayfever since childhood but rarely took any medicines. Outside the grass-pollen season, he was fine, free of allergies and very fit. Then, when he was 35 he bought a run-down cottage in the country. The cottage was very damp and dirty.
The previous owner of the cottage, an elderly man, had died, and everything was much as he had left it. Tony moved in with his wife in late summer, and they began pulling out all the old carpets and furniture. Many of the windows would not open and there were dank musty cupboards and attics to be cleared. Dust filled the air – and Tony’s nose. He began to sneeze a little and within a few days he had a strange and unfamiliar feeling of tightness in his chest. During the following weeks, harvesting began in the surrounding fields, with several huge combine-harvesters working away all day and night. Tony noticed that, when out of doors, his eyes began to stream and the tightness in his chest became more noticeable. A few more days passed, and Tony found it harder to breathe, so he reluctantly went to see the doctor. The diagnosis was asthma. Skin-prick tests showed that Tony had allergic reactions to house-dust mite and moulds.
Tony’s case shows how someone who is already sensitised to an allergen – pollen in this case – may be vulnerable to developing new sensitivities, and new symptoms. It was almost certainly the dust mite and mould spores in the cottage that sparked off the trouble, followed by the mould spores from the cereal leaves, dispersed during harvesting.
For people with a tendency to allergies, the dangers of heavy exposure to potential allergens are something to bear in mind. It is surprising how many people with asthma had their first major attack while away from home, sleeping on an old sofa or in a friend’s dusty spare room. The dose of dust-mite allergen that you get from an ancient mattress or eiderdown can be massive.
Managing your allergy symptoms
As well as avoiding the development of new allergies, you need to manage your existing symptoms, and make sure that they interfere with your life as little as possible. For this you need good information and advice, support from your doctor, optimal drug treatment, and careful avoidance of your allergens.
Quite often people have all the information and drug treatment they need, but they still don’t stay on top of their health problems. There can be two distinct reasons for this: either they are not wholehearted about wanting to be well (ambivalence) – or they have never really accepted that they are ill (denial).
Ambivalence
Sometimes being ill has certain benefits – or being entirely well has certain disadvantages. Our state of health determines how people treat us, especially within the family, and the expectations people have of us. It may be comforting to be ill because others are more supportive then, or it may be less risky, because we are not forced to try things (such as sports or other physical activities) at which we might fail or look foolish. Being ill as a child often sets up a pattern for how we interact with the world, which revolves around caution, the comforts of familiarity, and holding back from new situations.
These habitual patterns can survive in the mind long after any real advantages have evaporated. Many people become stuck with a way of thinking and living where ill-health is a cornerstone of their existence. Doctors at the Chelsea and Westminster Hospital in London, who have developed a radical programme for treating atopic eczema (see pp. 46-8), have noticed this in their patients. ‘Old habits die hard and living with a little bit of eczema is a very tempting prospect for many patients, rather than clearing the skin completely…. As atopic skin disease begins for many in the first year of life, causing sometimes understandable alarm and despondency in the parents, the child learns how relevant their condition can be in their relationship with the external world, and with their parents in particular. Before they are able to speak, they have a powerful means of gaining parental attention which can have long-standing effects in the development of their personality. For some, to live without eczema is understandably a daunting prospect. This can be consciously appreciated and spontaneous-y referred to by some patients, while for others the issue will be buried from view, deep in their unconscious.’
If any of this rings bells with you, try to tackle the problem at source. Such mental blocks are not immovable. Indeed, simply recognising that the block is there can start to change things for some people.
Others may need professional help to overcome these longstanding habits of mind. Counselling or cognitive therapy can be very valuable, and your doctor may be able to help in locating a suitably qualified person for this.
Denial
At the opposite end of the spectrum are those who want to deny that they have any kind of health problem. Often these people cannot quite accept that they have a long-term disease, such as eczema or asthma, so they forget to take their drugs, apply creams to their skin, or carry their inhalers. Ironically, these people frequently wind up having far more trouble with their allergies than they need to, and a very poor quality of life, simply because they neglect preventive treatments.
To be really well, you first have to admit that you do have allergies, and then sort out your conflicting feelings about what this means. Again, counselling, cognitive therapy or some other kind of psychotherapy can be helpful.
Dealing with doctors
The decisions that your doctor makes about your treatment are ones in which you should be fully involved. Quite a few allergy patients don’t feel happy about their doctor’s treatment plan, but they never say so to the doctor’s face.
The usual pattern is to accept what the doctor prescribes without any argument, but then halve the dose of tablets, or only put the cream on once a day instead of twice, or not use the Inhaler at all. Some people stop and start their drugs in a random way because they never quite make up their minds about whether drugs are a good thing or not.
This approach to allergies invariably leads to worsening symptoms. The risks are greatest with complex problems such as
atopic eczema or chronic sinusitis, where a vicious circle can easily be set up if the disease is not brought under control, and for those with a life-threatening condition such as asthma. In the case of asthma, neglecting preventative treatment can be fatal.
It is far better to say what you think in the surgery, and discuss any misgivings you may have about drugs with the doctor. That way you can agree on a treatment regime that you are prepared to stick to – which may or may not involve drugs. Most doctors would far prefer a little plain speaking at the outset to having a patient who is half-hearted about following the treatment plan and never really improves.
A more serious form of communication breakdown occurs when a doctor stops believing what a particular patient says. This usually occurs because the doctor has decided that some or all of a patient’s symptoms are due to psychological rather than physical causes. (This is far more likely to happen to those with intolerance or unusual forms of allergic reaction than to those with classical allergic diseases.) Sometimes doctors say what they think, but often they don’t – they just start treating the symptoms in a different way, or acting impatiently, or saying rather puzzling things that leave the patient trying to guess what is going on.
If you find yourself in such a situation, the main thing to do is stay very calm and be very rational. Getting upset, or challenging the doctor’s opinion in a manner that seems at all aggressive, instantly confirms the ‘psychological’ diagnosis. Unfortunately, insisting firmly that the symptoms are not psychological also confirms the diagnosis as far as many doctors are concerned (see p. 237) which can be extremely frustrating. To begin with, deal with the situation by informing yourself about your illness. Be tactful and patient but persistent with the doctor, trying all the time to keep the relationship pleasant and the channels of communication open. If, after giving it a fair try for some weeks or months, this approach isn’t working, you should look into the possibility of changing doctors (see p. 88).
Emergency alerts
An emergency alert bracelet or pendant should be worn by anyone who:
• is allergic to latex rubber, or to drugs such as penicillin
• has a severe allergy to insect stings
• suffers from exercise-induced anaphylaxis, or anaphylactic shock as a result of food allergy
• has very severe asthma attacks.
Key information is engraved on the bracelet, along with a telephone number which gives medical staff access to a computer database containing vital medical data about you. This valuable service is provided by a non-profit-making company called Medic Alert.
As everyone knows, a little knowledge is a dangerous thing. You can use the information in this book to help yourself, but it’s important to remember that there is no substitute for the comprehensive understanding of the human body that your doctor gained during many long years at medical school. Always check with your doctor before changing your diet, stopping your drugs, practising breathing exercises, taking a non-prescription medicine or trying any other experimental treatment.
The information about disease, diagnosis and treatment in this book falls into four categories:
• basic information about the disease that no doctor would disagree with
• the findings of new research, or research that has not become widely known, but which falls within the accepted medical model of the disease concerned. Your doctor may not know about some of this research (there is a terrifying amount of new information bombarding doctors every week, and no one can keep up with it all) but he or she won’t find it unbelievable.
• evidence from research that is entirely valid, but which is widely ignored or dismissed because it falls outside the accepted medical model of the disease concerned (see pp. 86-7)
• information based on the repeated observations of doctors, or of patients – this does not amount to scientifically valid evidence, but it’s included here if it seems plausible and if it could be useful to some readers.
You should be able to tell, from the context in which it is presented, which category any item of information falls into. When talking to your doctor about items that belong in the last two categories above, be prepared for a certain amount of scepticism or possibly outright dismissal.
The important thing to ask the doctor is if there is good reason why you should not try the suggested measures, in addition to your usual treatment – is there any risk involved, given your particular state of health? Make it clear that you want to try the additional treatment with an open mind and will drop it if it is not helping. Ask for the doctor’s help in assessing the effects of the treatment objectively.
Managing asthma
Of all the diseases described in this book, asthma is among the most difficult to live with, especially severe asthma. Learn to recognise asthma symptoms before they get out of hand, and take immediate action.
Studies of patients who die from asthma attacks find that the deaths could, in almost all cases, have been prevented. Factors contributing to fatal attacks include:
• heavy exposure to allergens just before the asthma attack
• cigarette smoking
• failure to use preventer drugs
• repeat prescriptions for inhalers being given without the patient seeing a doctor
• delays in seeing an asthma specialist
• depression in the asthmatic leading to neglect of treatment.
For the day-to-day management of asthma, you should have a written management plan prepared by your doctor or asthma nurse.
This should tell you how often to take your drugs under normal circumstances, and what to do if your symptoms change or you develop a cold or chest infection. The actual brand names of your drugs (or the colour of the inhaler) should be included on the management plan. Assuming you have a peak-flow meter – and you really should have one –specific peak-flow values should be included on your management plan, with instructions for how to respond if your peak flow falls to these levels.
Your plan should tell you how to recognise a severe attack coming on, and what to do at the various stages of the attack. (This personal management plan is specifically geared to you or your child. Although pp. 100-101 give generalised advice, your own plan is invaluable.)
Be sure that you know exactly how the advice in the plan relates to the sort of real-life situations you experience. No matter how good your plan, real life can sometimes be far more complex than anyone anticipates, so there may be times when it is difficult to know what to do. When this occurs, make a note of the situation, and the reasons why you are unsure how to implement the plan. Call your doctor immediately if your asthma is getting worse, and get the asthma attack under control. Save your notes and, at the next opportunity, check with the doctor what you should have done in those circumstances. This will help you to build up your detailed knowledge of how to manage your asthma, or that of your child.
Research shows that asthmatics can, with training, develop a greater awareness of how narrow their airways are – this helps you to detect worsening asthma before things get too serious. You can train yourself in this art by guessing what your peak flow will be and writing your guess down before you use your peak-flow meter (see right) each day. Over a period of weeks, you should find your guesses getting closer to the true value.
A key part of asthma control is having everything with you that you need in case of an attack. It’s tedious, but you have to do it. You should take your reliever inhaler with you wherever you go. Those with severe asthma can also benefit from carrying a collapsible spacer (ask your pharmacist or see p. 255 for contact details of suppliers).
For a long day out, or a stay away from home, check that you also have:
• your management plan
• your peak-flow meter
• your preventer inhaler
• steroid tablets, if you sometimes need these
• your doctor’s phone number.
A little lateral thinking may be needed regarding the problem of carrying all this kit around. One asthmatic friend of mine carries his inhalers in a trendy-looking camera bag that goes everywhere with him. Mothers of asthmatic children have solved the problem by making an ‘inhaler pouch’ from a sunglasses case and attaching it to a favourite belt or by enlarging the pocket in a teenager’s jacket to accommodate inhalers.
Anyone with severe allergies to food or insect stings should take similar steps, so that carrying their auto-injector everywhere is a simple matter.
Peak-flow meters
A peak-flow meter can detect narrowing of your airways – the beginnings of an asthma attack – before there are any obvious symptoms. It measures the maximum speed at which you can force air out of your lungs. The signs of worsening asthma include:
• a morning reading which is less than 75% of the evening reading
• average readings less than 75% of your best-ever reading. (If they get to less than 50% of your best reading, this is a severe and possibly life-threatening attack.)
To use a peak-flow meter:
• push the pointer to zero and hold the meter horizontally
• keep your fingers away from the scale and the pointer
• breathe normally before you start
• stand up and take a deep breath, but don’t puff your cheeks out and don’t hold your breath before you blow
• seal your lips tightly around the mouthpiece
• blow hard into the meter, as if blowing out candles on a birthday cake; don’t move your tongue while doing this
• repeat three times, and record the highest reading of the three.
You must learn how to use a peak-flow meter from your doctor or asthma nurse, who should also check your technique regularly – it is very easy to get into bad habits.

Atopic eczema
A Greek word meaning ‘to boil over’ or ‘to erupt’ is the source of the medical term ‘eczema’. It refers, of course, to the way in which the skin erupts into a rash, but it could equally well describe the eruption of controversy around this disease. No other allergic disease is quite such a cauldron of dissent - indeed, even the question of whether it is an allergic disease remains unresolved. These controversies directly affect the treatment of atopic eczema, so it is useful to understand them if you or your child have eczema.
The disagreement begins with the question of what causes atopic eczema.
Let’s start with the one point that everyone agrees on: dry skin plays a fundamental role. Those with atopic eczema have dry skin, not just in the eczematous areas, but in other parts as well, sometimes all over the body. The skin cells are less efficient than normal skin cells at retaining water.
Everyone would also agree that there is inflammation of the skin – a reaction that is produced by the immune system. But when it comes to the question of what starts off the inflammation there are huge differences of opinion among specialists treating atopic eczema – these specialists include dermatologists, allergists and paediatricians.
Since people with atopic eczema are atopic (allergy-prone), and most have
huge amounts of the allergy antibody, IgE, going round in their blood, it might
seem plausible that an allergic reaction to some external item kicks off the
inflammation. And when skin-prick tests (see p. 91) to common allergens such
as house-dust mite are tried, there are usually a large number of positive results.
But many of these turn out to be false positives – when tested more directly,
the allergen concerned does not actually play a part in causing the skin symptoms.
This has led some specialists working with eczema, mainly dermatologists, to
What the words mean
Eczema is not a disease in itself. The word refers to a certain type of reddish rash — a rash which can be caused in a variety of ways. The type of eczema that affects people of an allergic disposition (atopics), is called either atopic eczema or atopic dermatitis.
The word dermatitis just means inflammation of the skin. Most doctors consider it to be synonymous with eczema, but some give it a slightly broader meaning.
believe that allergic reactions play little part in either initiating or perpetuating atopic eczema. In their view, the basic cause of atopic eczema is dry skin and a generally overwrought immune system, not specific allergic reactions.
To some of these doctors, positive skin-prick tests are all false positives in atopic eczema – that is, irrelevant to the disease process. A positive skin-test result, in their opinion, simply indicates that the skin of atopic eczema sufferers is in a highly sensitive state, not that the allergen concerned plays any causative role.
Allergists tend to take a different view of this, as you might expect. And recent research shows that they are correct – allergens often do play a significant part in provoking atopic eczema.
Research using direct challenge tests (see p. 90) has identified some of the things that could provoke such sensitivity reactions:
• house-dust mites, pollen or moulds
• cats, dogs, rabbits and other furry pets
• cow’s milk or other food – a prime suspect in babies and young children (see p. 68). The response to food is usually delayed, occurring some hours after the item is consumed.
With mite, pollen and pet allergens, the eczema symptoms can be provoked either by allergens falling on the skin, or by direct contact (e.g. mite allergens in the bed, skin contact with pets, or lying on grass for those with grass-pollen allergy).
The rash tends to occur on skin not covered by clothes, as you would expect. But it can sometimes occur only on particular exposed areas – usually the most sensitive areas of skin. For example, there are people who react to house-dust mite but have eczema on the eyelids only.
Additionally, experiments show that even when an airborne allergen is only inhaled it can sometimes provoke eczema symptoms. The allergen probably reaches the skin in the bloodstream. (Alternatively, it might provoke an immune reaction in the airways which generates chemical messages of the kind that promote inflammation – these then reach the skin in the blood.) This means that the skin reaction could occur anywhere on the body, not just on exposed skin.
In the case of food, the molecules of food that cause the trouble are probably being absorbed from the stomach without being completely broken down. They then reach the skin via the blood to provoke a reaction there. (Or, again, it could be an inflammatory messenger chemical travelling from the gut to the skin in the blood.)
When food gets directly onto the skin – which it frequently does with small children, of course – it can provoke a reaction that way too. This may be a slow eczema-causing reaction, or a much faster reaction known as contact urticaria (see pp. 50-51). Reacting to food with contact urticaria is quite common in children with atopic eczema – but the same food doesn’t necessarily provoke atopic eczema when it is eaten. (However, eating these foods can sometimes trigger anaphylaxis – see pp. 58-9. They should therefore be treated with great caution.)
At the same time as all this research – which shows for sure that allergens play a part in atopic eczema – others have been asking what actually happens when skin reacts to an allergen. Their studies have turned the accepted understanding of allergies upside-down. They show that when something like egg or pollen provokes atopic eczema, what is occurring isn’t necessarily an allergic reaction of the usual sort, with IgE and mast cells (see
box on p.12). Instead, other immune cells are causing the trouble. Sometimes IgE is involved, but without mast cells. Sometimes neither is involved. These revolutionary discoveries are described in more detail on pp. 18-19. One interesting realisation from this research is that in different eczema sufferers, different immune reactions may be producing the rash – even if they are reacting to the same allergen! This helps to explain why the results of skin tests are so inconsistent and puzzling.
The wandering rash
For a baby with atopic eczema, the face, and especially the cheeks, are commonly affected, but there may be a rash all over the legs, the backs of the arms, and the back. As the months go by, the rash settles on the lower legs, and spreads to the fold of the elbow, and then the fold at the back of the knees — by about three years of age, this flexure eczema is the main problem for most children.
In adults, eczema is often found in quite restricted areas, such as the hands, scalp, lips, eyelids or chest. It may be located around the nipples — a sensitive spot where rubbing by clothing is enough to initiate a rash.
Atopic eczema is always in a process of change, and different parts of the body may display different stages of the rash:
• The rash is red and usually dry at first, and there may be not a great deal to see. In this early stage the visible signs may be minimal, while the itchiness can be colossal. Sometimes there is oozing of clear fluid.
• Occasionally the first phase is more marked, with dense patches of small red bumps or tiny blisters. On the hands, these may merge to form larger blisters.
• Infections tend to change the appearance of the rash (see p. 44).
• With time the skin becomes thicker, paler and scaly. It may form leathery patches (called lichenification), especially if there is habitual scratching or rubbing. This is chronic eczema.
• When the eczema clears, there may be an area of skin that is lighter in colour, or darker, than the surrounding skin.
The next step
Whatever causes atopic eczema, it provokes the most horrendous itching, as every eczema sufferer knows. The itch cries out to be scratched, and scratching is the major cause of the visible rash. If left untouched, the skin does not erupt into eczema, although it may well turn red, and there are still distinct changes in the skin that can be seen with a microscope.
Once eczema has erupted, the skin is no longer an intact protective layer that neatly separates ‘in-here’ from ‘out-there’. The skin becomes more permeable and loses its own natural moisture far more readily, so the dryness gets worse. At the same time allergens and irritants penetrate far more easily, causing yet more inflammation.
Something else compounds the damage: once atopic eczema is established, the immune system starts making IgE antibodies to the body’s own proteins, especially those found in skin cells. This helps explain why atopic eczema can become so severe and so entrenched.
Infections — another vicious circle
When eczema erupts and the skin barrier is breached, infections often become a problem. A regular source of trouble is the bacterium Staphylococcus aureus, a cause of the infection impetigo. This microbe invades eczematous skin far more readily than healthy skin, causing a prolific ooze with golden-yellow crusting.
Staphylococcus aureus produces a toxin known as a ’super-antigen’ which revs up the immune system to even more furious effort. This effort does not, unfortunately, oust the bacteria, but it does make the skin inflammation even worse. To add to their woes, many who are afflicted with atopic eczema start making IgE antibodies against Staphylococcus aureus toxins.
Infection with fungi (yeasts and moulds) is also a problem in atopic eczema (see p. 49), and there may be sensitivity reactions to these fungi.
The herpes virus, responsible for causing cold sores, can also invade eczematous skin, though this is much rarer. It worsens the eczema and produces fever and general weakness. There may also be flocks of small red bumps, each with a tiny dimple or blister at the centre. Any symptoms of this kind indicate that the patient needs urgent treatment.
Irritants and stress
People with atopic eczema are far more susceptible to everyday irritants such as wool and rough synthetic fabrics, soap, and traces of detergent left behind in clothes. Chlorinated water, either in swimming pools or from the tap, can also aggravate the skin, and even ‘hard’ water (found in areas with chalk or limestone bedrock) may be a factor.
Some air pollutants may play a part in atopic eczema. Researchers in Germany have found that children living close to busy trunk roads, or in homes with a gas cooker and no extraction hood (see pp. 128-9), were more likely to develop eczema. Formaldehyde fumes, often found in modern houses (see p. 129), are sometimes a factor when eczema affects the face and hands.

A blocked or runny nose in Allergy
THAT LASTS ALL YEAR
`Everyone has heard of hayfever, but it’s news to most people that you can have this sort of problem all year round,’ complains Elizabeth. ‘Before we got the treatment sorted out, Benny was “the kid with the constant cold”, and I did notice other mothers looking less than enchanted at the prospect of his coming over to play.’
Benny suffers from allergic reactions to house-dust mites and cats which cause hayfever-style symptoms (26) all year round. This condition doesn’t even have a common name – the medical one is perennial allergic rhinitis – yet it is one of the most common allergic diseases.
Any airborne allergen that is found in the air all year round can cause perennial allergic rhinitis:
• House-dust mite is the number one suspect in most parts of the world. Particles from other insects, such as midges and mosquitoes outdoors, and cockroaches, house flies, bloodworms (used for fish food) or carpet beetles indoors, can also cause nasal allergies.
• Mould spores can be the problem: they are found both indoors and out.
• In some regions, certain types of pollen are airborne all year round (27).
• All pets other than fish produce allergenic particles (even snakes).
• Allergens encountered at work (133) can also produce symptoms in the nose. This is a warning sign gn you should not ignore – it often means that occupational asthma is on its way (132).
Occasionally, the offending substance is being eaten not inhaled. This is less common, so you should investigate inhaled allergens first, before trying an elimination diet (29).
Skin-prick tests (91) will help to identify any airborne allergens that are responsible, but where food is the culprit, skin-prick tests are often negative (69)
Triad and NARES
Diagnosis of perennial allergic rhinitis is complicated by the fact that there are two other conditions – called triad and NARES – which produce similar symptoms and involve the immune system but are not, strictly speaking, allergies.
Triad is so called because it involves three distinct symptoms:
• perennial rhinitis
• polyps in the nose – little fleshy growths that can kill your sense of smell
• asthma.
People with triad tend to collect all three symptoms gradually, in no fixed order, over a period of years or even decades. Many are sensitive to aspirin and related drugs, and almost everyone with triad develops this sensitivity eventually.
Aspirin sensitivity can come on very suddenly and produces a reaction akin to anaphylaxis (101). This can be fatal, so it is probably best to avoid all aspirin-like drugs if you have triad, even though you have not reacted to aspirin in the past Aspirin-like drugs are found in painkillers, arthritis drugs and cold remedies – check with a pharmacist before you buy (151).
If you have asthma, think twice about operations on the nose to remove polyps – they can make the asthma much worse.
The initial letters of Non-Allergic Rhinitis with Eosinophilia have been stretched a bit to get NARES. (This is a medical joke –the Latin word Hares means nostrils.) The problem is caused by eosinophils (19), which flock into the nose and cause severe inflammation. Some people with NARES go on to develop triad.
Collateral damage
Having the nose swamped with mucus can lead to knock-on problems in the ears, sinuses and airways.
If the tube that leads from the ear to the nose (the Eustachian tube) becomes blocked, then fluid cannot drain away from the middle ear. This is called secretory otitis media, or glue ear - it dulls the hearing and causes an unpleasant ‘popping’ sensation. The ears may also feel blocked and itchy, but if children have had this problem since they were tiny they may not complain because they assume that’s just the way ears are supposed to feel. Deafness is often the first sign anyone notices.
Sinusitis is another possible complication, because fluid from the sinuses should also drain into the nasal cavity. With the ouflow blocked, mucus builds up in the sinuses and can become infected by bacteria (30).
Post-nasal drip can also occur with perennial allergic rhinitis. The over-abundant mucus runs down the back of the nose, into the throat and then the airways. This produces a persistent phlegmy cough, which may occasionally be mistaken for asthma.
When the rhinitis is treated effectively, all these problems should sort themselves out, although additional treatment is usually necessary in the case of persistent sinusitis (33).
Treatment
Where an allergen such as house-dust mite or mould spores has been identified as the source of the problem, eradicating it from your house (see Chapter 4) will make a huge difference, and may avoid the need for drugs. If the allergen is unavoidable, immunotherapy (see pp. 164-8) or some alternative form of desensitisation (see pp. 210-13) could be very helpful.
Where drugs are needed, nose drops are best. They get the drugs right to the target so doses are minimal, which means very few side effects. The drugs used are:
• cromoglycate to prevent the allergic reaction before it starts (148)
• antihistamines to block the allergic reaction before it produces inflammation (138)
• steroids to calm down inflammation (144). Steroid nose drops are also useful for NARES and triad. If you are taking steroid drops continuously, your doctor should check the membranes inside your nose every six months. Make sure you put the drops in correctly, especially if you have polyps (144).
If you suffer stinging, burning or dryness, it might be due to preservatives in the drops, not the drug itself (see box on p. 33), so talk to your doctor about a different formulation.
Don’t use over-the-counter decongestant drops: they do nothing to treat the allergy or inflammation, and are little more than a ‘chemical crowbar’ to open up the nose. Your nose gets addicted to them in a few days, and when you stop using them you get ‘rebound congestion’ - absolute and total blockage. It does wear off eventually, but is unpleasant meanwhile. If you are suffering this problem at this very moment, don’t put more decongestant drops in - your nose needs to go ‘cold turkey’ to recover, not have its addiction fed!
If none of the anti-allergy drugs work, but decongestant drops do, then you probably have a non-allergic disease called vasomotor rhinitis. The symptoms are very similar to allergic rhinitis, but without the sneezing and itching. See your doctor again, because there is an effective treatment that uses anticholinergic drugs (see box on p. 156). Acupuncture (see below) can also be helpful.
An elimination diet (194) will diagnose any food reactions. It works wonders for some people with severe and unexplained perennial rhinitis, Including people with such a flood of mucus that they can scarcely work or live normally. You should certainly give this diagnostic diet a try if there are clues that suggest food is the culprit (69) or if no airborne allergen can be identified. Yeast - found in bread, beer and B-vitamin tablets -is quite often the culprit in rhinitis, but it could be any food.
Acupuncture is worth trying, to reduce the blockage in the nose and stem the flow of mucus, because the autonomic nervous system (see box on p. 235) plays some part in the symptoms of allergic rhinitis (and is the sole cause of the symptoms for those with vasomotor rhinitis). For those with severe sinusitis, osteopathy can be good for draining mucus from the sinuses.
Very occasionally, psychological or emotional reactions play a part in perennial allergic rhinitis, with symptoms getting significantly worse during stressful events. One possible manifestation of this is post-coital rhinitis, where sex brings on rhinitis (and sometimes asthma as well). In such cases, psychotherapy should be considered. (But check you are not just allergic to the dust mites in your bed first…)
A nose by any other name…
Rhinitis means inflammation (-itis) of the nose (rhin-). The same Greek word gives us rhinoceros - ‘nose-horn’.

Cross Reactions in Allergy

For the rabbi’s doctor, discussing the results of the allergy tests with his patient, it was an embarrassing moment. An allergy is not inborn, it is an acquired reaction — a response by the immune system to a substance it has already encountered at least once. So, in theory, nobody can be allergic to a food they have never eaten.
Naturally enough, the rabbi had never eaten shellfish - like pork, it is a forbidden food in Judaism. But the nurse carrying out the skin-prick tests was unaware of this, and she had been told to test for all the common food allergens, so shrimp allergen was included. The test came up positive.
Fortunately, the rabbi had also been tested for inhaled allergens and had given a very strong positive reaction to house-dust mite. The likely explanation was clear: the rabbi had formed antibodies to a muscle protein of house-dust mite called tropomyosin, which is also found in shrimps and prawns. His antibodies against house-dust mite had cross-reacted with shrimp tropomyosin.
This does not mean that everyone who is allergic to house-dust mite will also react to shrimp. Firstly, they must have made antibodies to tropomyosin, rather than some other dust-mite antigen. Secondly, the antibodies must be recognising a particular feature of dust-mite tropomyosin that closely resembles (chemically speaking) a particular feature of shrimp tropomyosin.
The important point about antibodies is that, on the one hand, they achieve results by being specific for their antigen , but on the other, they do make mistakes. In the case of allergies, this is sometimes an added problem for patients but is rarely life threatening. More seriously, there are other conditions, like coeliac disease, where cross-reactions initiate attacks on the body’s own components, causing severe symptoms.
Antibodies make mistakes because they recognise antigens by homing in on tiny chemical markers, not by looking at the antigen as a whole (see box on p. 15). Although this is a nuisance for allergy sufferers, it can be a bonus in fighting diseases. For example,
Antigens and allergens
An antigen is anything which elicits an antibody reaction. Each antibody is specific for a particular antigen.
When they tend to cause allergies (by provoking IgE antibodies rather than other kinds of antibody -  these antigens are called allergens. Something such as grass pollen is both an antigen (because it elicits an antibody reaction) and an allergen (because it often elicits IgE antibodies in those who are allergy-prone).
when viruses (such as those that cause influenza) revamp their outer coat proteins to evade the immune system, the chances are that some antibodies will still recognise them because a few of the original chemical markers persist.
Understanding cross-reactions
Many cross-reactions are between related species, and this makes sense in biological terms. The tropomyosin story is a good example - not only is tropomyosin found in dust mite and shrimps, but it also occurs in other crustacean shellfish, such as crabs and lobsters, in molluscan shellfish such as clams and oysters, and in insects. If one goes back over 300 million years, all these animals were just a twinkle in the eye of some primeval invertebrate, the common ancestor of them all.
Tropomyosin is one of those triumphs of the evolutionary process - a protein that reached near-perfection hundreds of millions of years ago, in the long-vanished ancestral species, and remains so good at its job that it has only been tinkered with by natural selection since then, never radically altered. In other words, because it works so well, it has been ‘conserved’ by the various animal groups descended from the shared ancestor. Although there are some differences between the tropomyosins from different descendants, the similarities are considerable.
Relatedness counts here. Shrimps and prawns are pretty closely related, as anyone can see by looking at them. Their tropomyosins are extremely similar, as are many other allergens. You’re unlikely to be allergic to prawn but not shrimp. The more distant the relationship, the more differences accumulate in the antigens, so a cross-reaction between dust mite and shrimp is far less likely (the rabbi was unlucky).
Another conserved protein, parvalbumin, explains why people who are allergic to one type of fish are usually allergic to all kinds of fish (in spite of the fact that fish belong to several different families which are only distantly related). Those allergic to hen’s eggs will probably be allergic to the eggs of all birds, because the primary allergens (e.g, ovalbumin) are so similar.
These conserved proteins produce cross-reactions across huge gulfs, in terms of zoological and botanical relationships. Far more easily understood are the cross-reactions between close cousins, such as dust mite and storage mites, wheat and rye, pine pollen and pine nuts, or ragweed and sunflower (both members of the daisy family).
Relatedness can be useful in explaining cross-reactions, but often fails when it comes to predicting them. Some related species do not show as many cross-reactions as one might expect. Peanuts are legumes, and highly allergenic. One would expect some peanut-allergic individuals to be allergic to other members of the legume family, such as peas, beans, carob and soya. In fact, although some patients give positive skin-prick tests, very few show actual symptoms when they eat these foods. Where symptoms do occur, they tend to be mild.
Paradoxically, those who are allergic to peanuts very often develop an allergy to tree nuts, and this usually spans several different kinds of tree nuts – yet botanically all these are very distant relatives. No tree nut is a legume and while walnuts and pecans belong to one plant family, almonds belong to another, hazelnuts to another, cashews to a fourth, and Brazils to a fifth different plant family. Here relatedness seems irrelevant, and it is shared lifestyle (surviving as a nut-producing plant) that is crucial.
A nut is just an over-sized seed that has to survive being buried in the soil – either by the plant itself (in the case of peanuts) or by a nut-eating animal such as a squirrel. All nuts must resist rotting in the soil until the following spring, and therefore contain powerful bactericidal and fungicidal compounds. Some of these may have chemical similarities that cause cross-reactions.
These functional ‘lifestyle’ allergens of nuts may be even more widely shared, with many seeds having something similar: recent research shows potentially cross-reacting allergens in wheat, rye, hazelnuts, sesame and poppy. It is interesting that many of those developing new allergies to sesame or poppy are already allergic to wheat and nuts.
A few cross-reactions seem to defy any explanation, such as that between house-dust mite and kiwi fruit – this appears to be just a case of chemical coincidence. Other cross-reactions can appear equally bizarre but actually have a biological basis, notably that between latex (as used in medical gloves) and various fruits and vegetables, principally chestnut, banana, avocado and kiwi fruit. This cross-reaction is due to a shared enzyme called a chitinase that protects plants against insect pests. Latex, of course, comes from the sap of the rubber tree: the tree needs such insect-protection and its sap is richly laced with chitinase.
How antibodies work - and why they make errors
Antibodies are catapult-shaped, with two antigen binding sites at the ends of the two arms. The other end of the antibody molecule – the handle of the catapult – is free to bind to cell receptors.
When an antibody binds to its antigen there is a ‘chemical handshake’: a very specific recognition event involving one of the antigen binding sites and a particular small site on the antigen molecule called the epitope. The two lock together. Different antibodies may recognise different epitopes.
The antibody is recognising its antigen, but it is as if we recognised other people by homing in on one small part of them, choosing a different feature for each person, whatever is most distinctive about them – the quirky right eyebrow, the hook in the nose, or the mole on the cheek. The antibody does not ‘look at’ the whole antigen molecule, but simply recognises a characteristic cluster of chemical features at the epitope.
Cross-reactions can occur so readily because an antigen molecule only has to resemble another molecule in one or two small areas (the epitopes) for a mistake to occur.
antigen antibody molecule binding sites
cell receptor antigen molecule
epitope
surface of immune cell
(e.g. a mast cell)

Allergies and
inheritance
WHY IT RUNS IN
FAMILIES
`My father had asthma as a child, and his sister had it too. In fact she died from it. My mother has never had any allergies, but one of her brothers had terrible hayfever all his life. Out of us four, only my brother Peter is completely allergy-free. I had bad eczema when I was small, as did my sister. So when our son developed eczema, and then asthma, and an allergy to house-dust mite which made his nose run all the time, I wasn’t entirely surprised.’ What Janet’ is describing is a good example of an atopic family — one where classical allergies, of one kind or another, affect several family members. The members of such a family are called atopics.
Atopics have an underlying tendency to allergy which, with luck, may never be expressed. But if they are unlucky, the tendency will lead to allergies, which can settle on the skin (atopic eczema), the nose (hayfever or perennial allergic rhinitis), the airways (asthma) or the mouth and digestive tract (food allergy). These diseases, which recur down the generations in atopic families like Janey’s, are known as the classical allergic diseases.
The atopic tendency is coded into our DNA –in the genes that are passed from parent to child. There are also other genes that make asthma more likely to develop, and these can work in concert with the allergy-promoting genes to produce asthma in a child. And there are probably genes for dry skin, which contribute to atopic eczema.
Genes alone are not enough, however. Environment (which means, in medical terms, everything external that affects an individual,
including diseases, diet, air, allergens such as dust mite or pollen, and even medical treatment) also plays a large part in promoting allergic reactions. In other words, genes and the external world interact to produce allergic disease. What happens in the months and years immediately after birth seems to be a crucial element.
This helps to explain why allergies are on the increase even though we are, genetically speaking, not so different from our grandparents or great-grandparents. It is also a cause for optimism, since it means we can largely reverse the trend in coming generations. All we have to do is adjust the environment, especially for newborns and young children. Luckily, most of the problem factors are ones over which we have personal control, such as smoking by parents, diet, infant feeding, hygiene (less is better), antibiotic treatment, house design and furnishings Generally speaking, inherited traits such as height or skin colour are governed, not by a single gene with a large effect, but by a great many genes each with a small effect. This is called multi-gene inheritance. The many small effects add up to produce the final outcome. Atopy is probably inherited in a similar way, which would explain why some people have a very strong tendency to allergies (they have lots of the wrong genes) while other people have only a mild tendency (they have just a few).
Current estimates hold that at least twenty different genes are involved in determining atopy. This means that no two atopic individuals are going to be quite the same, because each will have a different combination of the possible variants on these twenty genes. In the words of Dr Vincent Beltrani, of Columbia University, New York, ‘it is not surprising that, as a result of all the possible genetic combinations and permutations, each atopic individual possesses a unique “allergic fingerprint” and that not all atopic individuals have identical findings’.
Multi-gene inheritance has another important effect, in terms of predicting who will develop allergies. The genetic risks from the two parents add up, so if both parents have allergies themselves or come from atopic families, the risks of the child developing allergies are much higher than if only one parent is atopic. The actual figures are uncertain because the results vary considerably from one study to another. If one parent is atopic, the risk can range from 20% to 58%, whereas if both parents are atopic, the risk ranges from 50% to 80% or even more.
Note that these are just risks: there are no certainties here because the actual mix of genes that a child receives is a selection – half of the mother’s genes and half of the father’s. There’s no saying which half a child gets, because this is a random selection process, similar to the shuffling and dealing of playing cards. Luck plays a big part.
Naturally enough, both atopic parents and their doctors have asked whether there is any test that could assess the number of pro-allergy genes in a newborn and so predict the chances of allergy developing in particular children. That would allow more stringent anti-allergy measures  to be taken for the children most at risk.
Various tests have been tried, and one does work, to a limited extent. It involves measuring the level of the allergy antibody, IgE, in a blood sample taken from the umbilical cord just after birth. Very high levels of IgE give some indication of the chances of allergies developing later, but the accuracy of the prediction is, unfortunately, not that good when the test is carried out in atopic families. The test doesn’t reveal much more than is already known – that the baby has atopic parents.
This same test, when carried out on newborns who are not from atopic families, sometimes gives a much more useful and accurate result. In one study, 75% of those babies with high levels of cord-blood IgE developed allergies a few years later, compared to only 6% of those with low levels. Unfortunately, the test does not always give such impressive results, and some disappointing studies have led doctors to conclude that it is not worthwhile as a standard test for all newborns.
This finding of high IgE in children from non-atopic families highlights an important point: pro-allergy genes are everywhere. A lot of healthy people have them, but at levels which do not cause any symptoms – yet. This explains why, with the allergy epidemic, many new allergy sufferers are coming from families never affected by allergy before. As our lifestyle becomes more pro-allergy, a baby needs fewer of the pro-allergy genes to grow into an allergic individual.
Other forms of sensitivity
The multi-gene inheritance of classical allergy is very different from the inheritance of diseases such as primary lactase deficiency  where there is a single gene that is at fault. Generally, speaking, all metabolic abnormalities are inherited in this straightforward way, so they are an all-or-nothing affair: one child in the family gets the defective gene while another does not. No environmental triggers are needed to activate the defect.
In the case of food intolerance, if minor metabolic abnormalities play a part, as they may do for some sufferers, then there could be inheritance of the defect, but this will not necessarily lead to symptoms unless other intolerance-promoting factors (such as disturbed gut flora) are present. Those who suffer from both food intolerance and chemical intolerance (also called chemical sensitivity) are the most likely to have metabolic abnormalities, and it is interesting that such problems do sometimes affect several members of the same family. (Doctors who are sceptical about such diseases will dismiss this as simply ‘learned illness behaviour’ among family members, a theory that is difficult to test without a lot of expensive research.)
Inheritance plays a part in several other forms of sensitivity. It is very important, for example, in coeliac disease and dermatitis herpetiformis , which both stem from the same genetic feature. They are only expressed when wheat is eaten but the timing is important here – introducing wheat into a child’s diet later, rather than during the first year of life, seems less likely to provoke the disease. When coeliac disease comes on in adult life, it suggests that some other environmental trigger was needed, in addition to eating wheat, to start off the disease process.