Posts Tagged ‘atopic eczema’

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.

Various anti-allergy drugs
An allergic reaction is a lengthy, complex process, and the various anti-allergy drugs all work on different stages of that process. That is why it often makes sense to use several different drugs for the same allergic condition: they each tackle the problem in their own way.
Steroids (see p. 140) intervene at a very late stage, quelling the inflammation that follows on from an allergic reaction. Using a steroid is rather like calling the fire brigade to put out a fire, whereas using an antihistamine (see p. 138) is like having fire-proof doors, to prevent the fire spreading at an early stage. Cromoglycate-type drugs (see below) intervene at an even earlier stage. They are like basic fire prevention - teaching children not to play with matches, or fitting smoke detectors.
Anti - leukotnene drugs (see p. 149) work at roughly the same stage of the process as anti-histamines but tackle an entirely different aspect of the allergic reaction.
Cromoglycate-type drugs
These drugs are also referred to as mast-cell stabilisers or mast-cell Mockers.
There are three drugs in this group, sodium cromoglycate (also spelled cromoglicate), nedocromil sodium, and lodoxamide. All operate at an early stage of the allergic reaction, stopping it before it actually starts. They stabilise the outer membrane of the mast cells (see box on p. 12), which prevents the allergic response from occurring.
Some common brand names
Common brand names of cromoglycate-type drugs include:
inhalers - Cromogen Easi-Breathe, Intal, Tilade
eye drops - Hay-Crom, Opticrom, Rapitil, Vividrin, Viz-on nose sprays - Rynacrom, Vividrin
capsules - Nalcrom
This is a far more satisfactory way of dealing with an allergic reaction than trying to tackle it after the reaction has occurred. But from a purely practical point of view, it has a drawback. I order to work at all, these drugs must reach the mast cells in advance of the allergen. They are of very little use if taken after the allergic reaction has begun.
For those who are taking cromoglycate-type drugs on a regular schedule, several times a day, it is very important to be conscientious about taking them on time. This maintains the protective effect of the drug, without any gaps.
If you are using these drugs on an ‘as-needed’ basis, you should take them 30 minutes before an allergen is encountered. or 30 minutes before a bout of exercise, if they are being prescribed for exercise-induced asthma. (Note that children sometimes respond differently, getting protection from these drugs immediately.)
The effect of these drugs takes time to build up. You should take them regularly for at least four weeks before deciding whether they are helping you or not.
One point in favour of cromoglycate-type drugs is that they are extremely safe, with few or no side effects in most people. Sadly, they do not work for everyone. A fairly high percentage of children respond well to them, but the response rate is much lower for adults. Nevertheless, adult allergy sufferers, especially those who need steroids to control their symptoms, should always be given the opportunity to try out these drugs. When cromoglycate-type drugs do work, they are very effective and almost always trouble-free, so they are a good alternative to steroids.
Both sodium cromoglycate and nedocromil sodium are available in inhaler form for asthma (see p. 157). Sodium cromoglycate is also available as nose drops for hayfever and other nasal allergies.
All three drugs are available as eye drops. Recent evidence suggests that sodium cromoglycate drops are less effective than the other two, particularly for the treatment of severe allergic conjunctivitis (inflammation of the eye).
Sodium cromoglycate is available in capsule form for food allergy. Note that these capsules are of very limited value in food allergy, and are certainly not a substitute for food avoidance. They do reduce sensitivity a little and can sometimes be helpful for those with multiple food allergies (see p. 67).
Side effects
There are no serious side effects at all for nedocromil sodium. cromoglycate can, very rarely, cause joint pain and swelling. An allergic reaction to the drug itself is even more uncommon. Stop taking the drug and see your doctor promptly if either of these occurs.
The only other side effects that have occasionally been reported are headache, nausea and vomiting. None of these indicates any damaging effect by the drugs – they are all minor side effects.
Eye drops containing these drugs may cause stinging and burning when inserted, but this is a minor side effect and usually wears off. Flushing and dizziness have sometimes been reported with lodoxamide eye drops.
Nose drops may also cause local irritation. This could be due to the drug itself, in which case it is a minor side effect. Alternatively, the irritation may be due to the preservative used or some other non-drug ingredient (see box on p. 33).
Occasionally cromoglycate nose drops cause bronchospasm – contraction of the airway muscles – but this tends to wear off quite quickly. Bronchospasm can also occur when cromoglycate-type drugs are inhaled (see p. 157).
Anti - leu kotriene drugs
These drugs, which have a set of very specific effects (see p. 159), were originally designed to treat asthma. Their potential for treating other allergic diseases is currently being explored:
•    Several studies show that they work well for perennial allergic rhinitis brought on by allergens such as house-dust mite. They also have some effect on hayfever, but standard treatment (such as antihistamines plus a steroid spray for the nose) is more effective.
•    They are especially useful for both rhinitis and asthma in patients suffering from triad (see box on p. 28). Research shows that they also reduce asthmatic reactions to very small test doses of aspirin, but they don’t give protection against anaphylaxis brought on by normal doses.
•    They have also been used successfully in cases of chronic urticaria and for some patients with delayed pressure urticaria. It seems plausible that they would also be helpful for chronic urticarla linked to aspirin sensitivity.
•    Preliminary trials suggest that these drugs might be useful in atopic eczema. Some studies show a very good response that allows a reduction in steroid creams.
•    Montelukast works very well for eosinophilic gastroenteritis and eosinophilic oesophagitis (see p. 72), according to some new studies.
For side effects of these drugs see pp. 159-60.
Anti-IgE drugs
Since the antibody IgE (see box on p. 12) is such a crucial player in allergic reactions, developing drugs that disable this antibody should help allergy sufferers. The first such drug is omalizumab (brand name Xolair) which was licensed for use in the United States in 2003. It is expected to become available in Britain some time in the next few years.
Omalizumab binds to IgE antibodies and stops them from interacting with mast cells, so blocking any allergic reaction. The drug is given as a ‘depot injection’, just under the skin, every 2-4 weeks. It is gradually released from the injection site and moves around the body in the blood, mopping up IgE molecules.
At present, omalizumab is used for severe hayfever and for people with asthma who are not responding well to the usual treatments. It is only worth using if there is clear evidence that allergies play a part in the asthma. Patients who use omalizumab are often able to reduce their dose of inhaled steroids – and they suffer fewer serious asthma attacks and have better lung function. Some patients can even stop using steroids completely.
Other anti-IgE drugs are in the pipeline. Pilot studies show that one works very well for peanut allergy: after just four injections, sensitivity to the allergen falls sharply, reducing the risk of anaphylaxis from traces of peanut eaten accidentally.
More powerful anti-allergy drugs
Occasionally people with severe allergies, who are on constant high doses of steroid tablets, or who fail to respond to steroids, need treatment with powerful anti-inflammatory drugs, such as methotrexate or cyclosporin. These suppress the immune system, and extremely careful monitoring for side effects is needed.
Adrenaline (epinephrine)
Anyone who has suffered anaphylactic shock (see p. 58) should be carrying a special syringe, called an auto-injector, loaded with adrenaline. The injector is very simple to operate and is designed for emergencies. Most allergy sufferers, even children, can give themselves the injection – or a parent or other adult can give it.
Some asthmatics, and those with food allergy who suffer swelling of the throat, may be given adrenaline in inhaler form as well (see pp. 155-6). This can be useful as an additional treatment but it’s definitely not a substitute for an injector.
See pp. 98-9 for instructions on using adrenaline in a crisis.
Wherever you go, take your injector with you. Always keep it close at hand: you need to be able to use it within minutes of the allergic reaction starting. You may be unable to speak (and therefore unable to ask someone else to fetch it) quite soon after the attack begins. The injector must never be refrigerated. It can also be damaged by sunlight and excess heat.
If you live in the countryside or in an area with a poor ambulance sevice, or if you are going camping or hiking somewhere remote, ask your doctor for a second injector, or one that can deliver multiple injections. Also ask about the maximum number of injections that can be given, and never exceed this total. Some doctors believe everyone should have two injectors, just in case the first dose doesn’t do the trick and help is slow in coming.
It is vital that you are shown exactly how to use the auto-injector. Canadian researchers discovered that only one in four
Some common brand names
Common brand names of adrenaline preparations include: auto-injectors – Anapen, EpiPen
inhalers – AsthmaHaler Mist, Bronkaid, Epiphrine
health professionals got the technique correct when demonstrating how to use an auto-injector In this study, pharmacists were much the best as regards accurate instructions. Dummy injectors are useful for training purposes and most pharmacies have them.
When the adrenaline auto-injectors expire, they can be very useful for practising with, or for showing a new baby-sitter or teacher – practise on an orange or grapefruit.
If you are taking beta-blockers (e.g. for a heart condition or anxiety), adrenaline may not have much effect.
Heavy daily use of beta-2 relievers for asthma (see p. 152) will also make adrenaline less effective when you need it.
Side effects
The important side effects of adrenaline involve the heart. Anyone with a heart condition should be given special advice in advance by their doctor about using adrenaline. The same goes for people with diabetes, hyperthyroidism or high blood pressure, and anyone taking tricyclic anti-depressants. There are quite a few minor side effects from adrenaline, such as anxiety, trembling, nausea. sweating, dizziness and cold extremities. These soon wear off.
Drugs that can make you worse
Aspirin and its relatives have a very bad effect on some people with rhinitis and/or asthma (see box on p. 151). Unfortunately, recent research shows that paracetamol is not safe either. It makes asthma more likely to develop in those who do not yet have the disease, and increases the severity of asthma symptoms for those who do. Unlike aspirin, paracetamol affects everyone, because it lowers the levels of a natural antioxidant, called glutathione, which the body makes to protect the lungs from oxidants. The greatest effects are seen in people who take paracetamol regularly (once a week or more), but even an occasional dose makes some difference.
All the other drugs that can make you worse are prescription drugs, and your doctor should be alert to the dangers. But doctors are overworked and sometimes forget, so it is sensible to know about the risks for yourself. If you have any doubt about the drugs you are taking, ask a pharmacist.
Beta-blockers are a major hazard for people with allergies. They can make the airways contract, and can bring on a serious asthma attack. They also make anaphylaxis more likely in someone who already has allergic reactions (see p. 59) and they increase the risk of a severe reaction to
immunotherapy (see p. 166) or skin-prick tests (see p. 91). Beta-blockers are prescribed for high blood pressure, angina and other heart problems, migraine and thyroid disease. There are alternative drugs in all cases. Sometimes asthma develops in people who have been taking beta-blockers for years. The beta-blockers are not responsible for this, but once asthma has begun, they will make symptoms worse. Eye drops for the treatment of glaucoma may also contain beta-blockers and can have a bad effect on asthmatics.
ACE inhibitors, used for heart conditions, may cause a cough and airway narrowing. They may also increase the risk of a severe reaction to immunotherapy.
Female hormones affect asthmatics, so taking the contraceptive pill or hormone replacement therapy (HRT) may make asthma worse. Progesterone-only contraceptive pills tend to cause fewer problems.
The drug isoniazid (INH), prescribed for tuberculosis, makes the body far more susceptible to histamine in foods (see p. 200).
An allergic reaction to a specific drug (e.g. penicillin) can also occur in some people, resulting in urticaria, or even anaphylactic shock.
Aspirin sensitivity
Aspirin sensitivity is not an allergic reaction, because neither IgE nor mast cells are involved. What causes this problem is a metabolic abnormality — a malfunction in one aspect of the body’s chemistry. The details of this are very complicated: you may want to skip the next three paragraphs and
simply read about how to cope with the problem.
The exact nature of aspirin sensitivity is still far from clear, but it seems to involve a relatively poor production of prostaglandins, combined with a plentiful production of leukotrienes. Both these substances are messenger chemicals which, broadly speaking, promote inflammation. But the details of their pro-inflammatory activities differ. It seems that, ideally, the body should have a harmonious balance between the two, and an imbalance produces problems.
Both prostaglandins and leukotrienes are manufactured from certain fats that are found in the diet. These fats, the raw materials, are worked on initially by two different enzymes — one that leads to the production of prostaglandins and another that leads to the production of leukotrienes.
If one of these enzymes is defective, it may mean that the other is oversupplied with raw materials, resulting in a serious imbalance between prostaglandins and leukotrienes. In those with aspirin sensitivity, or at risk of developing aspirin sensitivity, the enzyme that produces prostaglandins seems to be defective.
Even in the absence of aspirin, this imbalance in the production of prostaglandins and leukotrienes causes problems. It leads to symptoms such as chronic urticaria (see p. 51) or rhinitis, nasal polyps and asthma (a cluster of symptoms that is commonly called triad — see box on p. 28).
Taking aspirin can make the imbalance between prostaglandins and leukotrienes even worse in a person with this underlying abnormality. Aspirin exerts its painkilling effects by disabling the main prostaglandin-making enzyme — the enzyme that is already defective.
When someone with aspirin sensitivity takes aspirin, they may suffer worsening asthma, a severe asthma attack or — the worst-case scenario —collapse. This is a potentially fatal reaction, similar to anaphylaxis, requiring emergency medical treatment (see p. 101).
The greatest puzzle about aspirin sensitivity is why it often takes so long to develop in someone who already has the symptoms of triad —indicating the basic metabolic abnormality. It may be as much as 20 years from when someone has their first triad symptoms to when they begin reacting badly to aspirin.
If you have triad symptoms already, but no aspirin sensitivity yet, what should you do? Unfortunately, there are no safe tests for aspirin sensitivity at present — taking a small dose of aspirin and seeing what happens is very hazardous. It is probably best to assume that you are going to become sensitive to aspirin at some stage, and avoid all aspirin and aspirin-like drugs. Caution is the best plan here because aspirin sensitivity can come on very suddenly, and be life-threatening the very first time it occurs. Note
that some triad sufferers have polyps and rhinitis but no asthma until they actually develop aspirin sensitivity — a dose of aspirin suddenly brings on their first asthma attack plus other symptoms of aspirin sensitivity.
Avoiding aspirin itself is not difficult, but aspirin-like drugs pose more of a problem. Every year there are a number of deaths from these drugs. Some cases occur because a busy doctor momentarily forgets that a patient should not take these drugs. The drugs that need to be avoided are all known as non-steroidal anti-inflammatory drugs (NSAIDs), COX-1 inhibitors or COX-2 inhibitors. However you will not see any of these names on the packet. These drugs are very widely used for pain relief (e.g. in headache and backache remedies such as Nurofen), for the treatment of arthritis, and for several other inflammatory diseases.
There are dozens of non-steroidal anti-inflammatory drugs available, and many are sold under several different brand names. The list grows every year, as new drugs or new brands are launched. The only way to avoid these drugs is to be very cautious:
•    When buying any cold- or flu-remedies, painkillers, medicines for sprains or sports injuries (including those you apply directly to the skin), headache tablets or migraine tablets, always buy them at a chemist’s shop rather than a supermarket, and check with the pharmacist that they do not contain aspirin or aspirin-like drugs.
•    Be cautious also about remedies for an upset stomach. A few (e.g. Alka-Seltzer) contain aspirin.
•    Don’t take any drugs unless you are 100% sure of what they contain. Remember that the ingredients of a familiar brand name can sometimes change — read the label every time.
•    When a doctor prescribes any new drug, always mention that you are sensitive to aspirin, or that you have triad symptoms. Alternatively, check with the pharmacist when the prescription is filled.
•    Aspirin-free painkillers almost always contain paracetamol, a drug which can cause a severe reaction (similar to the collapse induced by aspirin itself) in about 5% of those with aspirin sensitivity. If you are taking paracetamol for the first time, start with half a tablet. Be sure that, for the next 2-3 hours, you have a way of getting to hospital quickly should you start to feel ill. (Note that paracetamol has another entirely separate effect, increasing the severity of asthma, and it is best not to take it too often — see box on p. 150.)
Avoiding all aspirin-like drugs will prevent you having anaphylaxis or severe attacks of asthma. Unfortunately, triad symptoms will not go away however careful you are about avoiding aspirin.
It is well worth trying the new anti-leukotriene drugs (see p. 149), especially if you have aspirin-induced asthma. They seem to help with triad symptoms by curtailing the activities of leukotrienes and so redressing the balance between leukotrienes and prostaglandins.

FOOD SENSITIVITY IN ASTHMA, ECZEMA AND OTHER ALLERGIC DISEASES
In 1995, medical researchers in North Carolina, USA, asked over a hundred dermatologists how they treated atopic eczema. All used standard treatments such as moisturisers and steroid creams, but only 14% mentioned the possible role of food to the parents of children with eczema.
Between them, the dermatologists in this study treated about 17,000 children with atopic eczema per year. Using the most widely accepted estimates for food sensitivity in atopic eczema –38% of eczematous children are sensitive to food – one can calculate that there were over 5000 children in this study area who might perhaps have benefited from avoiding a problem food, but whose parents were never told about this treatment option.
North Carolina is by no means unique. The situation is much the same in other parts of the world, which adds up to millions of children and parents not even being told about a treatment that is frequently effective.
Other allergic diseases (see right) can also be triggered by food, although the percentage of patients affected is much lower than for atopic eczema. Here too, many doctors are unaware of (or sceptical about) the possible role of food.
These reactions are best described as ‘food sensitivity’. They cannot be called food allergy (see p. 62) if there are no symptoms in the mouth or gut and if skin-prick tests are negative – as is often the case. Negative skin tests suggest that the reaction is not IgEmediated (see box on p. 12).
However, in some children with atopic eczema. the skin-prick tests to culprit foods are positive. When these foods are eaten after a period of avoidance, such children sometimes suffer an
immediate reaction, with symptoms typical of true food allergy. For these individuals, their atopic eczema seems to be a symptom of IgE-mediated food allergy.
How can an atopic eczema reaction in response to food be IgE-mediated in one individual and not in another? Research is finally beginning to answer this question (see pp. 18-19).
The allergic conditions that may sometimes be induced, or simply aggravated, by a non-immediate reaction to food are:
• atopic eczema (atopic dermatitis)
• asthma
• perennial allergic rhinitis (constantly blocked or runny nose)
• chronic sinusitis
• secretory otitis media (’glue ear’).
In all of these conditions, many other causes exist. Except in the case of eczema, the other causes are far more likely than sensitivity to food. This fact will weigh heavily with your doctor, whose instinct, quite sensibly, is to look for likely causes first.
Taking asthma as an example, food sensitivity is relatively unusual as a primary cause, whereas allergy to airborne items. such as pollen or house-dust mite, is very common. Food probably affects only 8-10% of asthmatics overall, but is much more important for those with brittle asthma (the most severe and unstable form), affecting as many as 60% in a recent study.
The pollen connection
People who suffer from both birch-pollen allergy and atopic eczema may have worsening eczema when they eat certain fruits and vegetables, e.g. apples and carrots. These same foods cause Oral Allergy Syndrome (see box on p. 63) in some with birch-pollen hayfever, but they can aggravate eczema without causing Oral Allergy Syndrome.
Diagnosis
Consider other likely allergens first. Look at p. 28 for the airborne allergens that could play a part in perennial allergic rhinitis, chronic sinusitis, secretory otitis media (’glue ear’), and asthma. Only in the case of children with atopic eczema is food a prime suspect (between 38% and 69% of children with atopic eczema are affected by food), but even here there are a lot of other factors to consider (see pp. 43-4).
If you do decide to investigate the role of food, don’t abandon basic treatments in the meantime. By neglecting these. you could make the whole problem a great deal worse.
There are various clues that food is at fault:
• If you have other symptoms that suggest food intolerance (see p. 76). These problems often seem to go together with food-induced asthma or rhinitis.
• If you have noticed that a particular food makes your symptoms worse. Where there is intolerance to one food, there could well be intolerance to another, which you have not noticed.
• If you have exercise-induced asthma (see p. 41) and sometimes respond severely to exercise but sometimes have little or no reaction. Sensitivity to a food or foods may be instrumental in changing the response to exercise.
• If you have brittle asthma – but you must get your doctor’s consent for an elimination diet. Foods must be tested under medical supervision as severe life- threatening asthmatic reactions can occur on testing.
• If there are also digestive problems such as diarrhoea, vomiting or belching. This is a strong clue in the case of children with atopic eczema. Symptoms such as diarrhoea frequently precede atopic eczema, and it seems likely that a reaction to food in the gut increases the leakiness of the gut wall, allowing more food molecules through to the blood.
• If there is pronounced eczema around the mouth in children (but this can also be due to constant licking),
• For adults with atopic eczema, if there is a persistent rash on the hands, or the lips. Where there is a blistering rash on the hands that erupts at regular intervals, food is often the problem – or it may be metal contaminants of food such as nickel (see pp. 55-6). In general, food sensitivity is rarer among adults with atopic eczema than it is among children.
Skin-prick tests (see p. 91) for commonly eaten foods are worth
trying in all the diseases – if they give a positive result, they should
be noted, but if they give a negative one, they should be disre-
garded. The many alternative tests being marketed (see p. 93) are
highly inaccurate and unlikely to help.
Research from Tampere University Hospital in Finland suggests that babies are much more likely to give false-negative skin-prick tests for food than older children and adults with atopic eczema. The Finnish researchers found that 52% of babies with atopic eczema give a negative skin-prick test despite having a genuine reaction when tested by food challenge. In an attempt to tackle this problem, they have devised a patch test, similar to those used for contact dermatitis. The patch test, in which food is applied to intact skin and left there for two days, gives false negatives in only 39% of babies.
The best way to detect food-sensitive eczema, according to Dr Erika Isolauri. who heads the Finnish research team, is to use both tests, and take note of a positive reaction to either. This detects 80-90% of eczema-causing food reactions in infants.
Few other doctors are currently using patch tests for atopic eczema; because so much controversy surrounds this topic, and no standardised method has yet been devised. You may be lucky and find a specialist who does these tests.
To confirm the role of particular foods in atopic eczema, a food challenge test is essential, having first avoided the food carefully for two weeks. Great care is needed in testing (see p. 198).
If you cannot get suitable tests done. a simple elimination diet will be needed (see p. 198).
Treatment
There is a choice here, between avoiding the offending food, or eating normally and controlling the symptoms with drugs.
The difficulty comes when parents have to make this decision on behalf of their children. Unfortunately, there is insufficient evidence as regards the consequences of this decision. Treating food sensitivity can reduce the eczema symptoms substantially in the short term, but it does not necessarily improve the long-term prospects for the child. Orthodox doctors tend to think that eating a normal diet is much better for a child nutritionally and socially, and they have a point.
Doctors with a special interest in food sensitivity generally believe that treating the problem at source, rather than just suppressing the symptoms with drugs, must take the pressure off the child’s immune system, and give the child a better chance of growing out of sensitivity reactions in the long run.
The decision is yours – but it is vital that the diet is not more of an encumbrance than the disease itself, and that the child’s interests come first (see pp. 170-71). Whatever you do, don’t allow a child to become malnourished (see p. 198).

Various other things can irritate the skin and make atopic eczema flare up:
• cold weather
• dry air
• long car journeys
• sweating heavily; clothes or shoes that trap sweat may also cause problems
• dust mites, which can act as an irritant, even if not an allergen
• tobacco smoke
• solvents and other chemicals encountered at work
• skin contact with fruit (especially citrus), vegetables, and sometimes other foods. The spray generated by peeling potatoes can even produce eczema on the face.
Anything which increases blood flow through the skin makes the itching worse:
• heat, especially a hot bath or being too hot in bed
• anger or embarassment
• hot drinks of any kind
• coffee, tea and alcohol because of the drug-like substances they contain
• vinegar and spicy foods
• chocolate, soy sauce, yeast extract, orange juice, tomatoes and other foods that are rich in amines (see p. 200).
Various changes in the body can make the eczema worse:
• teething, in babies
• colds and other viral infections
• in women, certain phases of the menstrual cycle.
Many eczema sufferers are aware that their skin gets worse when they are upset, stressed or anxious Oust before examinations, for example). Like other allergic diseases, atopic eczema is not primarily psychological but, once it has begun, psychological factors can play quite a big part.
The good news…
…for children and teenagers, is that if you have eczema as a child, your chances of developing acne during your teens are greatly reduced.
Contact dermatitis too?
People with atopic eczema can develop contact dermatitis (see p. 54) in addition to their existing rash. There is always this risk with regularly applying creams to your skin, especially anything containing fragrance or lanolin. Antihistamine and antibiotic creams also carry this risk.
Even the ingredients in the creams prescribed for eczema – such as moisturisers and steroids – can sometimes provoke contact dermatitis. Creams are more likely to contain sensitising ingredients than ointments. Very occasionally, the sensitivity is to a preservative or emulsifier that is widely used in different ointments and creams, which means that switching brands yields no improvement. Steroid suspended in petrolatum (white paraffin jelly) is the least likely to cause reactions.
The rash produced by contact dermatitis looks no different from atopic eczema, so this sensitivity will be far from obvious. It will just seem as though the atopic eczema is not getting better.
Talk to your doctor if you think there may be a problem of this kind. He or she can check by using the suspect cream on one side of the body, and a different-but-equivalent product on the other side. Patch tests (see p. 92) may also help to identify contact sensitivity.
Diagnosis
There are five separate aspects to diagnosis:
1 Is this really atopic eczema? There are no clear-cut tests for atopic eczema. Instead the diagnosis is based on a ‘points system’ – how many of the typical features of atopic eczema are present? The doctor adds them up, and if there are enough, then it’s atopic eczema. Sometimes all the typical features are there and this is obviously the right diagnosis, but in other cases there may be room for doubt. The doctor should rule out the possibility of contact
dermatitis (see p. 54), especially if you have eczema only, or mainly, on the hands.
2 What avoidable irritants are making the skin worse?
3 Is the eczematous skin infected? The signs of infection are usually clear, but not always, especially with fungal infections. Steroid creams can sometimes mask the overt signs of infections: if atopic eczema is not responding to treatment this possibility should be investigated.
4 Are there any allergic reactions to those infections? Or to the normally harmless microbes that live naturally on the skin (see p. 17)? Skin-prick tests or blood tests can reveal such allergic reactions where fungi are concerned. Adults with persistent atopic, eczema which is getting worse rather than better are the most likely candidates.
5 Are there allergic reactions (or other sensitivity reactions) to food, or to allergens such as house-dust mite?
This fifth aspect of diagnosis is where controversy is rife. Many dermatologists feel that atopic eczema is treated quite adequately with moisturisers (emollients) and steroid creams. The search for allergic/sensitivity reactions – in other words, for basic causes – seems unnecessary for most patients, or more trouble than it is worth. Indeed, some dermatologists believe that looking for such sensitivity reactions is actually mistaken because they are not basic causes (see p. 42).
Other specialists disagree, and feel that allergic/sensitivity reactions are a basic causative factor in atopic eczema. They concede that there are many false positives, but in their opinion, there are enough true positives in the skin-prick test results to make it worth sorting them out from the false positives. Except for patients with very mild eczema, such doctors prefer to identify and eliminate the root causes, if possible.
Patch tests are now used by some of these doctors (see p. 69) – yet another contentious issue! The time-honoured use for patch tests is in contact dermatitis, and there is a lot of resistance to using them for atopic eczema. Traditionally, the immune reactions involved in atopic eczema and contact dermatitis are seen as entirely different – the former involving IgE and being a quick reaction (identified by skin-prick tests), the latter involving other players and
Sweaty sock dermatitis
More correctly known as ‘juvenile plantar dermatitis’, this rash on the feet affects an awful lot of atopic children. It is frequently misdiagnosed as athlete’s foot, and treated with anti-fungal drugs. The important clue can be found by looking between the toes: if there’s no rash there, then it is not athlete’s foot.
being much slower (identified by patch tests). New research into atopic eczema shows this view to be overly simple (see pp. 18-19) – and it provides a rational basis for using patch tests.
If, as a patient or a parent, you are keen to search for fundamental causes, remember that this should never displace treatments to quell infection or moisturise the skin and restore its protective structure. When these treatments are neglected the whole problem can get far worse, because of the vicious circles that sustain atopic eczema.
Treatment
Treatment for atopic eczema has five possible angles:
1 calming the inflammation
2 avoidance of scratching and rubbing
3 caring for the skin and restoring its normal structure
4 treating infections
5 avoiding allergens.
One or more of these aspects may be neglected, depending on what kind of specialist you are seeing.
Calming the inflammation
Steroid creams are the mainstay of atopic eczema treatment because they calm the inflammation in the skin. The creams do carry a risk of side effects, but are safe when used correctly (see p. 147). An over-fearful attitude to steroids creams can mean that the eczema never gets under control, and this can mean using more steroids in the long run. When treating an outbreak of atopic eczema with steroid cream, it is vital to continue applying the cream until the ‘hidden healing’ has occurred (see p. 146) – don’t stop as soon as the skin looks better.
Promising alternatives to steroid creams now exist: these are tacrolimus and pimecrolimus ointments (see p. 147). Unfortunately they are much more expensive, and your doctor will probably prescribe them only if there is some pressing reason.
Tar-based ointments have a much milder anti-inflammatory effect, and can be helpful for areas of thickened skin. They were once widely used for atopic eczema, but are used less now, in part because they stain fabrics and smell unpleasant. Sometimes they irritate the skin, too, and there are concerns about safety: they contain carcinogens, and significant amounts are absorbed into the bloodstream. However no evidence has been found that these cause cancer, despite intensive searching.
Antihistamine tablets are sometimes used and while they
may not help the eczema much, some evidence suggests that
they could reduce the risk of asthma developing later (see p. 249).
Powerful drugs such as cyclosporin are sometimes used in
severe cases of atopic eczema, to damp down the immune
response. They are taken by mouth, and can affect other parts of the body, not just the skin. Very careful monitoring is needed.
Sunlight is often beneficial, because it suppresses the inflammatory processes in the skin. However, not everyone improves with sun exposure – some get worse. Careful experimentation is the only way to find out: build up the length of sun exposure very gradually, starting with less than an hour a day.
Medical treatment with UV (ultraviolet) light can produce the same effect as sunshine and suppress inflammation. This treatment may be prescribed, but you should not try it for yourself with a sun-lamp. In PUVA treatment, a plant-derived substance called psoralen is given by mouth, or applied to the skin, to enhance the response to UV light.
Kicking the scratching habit
Scratching is a substantial part of the problem in long-standing atopic eczema. Experiments with healthy people and mechanical ’scratching machines’ show that perfectly normal skin will erupt into eczema if it is scratched intensively.
There is no steroid cream powerful enough to counteract the effects of scratching. But if scratching stops, then the skin can –with the help of medication – heal up.
Note that ’scratching’, in this case, includes rubbing the itch (directly or through clothes; using a hand, wrist, chin, leg, foot, or any other part of the body), touching or picking at the skin, rubbing against sheets, furniture or another person, or using a towel, flannel or hairbrush to rub the skin. All these activities can be habitual and quite unconscious, if atopic eczema has been present for more than a few months – you just don’t realise you’re doing it most of the time.
For many with atopic eczema, another problem creeps in –scratching without itching. This may be just habit, a response to boredom, stress or anxiety, or even part of the family dynamics, in which scratching has become a form of emotional expression. Scratching alone can set off itching, and a scratch-itch-scratch cycle ensues.
The first step in combating scratching (for an adult or older child) is simply to notice how often scratching occurs. Doctors at the Chelsea and Westminster Hospital in London issue their patients with little hand-held counting devices (tally-counters), and ask them to press the button on the device every time they scratch or rub. Over a period of days, patients discover – usually to their own amazement – just how often they do scratch. The point of the exercise is simply to become conscious of the scratching impulse, and to notice the situations which typically provoke scratching. You could use a small pocket-sized notebook and pencil to achieve the same end.
Once this awareness has been gained, then you are in a position to break the scratching habit. The methods involved –called ‘habit reversal’ – were first developed by a Swedish dermatologist, Peter Noren. It takes about 2-4 weeks for most people, but the change is long-lasting. Most eczema sufferers find that they recoup their time investment rapidly, once they are free from the chore of dealing with chronic eczema.
When you notice that you are about to start scratching, and before the urge to scratch overwhelms you, take control and do something deliberate with your hands – for example, clench your fists, while breathing deeply and slowly. Think cool non-itchy thoughts. The urge to scratch may pass. If it doesn’t, then you can allay the itch by pinching the itchy area gently, or pressing your fingernail into it, or lightly applying a little moisturiser.
In the bath or shower, don’t use flannels, and never rub or scrub the skin. Dry off by gently patting with a soft towel.
The aim is to get scratching episodes down to fewer than ten per day. In achieving this goal, relaxation exercises, stress management techniques, hypnotherapy or autogenic training (see p. 222) can also be very helpful, especially if you sometimes scratch in tense situations.
With small children, the parents have to do the noticing. Most are unaware just how much their child scratches or rubs the eczema – babies often rub against the side of the cot.
Once the awareness is there, a child over four can usually be taught the habit-reversal technique described above. With a younger child, the parents must distract the child when scratching is imminent, by talking or playing. If the child is scratching while asleep, parents should pick the child up and, very gently, hold the child’s hands away from the body. Situations and activities which commonly provoke scratching should be avoided, or planned for. Give the child something to hold while dressing and undressing, for example – keep the hands busy. But never say ‘Don’t scratch’ – it usually has the opposite effect in the long run.
For the first four days and nights, while you are trying to break the scratching habit, the child should never be alone, even for a minute – someone who is able to distract the child from scratching should always be there, and awake. Fortunately, children lose the habit far more quickly than adults.
Keep a child’s fingernails very short, and smooth them with an emery board too, so that if any scratching does occur the effects are minimised. (Soft cotton mittens, to be worn at night, are often recommended, but the cotton itself can be used to rub the skin – observe your child carefully! The same is true of all-over cotton suits.)
For this anti-scratching programme to be effective in healing the skin, there must be a determined effort with drug treatment at
Will it clear up?
Small children with eczema generally grow out of it by the age of two. Those who have eczema after this age tend to show a big improvement at puberty. Sometimes, however, the eczema can disappear at puberty, only to reappear later: so continue to be careful with your skin.
Atopic eczema is frequently the first sign of a tendency to allergies (see p. 22). Given this early warning sign, parents should take steps to avoid allergies developing, or at least reduce their severity (see pp. 244-9). One small piece of good cheer: atopic eczema and life-threatening food allergies are very rarely found together.
People with both asthma and atopic eczema frequently notice that when one improves the other seems to get worse. There is no explanation for this as yet.
Moisturisers - how to use them
Moisturisers (emollients) do two things: they increase the amount of water in the skin, and they lubricate the skin, making it less brittle.
A moisturiser is designed to leave an oily layer on the surface of the skin which stops the skin’s natural moisture from escaping. The most effective preparations, from this point of view, are ointments made from white paraffin, such as Vaseline, which form an uninterrupted waterproof layer: these are sometimes called occlusives. They contain no water, unlike creams. Although a cream forms a less formidable barrier to the escape of moisture from the skin, it does provide some moisture itself, which can soak into the skin.
The most important thing is to have something that you like using, so that you apply it regularly. There are lots of moisturisers available, so ask the doctor for different ones to try.
Applying moisturiser well is crucial:
• Apply moisturiser before your skin gets dry, as a preventive treatment.
• There’s no need to rub in your moisturiser (this can be a form of scratching). Just apply it very lightly.
• A thin layer is all that’s needed. A thick layer keeps in heat which aggravates the skin.
• Always apply within three minutes of a bath or shower.
• In addition, apply every 3-4 hours during the day. Carrying moisturiser around with you is helpful – get a small tube of moisturiser for this purpose.
• Ask the doctor to prescribe moisturiser in large quantities, to make sure you have enough. But beware of infecting big pots with Staphylococcus bacteria and then reinfecting your skin. Pump-action dispensers are safer.
Moisturiser can also be smeared onto bandages which are then wound around the affected areas at night to reduce the itch – or you can use ready-made ‘wet-wraps’ (ask your doctor about these). As long as the bandages/wraps are immovable, they will reduce nocturnal rubbing and scratching.
Avoid lotions, and any non-prescribed creams, as they could be irritating to the skin. Choose bath oils with care – some contain alcohol which is an irritant.
the same time. You should be using a steroid cream of sufficient strength, twice a day, and plenty of moisturising treatment.
By taking this ‘Combined Approach’, as Dr Christopher Bridgett and his colleages at the Chelsea and Westminster Hospital call it, you should be able to clear the eczema completely, even if you have had it for years and have tried innumerable different treatments. Once this has been achieved, you can maintain an eczema-free state by watching carefully for any outbreaks of itching, redness or roughness, and treating them immediately with a short course of steroid cream (see p. 146).
Skin care
Firstly, avoid all the irritants which you think may affect your skin. Give clothes an extra rinse cycle in the washing machine, to remove all detergent. or use a non-detergent system such as Eco-balls or Aquaballs. Wash all new clothes before wearing them, to remove chemicals such as formaldehyde. Wear soft cotton or silk next to the skin.
Where eczema affects the hands, special care is needed (see p. 57).
Water can be both good and bad for eczema. When you soak in a bath, water is absorbed by the skin cells, which helps correct the dryness of the skin. But when you get out of the bath, and the skin dries, the outermost layer shrinks and develops microscopic cracks, making it even less waterproof than it was before. The way around this is to apply a moisturiser immediately after a bath or shower –gently pat the skin until partially dry, and apply the moisturiser immediately to trap the water in the skin.
For anyone with a severe flare of eczema, current recommendations are:
• soak in lukewarm water for 20 minutes, twice a day
• pat dry
• quickly apply steroid cream to the eczematous areas, then moisturiser over the top, and to all other dry-skin areas
• make sure the moisturiser goes on within 3 minutes of emerging from the water.
This works well for some people, but not all. For a few eczema sufferers, the effect of taking natural oils out of the skin (which soaking does, to some extent) may outweigh the benefits of putting water in. Or they could be sensitive to something in the tap water – the chlorine, perhaps, or pollutants. It may not be obvious that this routine treatment is not helping. As Dr Michael Tettenborn, a British paediatrician with long experience of atopic eczema, observes: ‘By the time they’re referred to me, children are usually on the standard regimen of two-soaks-a-day. One of the first things I do, as an experiment, is tell the parents to just bathe them once a week and use a moisturiser and tissues to keep them clean the rest of the time. Some children do a lot better after that.

Hayfever in Allergy

Foxtall grasses release their pollen - a potential source of hayfever symptoms.
`I gradually recognised that it was not an ordinary cold and that the symptoms were much worse on the

golf course or even during a nice day rowing on Loch Lomond.’ Dr John Morrison Smith, then a medical

student, began suffering from hayfever in the late 1930s. ‘At first I did not know what I had, and

neither did any other doctor I encountered in the next two or three years…’
All the classical allergic diseases (see box on p. 11) seem to be increasing, but none has exploded

quite so dramatically as hayfever. The physicians of Ancient Greece described asthma and food allergy,

and the Romans recorded allergy to horses, but there were no reports of hayfever. The only account –

and it is a doubtful one – comes from Persia in AD 925. Two hundred years ago, hayfever was unknown –

and careful research by medical historians has shown that this was not a case of it simply being

ignored, or misinterpreted as a cold.
The first case was reported in 1819, but even in the 1930s it was so rare that a succession of Scottish

doctors and medical students were baffled by Dr Morrison Smith’s symptoms. Today everyone knows what

hayfever is, since huge numbers of people sneeze and snuffle their way through the pollen season. There

are no certain explanations for this meteoric rise, but greater hygiene (21) may be an important

factor.
Symptoms of hayfever
The common symptoms of hayfever are well known:
• itchiness of the nose, mouth, throat and eyes – often the first sign
• a streaming and/or blocked nose
• frequent sneezing
• red, watery eyes (very rarely, hayfever affects the eyes only, with no symptoms in the nose).
Less commonly, there may be:
• dryness of the throat if the nasal blockage results in constant breathing through the mouth
• no sense of smell due to a blocked nose (but nasal polyps can also cause this – 30)
• a feverish sweaty feeling (but the body temperature is usually normal)
• swelling and inflammation of the eyelids, sometimes leading to blistering and ulceration: there

is a risk of blindness if this is not treated promptly
• recurrent sinusitis (30)
• earache, itching or a stuffy feeling in the ears, or ‘glue ear’ (29)
Some sufferers also experience:
• Oral Allergy Syndrome (an itchy tingling mouth) from certain fruits, nuts and vegetables (see

box on p. 63)
• a skin rash from pollen falling on the skin, direct contact with the leaves of the offending

plants, or with droplets of moisture from them – as when mowing a lawn or using a strimmer. If the skin

is cut or grazed, anaphylaxis can (rarely) result from direct contact with the plant (see pp. 58-9).
Even more rarely there can be:
• stomach upsets or even colitis (inflammation of the bowel) possibly due to pollen swallowed

with food or in the saliva
• irritation in the vagina
• migraine
• kidney inflammation (nephritis), leading to puffiness of the face and hands, and possibly other

symptoms
• joint pains.
The last two are probably caused by pollen allergens bound to their antibodies and carried in the blood

(13).
Diagnosis
The standard diagnostic tool here is the skin-prick test (see lo, 91). In diagnosing hayfever there are

three separate questions:
1 Is it actually hayfever?
2 Which pollen or pollens are responsible?
3 Are allergens other than pollen also involved?
Don’t be surprised if none of these questions is asked. In most countries, if you have hayfever-like

symptoms during the pollen season (i.e. when most hayfever sufferers have symptoms), the doctor will

conclude that you have hayfever - and that will be the end of that.
If hayfever seems plausible to you, and you respond to drug treatment, or manage well on pollen

avoidance (126), then -here is probably no reason to go further. Should you want a more thorough

investigation, you will need to be persistent. These are good reasons for requesting a full diagnosis:
• Your symptoms are worse in the pollen season, but they never really go away, suggesting that

you may be allergic to year-round allergens, such as house-dust mite or moulds, as well. It is worth

knowing which ones, so that you can avoid them. If you live in an area that is always warm (such as

California or Southern Australia) it may be that your culprit pollen is in the air all year round -

even so, knowing which pollen it is can help with avoidance. Around the Mediterranean, the pollen from

cypresses can keep hayfever going through the winter (or cause symptoms in winter only).
• Your symptoms are sometimes worse when they should be better, and vice versa. If you are

consistently worse indoors with the windows closed this could indicate that a seasonal indoor allergen

is the culprit - mould spores or cockroach perhaps (cockroach is often seasonal in regions with cold

winters - 118).
• Your symptoms begin before the pollen season begins, or go on long afterwards. Or the severity

of your symptoms does not match the daily pollen count for your suspect pollen. In Britain, the mould

Cladosporium herbarum produces spores in June, roughly coinciding with the grass-pollen season. Allergy

to this mould can easily be mistaken for grass-pollen allergy. You would need skin-prick tests for both

Cladosporium and grasses.
• You are much worse near home than elsewhere. It could just be a garden plant or tree. As one

California resident observed, ‘The worst offender was an olive tree on our front lawn. It’s been

removed.’
• You want to plan holidays free from the culprit pollen.
Moving house - especially to a region with different vegetation
- can be a spur to finding out exactly what your allergens are. If you are going for a full diagnosis

make sure it is done correctly. Don’t accept testing with ‘mixed tree and shrub pollens’ for example,

or ‘weed pollens’. The result tells you very little. Ask for tests with specific pollens.
Treatment
Too many people allow hayfever to spoil the summer months because they are anxious about taking drugs,

or feel that it is nobler to suffer. This book is not in any way complacent about the dangers from

drugs (see Chapter 5), but when it comes to hayfever there really is very little cause for concern. The

risks with drugs used for hayfever are absolutely minimal, and it is such a waste to miss out on the

best time of year.
Most hayfever responds very well to treatment with antihistamines (138). If they make you sleepy,

persist for a while, because this side effect often wears off - or ask for one of the new non-sedating

forms. The sleepiness is annoying, but it is only a minor side effect, and not an indication of the

drug causing any serious harm.
Cromoglycate drops (for the eyes or nose) do not work for everyone, but if they work for you, go for

them. These are absolutely the safest of the anti-allergy drugs. Steroid drops for the nose (144) are

also recommended. The dose of steroid involved is small, and very little gets into the bloodstream, so

there is no risk of serious side effects. 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). Steroid drops for the eyes

should be used cautiously (144). Don’t use over-the-counter decongestant drops for more than three days

(29).
Immunotherapy is standard treatment for hayfever in many countries, but in Britain you will have a

struggle to get it (see pp. 164-8). Some hayfever sufferers feel they do well with homeopathy (215) or

acupuncture (214).
Pollen asthma
Some people with hayfever also have pollen asthma. Their asthma is worse in the pollen season but it

usually persists all year round (either because there are other allergens or irritants involved, or

just because the inflammation of the airways is self-perpetuating) whereas hayfever itself clears up.

Treating the hayfever fully with antihistamines helps considerably with the asthma symptoms.

 

In medical terms, this article covers a lot of ground.
First there are the classical allergic diseases
 such as hayfever and immediate food allergy, which are caused by the allergy

antibody, IgE .
Then there is non-IgE immune sensitivity, a category which includes a number of quite different

diseases, caused in a great variety of ways. They also vary in severity - there are serious lifelong

problems such as coeliac disease and minor short-lived problems such as contact dermatitis from garden

plants.
Finally the chapter looks at diseases where the immune system seems not to be involved, or

plays only a minor role: the intolerance reactions to food and synthetic chemicals. These are diverse

and rather mysterious in origin. They would not be described as ‘allergies’ by most doctors, though

they often are by complementary therapists (6).
These categories are not nearly as neat and tidy as they might sound. Some problems refuse to fit

anywhere, such as atopic eczema caused by food. A percentage of children with this problem have IgE to

the food concerned, while others do not - so where does it belong?
If you were expecting an answer to that question, you will be disappointed. Nor, quite often, are there

any certain and honest answers to questions such as ‘Has my baby really got asthma?’ or ‘Can you be

sure it’s irritable bowel syndrome?’ There are no answers to
such questions because most diseases do not exist in neat compartments, and the words we use to

describe them really denote rather abstract concepts.
This does not mean that the terms used to describe diseases are invalid - doctors and medical

researchers invent them to try to make sense of a complex, confusing and largely foggy reality. They

also argue over them, split them, unite them and redefine them. There is a constant desire to get the

medical picture of that foggy reality more precise and accurate (although medical politics gets

involved too - 7 -which is unfortunate).
Over time, thanks to huge amounts of research effort, things gradually get clearer. You’ll no longer

hear a doctor talk about ‘rheumatism’ or ‘arthritis’, because it was long since realised that these

categories were useless - they included a number of diverse diseases. And while doctors might say ‘food

poisoning’ or ‘heart attack’ or ’skin cancer’ to a patient, they use much narrower and more precise

terms when talking among themselves, and when ordering tests or prescribing treatment. Each of these

categories has been split into several well-defined sub-categories.
Ideally, this process of splitting continues until each disease category has a set of well-defined

symptoms (this set is known as a syndrome), plus a few simple and definitive diagnostic tests. This

will probably depend on the cause of the disease (the mechanism in medical jargon) being clearly

understood. Once the mechanism is clear, then a disease category is a truly satisfactory tool for

diagnosis and treatment.
Of the disease categories mentioned in this book only a few, such as coeliac disease and hayfever, have

reached that happy state. The majority are still somewhat arbitrary and debatable.
Some disease terms describe a set of symptoms with no clear underlying cause, for example, ‘irritable

bowel syndrome’. Others describe a well-defined response by the body, that can be caused in many

different ways - an endpoint that can be reached by various routes. This is true of ‘asthma’ or

‘urticaria’.
A third type describes a much less well-defined cluster of symptoms. Idiopathic food intolerance,

chemical intolerance and yeast overgrowth all come into this category. A few doctors don’t even see

some of these clusters as real diseases because the symptoms involved are so vague and so widely

encountered. Some of the arguments used to dismiss idiopathic food intolerance are dissected on pp.

74-7. A key point made against these diseases is that the symptoms they produce are non-specific -

common symptoms such as headache, fatigue and diarrhoea, which can arise in a great variety of ways.

Ever since Pasteur and the germ theory, medicine has been based on the idea of each disease having

specific symptoms and specific causes, and it has roared ahead on the basis of this assumption. This is

the prevailing paradigm of modern medicine, and like all
paradigms it blinds people to facts that don’t fit. Evidence is accumulating that there are diseases

which have multiple, non-specific and variable symptoms. Chronic Fatigue Syndrome (CFS - see box on p.

85) is one of these, and its recent transformation from a doubtful diagnosis to a reputable disease

recognised by conventional medicine suggests that the paradigm might be starting to crack.
To sum up, the business of identifying and naming diseases is a complex and uncertain process, in which

the concept of most diseases is only ever that - a concept, subject to change and refinement. This does

not make it worthless - quite the opposite. These concepts are the best we can do at the present time,

and accurate diagnosis is the key to getting the best treatment available now.
As regards both diagnosis and treatment, this book covers a very wide spectrum of medical opinion, from

the entirely orthodox to the frankly whacky. I have tried to give an objective view of these different

opinions and approaches, using the evidence currently available, in the hope that it will help readers

to improve their health while wasting as little as possible of their time or money. In using this

information, you should always try to work closely with your doctor (96), respecting the depth and

breadth of knowledge that conventional medicine has to offer.

 

If you have a child with allergies, sooner or later some friend or relative will tell you not to worry

because your child ‘will probably grow out of it’. Your doctor may well say the same thing. But what

does this mean? Do all children shake off their allergic symptoms as they get older? If the symptoms

go, is the underlying disease completely cured? And why treat allergies if they disappear of their own

accord? The truth is that the relationship between allergy and age is incredibly complex, and doctors

only understand a tiny part of it. The best anyone can offer is a broad overview of how allergies

change with age, with few explanations of the underlying mechanisms, and absolutely no predictions of

what the future holds for any particular allergy sufferer.
It is certainly true that the classical allergic diseases, such as atopic eczema, hayfever and

childhood asthma (see box on p. 11), frequently disappear as children grow up. Babies tend to shrug off

food allergy and eczema by the time they are toddling, and a fair number of asthmatic children lose

their symptoms before they are ten years old, while others do so in their teens or early twenties.
Unfortunately, the disappearance of symptoms does not mean that the underlying disease has necessarily

disappeared, particularly in the case of asthma. Quite a few young adults find themselves wheezy and

breathless again in their late twenties or thirties, especially if they take up smoking. One study of

children who wheezed before the age of seven found that:
• 25% lost their asthma for a time – anything between two years and 25 years – only to get it

back again by their early thirties. Some recovered and relapsed more than once.
• Over 70% shook off asthma and were still symptom-free by their early thirties when the study

ended.
• Only 2% remained asthmatic throughout. Realistically, anyone who has ever been asthmatic should

regard themselves as ‘at risk’ indefinitely and never be careless with their health – don’t smoke, keep

away from smoky bars and clubs, eat a good diet with plenty of fruit and vegetables (206) and avoid

activities that involve an asthma risk, such as strenuous exercise in cold air.
Workplaces with high exposure to allergens, such as saw mills, bakeries or laboratories using animals

(see pp. 133-4) are not recommended for those with a history of allergy. Anyone who has ever had eczema

should also take care with cosmetics and soaps, choosing the gentlest brands. They should also protect

their hands (57) and avoid hairdressing or bricklaying as an occupation, or anything else where skin

irritation is likely.
Moving on
Growing out of classical allergies seems to be a consequence of the child’s immune system changing and

maturing as it grows. This same process, unfortunately, can also substitute one allergic disease for

another.
`When Alex developed eczema as a baby I hoped that she’d grow out of it in time. Well she did,

gradually, and by the time she was five it seemed to have cleared up, but then she started having a

snuffly nose that never really went away. A year or so later, she began wheezing whenever she got a

cold, and this has now developed into asthma.’ The pattern described by Alex’s mother Jenny will be

familiar to many parents, who watch their children slowly work their way through all the allergies in

the medical textbooks. Doctors call it the atopic march or allergic march.
Fortunately, even this type of allergic pattern can have a positive outcome eventually. Many such

children become allergy-free in time, and develop into healthy adults.
In the meantime, there are several itchy, wheezy or sneezy years to get through, and since childhood is

a time to be enjoyed, not endured, treatments that alleviate the symptoms of allergies are generally

welcomed. Being energetic, healthy, ‘normal’ and able to join in with sports and other activities is

particularly important for a child’s social development and self-confidence.
Treating the symptoms also prevents any long-term and irreversible damage, such as the thickening and

loss of elasticity that occurs in the airways of children with untreated asthma.
At the same time as treating the symptoms, it makes sense to maximise the chance of the child growing

out of the allergy. Parents can tip the odds in the right direction by providing an environment that

reduces the chance of new allergies developing. A detailed action programme is described on pp. 248-9.
Allergies that begin in adult life
What about those people who develop classical allergic diseases for the first time as adults - or even

in old age? Will they too ‘grow out of it’ with the passing years?
Only a minority of people develop such allergies for the first time as adults, although the numbers

seem to be increasing. The older you are when your allergies begin, the less likely you are ever to

throw them off. On the positive side, they are unlikely to get a great deal worse than they are at the

outset, especially if you take care of yourself and keep the air at home as unpolluted and

allergen-free as possible (see pp. 114-31).
In the case of asthma that develops in adulthood, there may not be an allergic reaction involved.

Whereas allergies play a part in asthma for 80-90% of children, the figure is thought to be lower for

adults. Nevertheless, it is well worth investigating the possible role of allergens, because avoiding

them is one of the most effective treatments.
The outlook for food intolerance
Food intolerance causes a wide variety of symptoms, from baby colic to migraine. A full list is given

on p. 76. Although far less is understood about food intolerance than about true allergies, there is

much more certainty about the future for affected individuals. With rare exceptions, people find that

the problem clears up as long as they totally avoid their problem food for a year or two. After this

period of strict avoidance, they can eat the food again in moderation but should never forget that the

problem can return. Eating the culprit food very regularly will turn the clock back and all the

original symptoms will return. This change for the worse may be irreversible for people with severe

reactions such as rheumatoid arthritis.
Safety first
Anyone who suffers the life-threatening allergic reaction known as anaphylactic shock (58) is probably

going
to have this for the rest of their days. Some children do become tolerant of food allergens in time

(allergies to milk, eggs or soya may well disappear, whereas fish or peanut allergy is probably going

to be permanent) but before concluding that there is no longer any risk, some extremely careful and

cautious testing should take place. Talk to your doctor about how to proceed. Skin-prick tests may be

helpful, but there must be resuscitation equipment close to hand as anaphylaxis can occur. Never give

the child any of the food to eat, until you (or, preferably, the doctor) have first tested it in other,

less risky, ways. For example, you can smear a little on the face to see if there is any reaction. If

there is none within 24 hours, put a tiny amount on the outer lip and watch again.
If both these tests produce absolutely no reaction then a very small amount of the food can be eaten as

a test: this should be done under medical supervision. The amount can be slowly increased with

successive tests, until it seems certain that no reaction will occur even with a normal portion.

`I can’t think of any of our friends where there isn’t at least one member of the family with asthma, and often it’s both children,’ says Dee Gill, a university lecturer from Melbourne, and herself asthmatic. Australia is one of the countries worst affected by the allergy epidemic. ‘If you go to a primary school sports day, you’ll see the teachers going along the line of kids, saying, “Have you taken your asthma medication?” It’s so much a part of everyday life now.’
The word ‘epidemic’ is now being freely used, even by the most conservative of medical scientists. All the classical allergic diseases seem to be on the increase, including:
• atopic eczema – in the United States, up from 3% of children in the 1960s to 10% in the 1990s; in Britain, more than 16% of 12- to 14-year-olds are now affected
• hayfever – extremely rare in the 1930s (26), affecting 3% of children in 1964, and now seen in 18% of 12- to 14-year-olds in many parts of the world
• asthma – the figures for children in one Scottish city are: 4% in 1964, 10% in 1989, nearly 20% in 1994
• peanut allergy has clearly been on the increase since the 1960s; a very alarming UK study shows that rates of allergy to peanuts have doubled in less than a decade (between children born in 1989 and those born in 1996).
To the question ‘why?’ there is no simple answer – the causes are many and various. But one thing is abundantly clear: this is a disease of modern, Westernised society. Travel to rural Africa or
Are other immune diseases increasing?
These two pages deal solely with the classical allergic diseases . Many doctors have the impression that eosinophilic disorders are also becoming more common, and some think that there are more cases of adult-onset coeliac disease than previously.
Asia, among people living a simple subsistence lifestyle, and you will find little or no sign of allergic diseases. There are no words in their languages for asthma or hayfever, because these are virtually unknown.
As soon as these people become more affluent, and change their lifestyle, allergic diseases appear, and the number of cases steadily rises over the years. Sometimes this coincides with a move to the towns, but it can also occur when people stay right where they are – as in Taiwan, where allergies rose dramatically with increasing affluence and a more Westernised way of life.
In the case of asthma, everyone is keen to blame air pollution, particularly traffic pollution. But a look at the research shows the link to be largely a myth. Certainly, polluted air can trigger off attacks in someone who already has asthma – but the effect is not huge, and this is not the same as causing asthma to develop in the first place. And while growing up in polluted air can increase the chances of children developing asthma, it makes only a small difference, one that simply cannot account for the massive asthma epidemic. The hollowness of the pollution argument is spectacularly evident when you consider rural New Zealand, where asthma rates are among the highest in the world, yet there are no factories, and sheep heavily outnumber motor cars.
Allergy to house-dust mites has also received a lot of publicity, and it does play an important part. Our warm, draught-free and thickly carpeted homes allow these tiny creatures to breed with abandon and many people with perennial rhinitis, asthma or atopic eczema have an allergy to dust mites. Recent research shows that dust mites play a far larger role than anyone previously suspected: the dust-mite allergen actually provokes immune cells, and once an allergy to dust mite has begun, other allergies become more likely.
But blaming house-dust mite as the supreme cause of the allergy/asthma epidemic (as some do) is as mistaken as blaming pollution. The proof in this case comes from the highlands of New Mexico where dust mites cannot survive because the air is much too dry. Allergies, including asthma, are just as common as elsewhere in the Western world.
Spoiling the immune system
Thanks to discoveries made during the past decade, we are now beginning to understand what has made the younger generations – those born since the early 1960s – so much more susceptible to allergies. The new data reveal that the way you bring up a child’s immune system matters as much as the way you bring up the child itself. You can ’spoil’ an immune system all too easily, by protecting it from life’s natural challenges and obstacles.
As a small child, I ate a spoonful of soil. My mother was horrified (she was still telling the story twenty years later) but research now shows that she should not have been. Exposure to certain bacteria in the soil, known as mycobacteria, is probably just the kind of education that a young immune system needs. These bacteria cause no 111-health, no symptoms at all, but they are thought to have an effect on the immune system, pushing it away from allergic reactions.
Children playing outdoors have probably always eaten soil, either intentionally or by accident – licking a grubby finger. Country people used to say, philosophically, ‘You eat a bushel of dirt before you die’, and they were probably right. Indeed, you may well need to eat a bit of dirt before you can live happily in an allergen-packed world. Now researchers are trying to make a vaccine using soil bacteria, to simulate this effect.
A study from the University of Bristol shows that children who wash their hands more than five times and have two baths a day are almost twice as likely to get asthma as children who wash their hands less than three times a day and have a bath every other day. The grubbier children are probably being protected from asthma by acquiring minor infections, with few or no symptoms. These infections could include both soil bacteria and germs that are spread from one child to another.
Other research reveals that children with older brothers and sisters are less likely to suffer from certain allergic diseases than only children or firstborn children. This may be due, in part at least, to the spread of infectious diseases, because mixing with lots of
other children in a nursery produces more infections but also gives protection against allergy. Studies from the former East Germany, where sending children to day nurseries at an early age was once the norm, demonstrate that if children from small families went to nursery aged 6-11 months they were substantially less allergy-prone than if they went later. The allergy risk was highest for only children who did not go to nursery until they were over two years.
Researchers in Colorado have recently tackled this subject from a different angle completely, analysing house-dust for the levels of bacterial endotoxin – substances that come from certain kinds of bacteria and which have a powerful effect on the immune system. If the house-dust contained high levels of endotoxin, babies brought up in that house were less likely to give positive skin-prick tests to common allergens such as cats, milk or house-dust mite. The babies from very clean houses, with low levels of endotoxin in the dust, were the ones with allergic reactions. (Fortunately, it is possible to have a dusty house with very little house-dust mite)
The hygiene hypothesis, as it is known, could also explain the strange history of hayfever. For the first century of its existence, hayfever was a disease of the urban upper classes, only gradually working its way down to the poor and to rural communities: this fits in well with the gradual spread of more hygienic ways of life. In most parts of the developed world today, it shows no class distinctions, but recent investigations have found a lower rate of hayfever among children raised on a farm with animals compared to children living in the same villages without farm animals.
In addition to greater hygiene, the following aspects of modern living appear to promote an allergic tendency in children:
• smoking by the mother during pregnancy and after, which may boost IgE levels
• breathing nitrogen dioxide from gas cookers, and formaldehyde from various household sources ; exposure to substances called phthalates, from plastics, may also be important; the poor ventilation of many modern houses, and the far greater time spent indoors aggravates the problem by increasing exposure to these irritants, and to allergens such as house-dust mite and moulds.
• taking antibiotics during the first two years of life
• bottle-feeding and/or abrupt and early weaning
• exposure to a virus called Respiratory Syncytial Virus (RSV) during infancy, which provokes an IgE-reaction (37)
• caesarean births; simply being born in a hospital might also raise the risks by exposing newborn babies to Staphylococcus, which adversely affects the immune system.

`When I first arrived in Charlottesville in 1982, the senior allergist said “I’ve got to warn you that here in Virginia we have patients who have very severe fungal infection of their feet, and they also have urticaria. If you treat their feet, their urticaria gets better.”‘ Professor Tom Platts-Mills of the University of Virginia in Charlottesville is recalling how his innovative studies of fungal infections and allergy began. That surprising observation about athlete’s foot (a fungal infection) and urticaria (nettle rash) was made by his predecessor, Professor John Guerrant,
‘I followed his advice,’ Platts-Mills continues, ‘and found he was right. Then I started noticing asthmatics in our allergy clinic who also had fungal infections of their feet. They were mostly men with severe adult-onset asthma. We gave them skin-prick tests with the fungus Trichophyton and these were positive – showing they had an allergic reaction to it. So we tried treating them with anti-fungal drugs and the asthma got much better.’
This discovery is not an isolated instance. Research over the last decade or so has revealed that allergic reactions to long-standing infections (chronic infection is the medical term) are far more common than anyone expected. Infections by fungi are frequent offenders.
An infection becomes chronic because, although the immune system tries to rout the infectious agent, it never succeeds. Making IgE may be part of that futile defensive effort. Once the immune system starts making IgE against the allergens produced by the infectious microbe, new symptoms may begin, or existing allergic symptoms may get much worse. The link between the infection and the allergy is far from obvious, however. Both the allergens and the IgE can be carried in the
Fungal infections
‘Fungus’ means everything from an edible mushroom or a huge bracket fungus to the specks of mould on stale bread or a shower curtain. Fungal infections are caused, not by mushroom-like fungi, but by inconspicuous mould-like forms, or by yeasts (which are single-celled fungi).
Once they are flourishing, some fungal infections may be seen as whitish or creamy-coloured patches. But at an earlier stage, the fungi are so small that they cannot be seen without a microscope. They spread as invisibly as bacteria or viruses.
Some infectious fungi can exist in two different forms – a mycelial form (long thin strands, as in a mould) or a yeast form (single cells).
bloodstream, so the symptoms may be somewhere else in the body, far away from the site of infection.
If the symptoms of the infection itself are relatively mild, they may not receive medical attention. Infection-plus-allergy often explains severe long-term allergic problems for which no cause could previously be found. This is the kind of case that gets labelled as ‘intrinsic’ or ‘endogenous’, because all the allergy tests have proved negative. Most patients in this category have had years of simply being treated with steroids (often at high doses) to suppress the symptoms.
Sometimes the infection-plus-allergy is part of a larger picture, with other allergens or irritants also contributing to the symptoms, but with no stunning improvements when they are avoided because the allergic stimulus from the infection remains.
The links between allergy and fungal infections – all those that have been discovered so far – are described below. In such cases, anti-fungal drugs, taken by mouth, usually in capsule form, could be of value. However, they must be taken for an adequate length of time, normally several months.
Bear in mind that, with the possible exception of chronic sinusitis, an allergic reaction to fungal infection is a relatively uncommon cause of symptoms. It is important that, with the help of your doctor, you start with the more likely suspects such as airborne or contact allergens. These are described in detail, for each allergic disease, in the relevant sections of Chapter 2.
Asthma
the common causes and usual treatment of asthma.
Trichophyton – the fungus that causes athlete’s foot – can provoke allergic reactions that contribute to asthma, as already described. This fungus may also infect other parts of the body. Trichophyton diseases have names that begin with tinea (athlete’s foot, for example, is tinea pedis). Other terms you may come across are intertrigo (an itchy rash which develops in skin folds) and onychomycosis (also called `ringworm of the nails’ or tinea unguinum). The research on the link with asthma was published in a respected medical journal, The Lancet, but has been widely ignored, so if you think you have this problem, you may have to be quite persistent with your doctor. Very thorough treatment with anti-fungal drugs (swallowed in capsule form) is required.
Chronic urticaria
many possible causes of chronic urticaria.
Trichophyton infections in any part of the body (see above) can provoke allergies, producing chronic urticarla. A great variety of other infections, including fungal, viral and chronic bacterial
infections, can be the root of the problem in chronic urticaria . However, this may not be an allergic reaction. It could be a direct effect of the infection, provoking the immune system in such a way that it triggers mast cells by itself, without IgE.
Chronic sinusitis
 the causes and treatment of chronic sinusitis.
Long-standing (chronic) sinusitis may be due to a fungal infection with a subsequent allergy. This is now called allergic fungal sinusitis. Some doctors believe that a sensitivity reaction to fungal infection (not necessarily an allergic reaction) could account for 96% of chronic sinusitis. However this is widely disputed .
Atopic eczema (atopic dermatitis)
the causes and treatment of atopic eczema.
The Trichophyton fungus can infect eczematous skin, though this is far less common than infection by Staphylococcus aureus (see below). Among patients infected by it, there can be an allergic reaction to Trichophyton which then makes the eczema worse.
There can also be an IgE reaction to a yeast, Pityrosporum ovale (also called Malassezia ovalis), in atopic eczema. This yeast is a commensal – i.e. a natural, and normally harmless, inhabitant of healthy skin. The inflammation of eczema makes the immune system far more tetchy so that it reacts allergically to this yeast, an innocent bystander which it normally disregards.
Candida  can also provoke an allergic reaction in eczematous skin. This is a more complex story, because while Candida is a commensal in the gut, it does not normally live on the skin. However, it may flourish in the disturbed skin of eczema patients.
Those with atopic eczema may also develop an allergic reaction to toxins from Staphylococcus aureus, a bacterium that often infects skin which is inflamed by eczema and damaged by scratching. Antibiotics are needed to treat the infection .
Seborrheic dermatitis
Not so long ago, this disease – which causes a red, scaly rash on the forehead, nose and cheeks, and sometimes on the chest –was labelled ’cause unknown’. Now most doctors believe that the yeast Pityrosporum ovale could well have a role in causing it. This yeast is part of the normal skin flora (see above), but it is found in greater numbers on the skin of seborrheic dermatitis patients. As well as overgrowth of the yeast, there is an immune reaction against it, usually involving the antibody known as IgG, rather than Fungi in the lungs
One form of infection-plus-allergy has been well recognised for many years - allergic bronchopulmonary aspergillosis, often shortened to aspergillosis.
The problem starts with the fungus Aspergillus fumigates, a ubiquitous mould that is found in special abundance in damp straw, compost heaps, bird cages and any decomposing material. Its spores are everywhere, and most immune systems quickly defeat them, but in some people, especially those with asthma, the spores begin to grow in the lungs. The fungus is found in the lung mucus, but does not actually invade the lungs. However, an allergic reation then occurs to the fungus.
This disease often goes together with asthma, or can be mistaken for asthma. There are three clues that point to aspergillosis:
• rubbery plugs of phlegm, either golden-
brown or green in colour
• fever whenever the asthma is severe
• worsening symptoms despite treatment.
Allergic bronchopulmonary aspergillosis is treated with steroids to control the allergic reaction, and physiotherapy to clear the mucus from the lungs.
Anti-fungal drugs have not proved very effective in the past. There are some newer anti-fungal drugs that may well be more useful, such as itraconazole and terbinafine. These are not widely used for aspergillosis at present, except in patients who also have cystic fibrosis or an immune deficiency. Because there has been no large-scale trial of these drugs, they are not usually given to people who simply have aspergillosis. However, they are sometimes prescribed for people who are unable to take steroids, or are not responding to steroid treatment. Anti-fungal drugs may become more widely used in the next few years, so it is worth discussing the possibility of this treatment with your doctor.
the allergy antibody IgE. Only about 12% of people who suffer from seborrheic dermatitis make IgE against the yeast.
One problem with seborrheic dermatitis is that, while it may improve with anti-fungal treatment, it usually comes back when the treatment stops. Doctors have therefore been looking for ways of keeping seborrheic dermatitis at bay after a successful course of anti-fungal treatment. One method that seems to work is to use a good anti-dandruff shampoo, in place of soap, to wash your skin once a week.
A medical earthquake
The recent discoveries about infection-plus-allergy have not posed any serious challenge to conventional thinking about allergy, because a disease of just this kind - aspergillosis (see box at left) - was already well known. A far more fundamental shake-up of traditional ideas about allergy and sensitivity has been necessitated by new research into atopic eczema. It is little short of an earthquake in the basic concepts of allergy and sensitivity.
To understand the extent of this earthquake, you need to know about the time-honoured system for classifying hypersensitivity reactions, which recognises four distinct types:
• Type I hypersensitivity — the IgE-mediated allergies  such as hayfever.
• Type II hypersensitivity - irrelevant to allergy, these antibody reactions mainly occur after transplant surgery, if the transplanted organ is rejected.
• Type III hypersensitivity - caused by a massive overload of antibodies and antigen in the blood. It is a feature of certain infections and autoimmune diseases, and can also occur in allergic reactions, though this is rare (13).
• Type IV hypersensitivity - the odd man out, because antibodies are not involved, or are not of central importance. Immune cells that can launch a direct attack are the movers and shakers here. These attacking-cells are sensitised for a particular antigen, such as dust mite or lanolin. Type IV hypersensitivity is a very slow reaction. Generally speaking, 48 hours pass, after an encounter with the offending substance, before the symptoms appear. The most common form of Type IV hypersensitivity is contact dermatitis (54).
Mystery has always surrounded atopic eczema. Although it crops up in the same atopic families that suffer from hayfever and asthma, and high levels of IgE in the bloodstream are typical of the disease, the actual role played by allergies in causing the symptoms is far from obvious.
The results of skin-prick tests - the standard test for an IgEmediated reaction - are puzzling. Patients tend to give a lot of positive results, many of which don’t mean much - the substances concerned do not provoke actual symptoms. On the other hand, skin-prick tests are often negative for substances that clearly do cause symptoms in challenge tests. Many children who regularly get eczema when they drink cow’s milk, for example, give a negative skin-prick test to milk. This conundrum has puzzled allergists for decades.
New discoveries about eczema do not entirely solve the puzzle, but they do go some way towards an answer, by revealing an immune response that cuts across the traditional categories. The most surprising fact is that even where skin-prick tests are positive and milk-specific IgE is involved in milk-induced eczema, this is not necessarily a standard IgE-mediated allergy.
While IgE antibodies may be involved, they are not necessarily teamed up with mast cells, their usual partners in crime (see box on p. 12). Instead, the IgE molecules are attached to special skin cells called Langerhans cells and dendritic cells. These have the role of picking up the antigen and showing or ‘presenting’ it to attacking-cells in the skin (a task called antigen presentation which is the ‘go’ signal that starts off all immune reactions).
The involvement of these attacking-cells, which are sensitised for a particular antigen, was a big surprise when first discovered. It makes this resemble a Type IV hypersensitivity reaction rather than a Type I.
IgE is not essential here, it seems — some patients do not have IgE for the substance that triggers their atopic eczema — but when Langerhans cells and dendritic cells are associated with IgE they do become far more zealous. This excitement is communicated to the attacking-cells, which mount a more powerful attack.
It looks as if what really matters in atopic eczema is the presence of antigen-specific attacking-cells in the skin, plus the heightened activity of the Langerhans cells and dendritic cells. If the individual has IgE for the antigen, it can play a part, but it is not essential.
In other words, this reaction cuts across two different categories of immune response — Type I and Type IV. (However, the kind of antigens that provoke the reaction are typical of IgEmediated allergy, rather than the kind of antigens that provoke contact dermatitis.) This has been exploited in a new and more sensitive set of diagnostic tests for food-induced atopic eczema (69).
Why atopic eczema is a feature of atopic families is the crucial question that remains unanswered. One factor may be that high levels of IgE in the bloodstream (not IgE for a particular allergen, but total IgE) make the whole immune system more excitable and prone to over-react. The next few years will no doubt solve this part of the puzzle too.
Peace-keepers or aggressors?
`It is bad enough having a child on an ultra-strict diet — Tim can’t have even a trace of cow’s milk or else he becomes violently ill. What makes it worse is when people — teachers, for example —ask what’s wrong. I take a deep breath and say “eosinophilic oesophagitis” then watch their eyes roll in disbelief.’
Tim’s disease is caused by a particular type of immune cell called an eosinophil. In the right circumstances, eosinophils can be valuable — like IgE and mast cells, they are geared to destroying parasitic worms . They produce some very toxic substances to kill these invaders, and it is the toxins that cause serious symptoms for Tim and others like him.
Any disease with ‘eosinophilic’ in the name involves vast numbers of eosinophils converging on some unfortunate part of the body. The stimulus that attracts them often remains unknown but once there, the toxins they generate cause inflammation (140) of a particularly violent kind.
It is only in recent years that doctors have begun to distinguish between patients such as Tim and children with classical food allergy, and to understand the cause of Tim’s symptoms. Several different forms of eosinophilic food sensitivity are now recognised (72). The exact relationship with IgE-mediated allergy remains a puzzle, because some sufferers make IgE to the culprit food but others do not.
That is not all — the eosinophil is finally coming out of the shadows and being recognised as an important agent in classical allergic diseases as well.
The fact that eosinophils appeared during the aftermath of an allergic reaction had long been known, but their role was misunderstood. What confused researchers was that eosinophils can break down histamine, the substance that kick-starts allergic symptoms. This ability gave eosinophils the appearance of peacekeeping troops, coming in at the close of battle to restore order. In fact, eosinophils are major aggressors — they do a whole lot of other things besides breaking down histamine, most of them pro-inflammatory. They can release toxins, just as they do in eosinophilic diseases, and they attract other inflammatory cells into the area. In short, eosinophils play a big part in keeping allergic reactions going once the initial burst of activity is over. This `Late Phase Reaction’ is enormously important .

 

how does allergy begin?
A mast cell, magnified about 10,000 times. The black granules contain histamine.
`At the beginning, I thought I just had a cold. I kept sneezing and coughing, and my nose was dripping. It got better at the weekend, and I thought — that’s good, it’s gone — but then on the Monday evening it started up again. The next thing I knew, I kept getting breathless. I’d been at the sawmill a month when it began. We were cutting planks of red cedar all day, and the dust was bad, it’s true. But I didn’t know that sawdust could cause you allergies. We were given dust masks, but they made you too hot. No one wore them. I found out later, from the doctor, that some men could work years at it before they got allergic to the dust, but with me it was just a month.’
Like many people with work-related allergy, Dan can actually pinpoint the time he became sensitised – when he began making IgE antibodies against the red cedar dust allergen. For allergies that are not caused by workplace allergens, this is rarely possible. The moment when symptoms begin may be obvious, but that is often long after sensitisation (making IgE to the allergen) first occurred. Long-term studies of children show that they may start giving positive skin-prick tests to pollens (a sign that they are making IgE to those pollens) while they are toddlers, but not develop hayfever until ten years later.
The basics of immunity
The immune system defends the body against infections and cancerous cells. One of its key jobs, before going on the offensive, is to recognise the difference between:
• self and non-self (e.g. the cells lining the lung, and bacteria trying to infect the lung)
• safe-non-self (e.g. a sandwich) and dangerous-non-self (e.g. Salmonella bacteria in the sandwich).
Through mis-regulation the immune system can cause:
• allergies (perceiving safe-non-self, such as pollen, as dangerous-non-self)
• autoimmune diseases (perceiving self as non-self).
The immune system consists of dozens of different kinds of cells (the immune cells) and a number of different antibodies – specialised ‘guided missiles’ (see box on p. 15) which are produced by certain immune cells.
There is also a huge array of messenger chemicals, which send general instructions (e.g. ‘calm down!’, ‘go for it!’ or’exterminate!’) from one type of cell to another.
Immune cells are self-contained units, many of them mobile and dispersed throughout the body. They travel around in the blood, and can move out of the blood vessels and into the surrounding tissues (skin, lung, nose, etc.).
These different components – immune cells, antibodies and messenger chemicals – interact in very complex ways. When an immune reaction occurs – i.e. the immune system recognises something, or mounts an attack on something – numerous different players are involved. All the reactions described in this book are very simplified versions of what actually happens.
Research shows that the first two years of life is the most vulnerable time as regards sensitisation to allergens. Very often, sensitisation occurs in the first few months, and sometimes even before birth.
Why is a young infant so easily sensitised? The answer lies not with the baby, but with the pregnant mother-to-be, whose immune system has to overrule its natural inclination to attack anything that is non-self. Potentially, a woman’s immune system could reject a foetus in just the same way that heart transplants are rejected. To prevent attacks on the foetus, the immune system is re-tuned during pregnancy, with one aspect of immunity – the part that’s most keen to attack a foreign body – being damped down.
This aspect of immunity is coordinated by cells known as T-helper-1 cells, or Th1 cells for short. To protect the foetus, these Th1 cells are asked to ease up during pregnancy. Meanwhile, since immune protection is still needed, their colleagues, called T-helper-2 cells or Th2 cells, become more active.
The classical allergic diseases
These four pages are concerned only with the classical allergic diseases, that is:
hayfever (an allergy to pollen)
perennial allergic rhinitis (a nasal allergy to a year-round allergen such as house-dust mite)
asthma where this includes an allergic reaction atopic eczema (42)
urticaria (nettle rash or hives) where this is allergic in origin, and the accompanying angioedema (swelling due to fluid escaping from tiny blood vessels into the surrounding area; it is sometimes called ‘water retention’)
anaphylaxis (a violent allergic reaction to food, insect stings, penicillin, latex, etc.)
food allergy (in most cases, an immediate and marked reaction to food, with symptoms in the mouth; there may also be anaphylaxis).
Running the immune system
T-helper cells are, in a way, mis-named, because they do not help at all – they just give orders.
These are the supervisors of the immune reactions, telling other immune cells either to lie low or to get busy. Where Th1 and Th2 cells differ is in the types of immune cells they send into action. Among those who get their go-ahead from Th1 cells are immune cells that attack directly, without producing antibodies – these are the ones that reject transplants and could, if given free rein, reject a foetus or retard its growth.
The Th2 cells, on the other hand, have among their preferred troops the immune cells that produce IgE antibodies – the allergy-causing antibodies. So one effect of protecting the foetus from rejection is to push the immune system towards a greater tendency to allergy.
This shift of emphasis occurs in the mother’s immune system, but it carries over into the immune system of the foetus because they are sharing the same blood supply, and the blood contains the messenger substances which fine-tune the immune system. Immediately after birth, the baby’s immune system is still following the same pattern, continuing to upregulate Th2 cells and downregulate Th1 cells. This is a crucial factor in setting the stage for allergic sensitisation.
Ideally, the world that the baby encounters just after birth should nudge the immune system in the opposite direction and get it operating in a non-allergic way. But the world in which we live is far from ideal in this regard.
For one thing, it is much too clean. As far as the immune system is concerned, ‘ideal’ would mean encountering quite a bit of dirt, such as garden soil, in the early stages of life. The soil contains harmless bacteria which do not cause any symptoms, but do tweak the immune system towards Th1 cells and away from Th2 cells. Bacterial products in household dust may do the same thing (21).
A long period of consuming nothing but breast milk would also suit the baby’s immune system rather better than being fed on cow’s milk formula or being suddenly weaned onto a number of highly allergenic foods, such as egg, wheat, soya (ubiquitous in The basic cause of classical allergy is an immune reaction involving mast cells and IgE antibodies.
Mast cells are plentiful in the lining of the nose, the airways, and the digestive tract. They have counterparts in the blood, called basophils.
Seen under the microscope, both mast cells and basophils look very granular inside. The granules are tiny storage compartments, containing stockpiles of messenger chemicals, notably histamine.
Histamine causes several different reactions:
• contraction of muscle around the airways. This reduces the diameter of the airway, producing an asthma attack.
• widening of blood vessels
• increased leakiness of the smallest blood vessels, allowing fluid and immune cells to escape into the surrounding area – for example, the skin or airway lining
• as a result of these two above effects, local swelling (called oedema or angioedema) and irritation – in the skin this is experienced as urticaria, or nettle rash, in the nose it causes blockage, itching and sneezing
• if sufficient histamine is released into the blood, a drastic fall in blood pressure, due to widespread opening of blood vessels, and leakage of fluid into the tissues; this occurs in anaphylaxis (58).
Histamine is released when mast cells are activated, a process called degranulation because the cells discharge their storage granules.
Mast cells release other substances at the same time, some of which attract more immune cells to the area, causing more inflammation. They help to produce a ‘Late Phase Reaction’ which occurs after the initial allergic reaction has died down, and lasts about 24 hours (13). Once activated, mast cells also start making messenger chemicals called leukotrienes which are highly inflammatory.
What causes a mast cell to degranulate? The answer is found on the surface of the cells, where the allergy antibody, IgE, sits. One end of the IgE molecule is bound to the mast cell, and the other end can bind to the allergen concerned. In someone allergic to egg, for example, egg allergen will bind, with great specificity, to egg-specific IgE antibody.
For the receptors to pass a message to the mast cell there have to be two IgE antibodies specific for the same allergen on the mast cell – and the allergen has to bind to both these IgE molecules, cross-linking them. This is the ‘go’ signal for the mast cell to degranulate.
processed foods), fish or peanuts, before it can handle them. Not taking antibiotics before two years of age would also help (although it might, of course, be very bad for the baby in other ways). Exactly why is not yet fully understood .
An ideal world for the immune system would also lack the by-products of cigarette smoking, whether in the blood of a pregnant woman or in the air that a baby breathes – both seem to promote the allergic tendency. In addition, the perfect world would lack central heating, fitted carpets, draught-proofing and thick upholstery. A house like this is heaven for house-dust mites but not for innocent young immune systems.
The problem with house-dust mites – apart from the fact that they breed like wildfire, and hole-up in mattresses, armchairs and soft toys – is that they produce a highly allergenic protein in their droppings. This protein interferes with the membranes of cells, making them less stable. It irritates various immune cells, including mast cells (see box at left), and can even make mast cells degranulate, as if there were a true allergic reaction happening.
Once mast cells have done this, they release messenger substances that arouse the immune system and make a genuine allergic reaction –beginning with the production of IgE to the dust-mite allergen – much more likely. In other words, dust-mite allergen is an agent provocateur, an aggressive substance that actually provokes the immune system into reacting allergically.
Until recently it was widely assumed that allergens were just inoffensive, passive substances which the immune system happened to take objection to, in a distinctly unreasonable way. The new discoveries about dust-mite allergen raise the question: could other allergens be more aggressive than previously thought? Certainly the peanut allergen, or other substances found in peanuts, seems to destabilise cell membranes, which may explain why this allergen so easily sensitises young children.
The role of genes
Faced with this non-ideal world, many children pull through without developing allergies, but others do not. This is where genes come in, making one child more susceptible to our allergy-promoting lifestyle and another child less so. Exactly how the genes make this difference is still not fully understood, but there are at least twenty genes involved , and it is clearly going to be a complex story. The overall effect of these genes is a greater tendency to make IgE, combined with mast cells and basophils  that are distinctly trigger-happy –much more eager to degranulate than in healthy individuals.
Given all the mayhem caused by mast cells and IgE, why does the body produce them at all? They cause a lot of damage to allergy sufferers and do little apparent good, at least for people in the Western world. The value of the mast-cell-IgE-reaction, for most of us, is historical – it wages war against large-bodied parasites such as tapeworms and schistosomes. (They are large by comparison with bacteria and viruses, and not easily tackled by other immune cells.) These unpleasant invaders have largely been eliminated in the developed world but are still rife in other countries. For millions of years such parasites were an inevitable part of human life, and this bit of our evolutionary past survives in our immune system.
The complexity of allergic reactions
`Each time the pollen season came around. I would start to get these pains, especially in my knees. I asked my doctor about it but she just looked at me rather oddly and said “take a paracetamol”. I couldn’t be sure it was linked to my hayfever, but the pains always came on just after the sneezing started. One year, it was all worse than usual, and I felt very tired too. My face was all puffy and I could feel that something was seriously amiss. That, as I now know, was because my kidneys were being affected. It was years before the doctor would refer me to an allergist, and I actually got an explanation for all this. I think for a long time my doctor thought I was making it up, or just imagining the pain in my knees.’
Karen suffers from a rare complication of hayfever involving an overload of pollen antigens and antibodies in the blood. Very large numbers of both are involved, and are bound to each other in dense tangled masses called immune complexes. Because these are carried around in the blood they are known as circulating immune complexes. They may be too large to be cleared quickly by the normal junk-munching systems that keep the blood clean.
Like a river choked with fallen leaves, which deposits some of the debris on its banks as it flows past, the blood inevitably
The other antibodies
Other than IgE, four main types of antibody exist – IgA, IgD, IgG and IgM. Although some of these antibodies help fight bacterial and viral diseases, they lack IgE’s ability to tackle certain large parasites. These other antibodies do not generally bind to mast cells, and therefore do not cause IgEstyle allergy. But they can be involved in various other sensitivity reactions – it is IgG antibodies that are active in coeliac disease for example, and IgA in dermatitis herpetiformis. And any kind of antibody can participate in circulating immune complexes, causing multiple symptoms (see below).
leaves behind some of the circulating immune complexes. They mostly become deposited in the tiny blood vessels called capillaries, particularly those in the skin, the kidneys and the joints. Inflammation (140) here can cause a range of symptoms.
This problem is known to doctors either as serum sickness or as Type III hypersensitivity. It is a well-known feature of several infections and of some autoimmune diseases.
Unfortunately, the potential for Type III hypersensitivity in allergies such as hayfever is much less well known among doctors, as Karen discovered. As well as affecting hayfever sufferers, Type III hypersensitivity can also be a complication of reactions to penicillin and certain other allergic reactions, such as insect-sting allergy.
When a reaction occurs to snake anti-venom – and it only occurs in an individual who has received snake anti-venom before – this too is Type III hypersensitivity. The snake anti-venom is cultured in horses, and the snake-bitten human who has received the snake anti-venom previously mounts a massive immune reaction to the horse proteins when snake anti-venom is injected for a second time. Large and numerous circulating immune complexes are formed, and although IgE is not involved, a very severe anaphylactoid reaction (see box on p. 59) follows.
Circulating immune complexes do not affect most allergy sufferers. But there are other immune responses that follow on from the initial allergic response in everyone with allergies –they are generally summed up as the ‘Late Phase Reaction’. This reaction starts 4-12 hours after the exposure to the allergen, and lasts about a day. It involves a number of different immune cells (including eosinophils – p. 19) and an even more varied array of messenger chemicals, making everything very complicated for medical researchers to investigate. When allergic symptoms become entrenched and difficult to treat, the Late Phase Reaction is usually implicated. But it has not been given much attention by doctors until recently, because the details are so complex and so poorly understood.

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.