Posts Tagged ‘allergic disease’

The simplest and most certain test for any sensitivity reaction is to expose the person concerned to the substance under suspicion and see what happens. This is known as a

challenge test. With true allergies, challenge tests are powerful tools, but they are also alarmingly close to reality. The risk of provoking a severe reaction requires a very

cautious approach.
By comparison, an indirect test – a roundabout way of seeing how the body responds, such as the skin-prick test (see p. 91) – has the advantage of rarely producing dangerous

reactions. The downside is that indirect tests can be misleading, precisely because they are not like the real-life situation. No indirect test is perfect – there are always

false positives and false negatives (see box on p. 91).
Challenge tests
If you undergo a challenge test with food or an airborne allergen, you will also be given dummy challenges with an innocuous substance which is indistinguishable from the item

being tested. Neither you, nor the tester who is scoring the reaction, should know which is which. This is called a double-blind trial because, to eliminate all possible bias,

both of you are in the dark. (The full name is a ‘double-blind placebo-controlled trial’ – the dummy challenge is also called a ‘placebo challenge’ or ‘control challenge’.)
The double-blind trial is a standard medical procedure and does not imply that the doctors think you are faking symptoms. Psychological forces are powerful things, and just

thinking that you might react to a test can be enough to produce a reaction – the process that generates the symptoms is largely unconscious.
Food challenge
A food challenge – eating the food that is under suspicion – is a key test for food intolerance (see p. 197). It is sometimes used for food allergy and other forms of food

sensitivity too, as a follow-up to skin tests. Some allergists use a food challenge only if the skin test is at odds with actual events reported by the patient. Other allergists

use food challenge more readily, to confirm skin-test results, and to assess the severity of the reaction.
Extreme caution must be exercised with immediate food allergy, because of the considerable risks involved. The test must be done under medical supervision with resuscitation

equipment to hand. A challenge test should never be done for true food allergy without some careful preliminary tests on the face and the lips (see box on p. 23). Even if these

tests produce no reaction, only tiny amounts of the food should be eaten to begin with.
Bronchial challenge
This type of test involves inhalation of an airborne allergen – such as pollen – suspected of causing asthma. Bronchial challenge carries the risk of provoking a severe asthma

attack, and few doctors use it unless there are compelling reasons to do so – such as demonstrating that someone’s asthma is due to an allergen encountered at work.
Skin-prick tests
This is an indirect method of detecting true allergic reactions. It is one of a family of skin tests that use a similar approach. The three different tests in this family are

known as: skin-prick tests or prick tests, puncture tests, and scratch tests.
For the skin-prick test – the technique used in Britain – a small drop of liquid containing an allergen, such as grass pollen, is placed on the arm. The doctor makes a small

prick in the skin, under the drop of liquid, allowing a minuscule amount of the allergen to get into the skin. A positive reaction is recorded if a red bump develops soon

afterwards. For accuracy, the bump must be compared to positive and negative controls (see below).
The puncture method is very similar to the skin-prick test but uses a slightly different technique for breaking the skin. The term prick-puncture test covers both techniques.
With the scratch method, the skin is scratched lightly, and the allergen solution is then applied over the scratch. This method gives less consistent results than prick-puncture

testing.
It is important to include a negative control in the test – a skin-prick test with plain salt water (saline). This should not produce much of a bump – if it does, the skin is

clearly over-reactive and the tests more difficult to assess. The doctor should also include a positive control – a skin-prick test with histamine, the substance that plays a

central role in allergic reactions. This should always produce a bump. If it does not, the skin is decidedly under-reactive, and the tests are invalid.
Taking antihistamines will make the skin under-reactive, and you should stop taking them before the testing, for a period ranging from a day to several weeks – it varies

depending on the particular antihistamine. Ask your doctor for specific instructions about stopping these and other drugs before testing.
Skin tends to be over-reactive to testing in people with dermatographism (see p. 52). Blood tests for specific IgE,
such as RASTs (see p. 92), are needed for anyone who has this condition. Eczema sufferers with a rash over large areas of the body may also require blood tests, if there is too

little clear skin for testing.
Skin-prick tests can produce both false positives and false negatives (see box below). Some allergic diseases will give a lot of false negatives and relatively few false

positives, while for others the reverse is true. The allergen itself influences the rates of misleading reactions: for example, tests for soya allergy are notoriously

unreliable, whereas those for peanut are far more accurate. The age of the person being tested also makes a difference. With all these influences at work, interpreting the test

responses is a real art, and the doctor’s experience counts for a lot.
All sorts of people offer skin-prick tests, including alternative practitioners. Get them done by a qualified doctor, preferably by an allergist, who will know how to make sense

of the reactions.
Note that the purpose of these tests, and of blood tests for specific IgE, is to identify the allergens that are bringing on your symptoms, not to predict how strongly you will

react to those allergens. The tests may give some Indication of the intensity of your reaction, but they cannot be regarded as a good guide to how you will respond to the

allergen in the future.
The safety record of skin-prick tests is very good. Occasionally a systemic reaction (anaphylaxis) occurs with these tests, but there are no records of any deaths. Nevertheless,

if you suffer from severe asthma or have experienced anaphylactic shock in the past, it is advisable for the doctor to have adrenaline and resuscitation equipment available.

Those with strong allergic reactions to latex may also react badly if they are tested with an allergen that cross-reacts with latex (e.g. cypress pollen), not just when tested

with latex itself. Taking beta-Mockers (see box on p. 150) increases the risk of a life-threatening reaction for anyone in these higher-risk categories.
False positives and false negatives
Apart from challenge tests, none of the tests used for allergy works with 100% accuracy. Most give both false positives and false negatives.
A false positive means that there is a positive test but no actual reaction when the allergen is encountered (e.g. eaten or inhaled). A false negative means that there is a

negative test result despite a genuine reaction (as shown by a challenge test, for example).
A test that gives relatively few false positives has good positive predictive value – in other words, if it suggests you are allergic to something, you probably are.
A test that gives relatively few false negatives has good negative predictive value. If it comes up negative, you are probably not allergic to that allergen.
Some tests for allergic reactions show good positive predictive value but poor negative predictive value, while for other tests the reverse is true.

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.

When Leonard Noon reported his first tentative experiments with immunotherapy for hayfever, in 1911 (see p. 164), he believed that pollen contained a toxin. Most people were

‘immune’ to this toxin, he said, in the same way that people might be immune to measles or diphtheria, but hayfever sufferers lacked this immunity. Noon thought that his

steadily increasing doses of pollen, injected just under the skin, were inducing immunity to the pollen toxin, in the same way that a smallpox vaccine could induce immunity to

smallpox.
Noon’s theory was all wrong, as we now know, but the important thing was that the treatment seemed to work. In fact it transformed the lives of some patients, especially those

who were very severely affected by hayfever. One spoke of a ‘marvellous cure’, another of going for walks to kick my old enemy the hay’.
So doctors kept using Noon’s treatment, and in time — when it became clear that Noon’s theory was flawed — medical researchers began trying to figure out how the injections

really worked.
Surprisingly, they have still not succeeded, even though a great deal is now known about the changes that can occur in people undergoing immunotherapy. Despite a wealth of

detailed knowledge (see p. 166), it remains impossible to say exactly how conventional immunotherapy reduces allergic reactions. Surprising discoveries about the effects of

conventional immunotherapy are being made all the time.
New methods of immunotherapy are still being devised today, and there are three different approaches being taken.
Firstly, there are doctors experimenting with modifications of the technique devised by Noon. For example, instead of injecting the allergen extract, some doctors are giving it

to their patients in capsule form. to be swallowed. Others are giving it as a liquid, to be placed under the tongue and held there for a few minutes, then swallowed (see p.

169). Sound scientific trials show that both these methods work well, at least with some allergens.
There are also experiments with speeded-up immunotherapy
(see p. 166), called ultrarush techniques — at the outset, injections are given at hourly intervals, or even more frequently (in hospital, of course, where severe reactions can

be dealt with immediately). Doctors have found that they can induce a remarkably rapid tolerance of the allergen in this way.
The second approach is to apply modern medical knowledge about allergic reactions and so develop entirely new methods of immunotherapy (see p. 168-9). Such research involves

working out, from first principles, novel ways of modifying the immune response in general, or the reaction to one allergen in particular.
This theory-led approach is certainly successful for classical allergies such as hayfever and perennial allergic rhinitis, where there is a good understanding of the basic

mechanism (i.e. the malfunctions of the immune system that produce the disease). But for those diseases where the underlying mechanism is only partially understood, such as

atopic eczema, this approach is not necessarily the best one. And for diseases such as food intolerance, where the cause of the illness remains largely unknown, it is a complete

non-starter.
The third type of approach is to devise a technique by trial and error, and then puzzle out the ‘how’ question later. This is the same sort of path as Noon originally took, and

some believe that this kind of pragmatic experimental approach — practising a method which seems to be effective, even though it’s a mystery how it works — is as valid now as it

was in 1911. Others disagree.
210 complementary therapies The two most widely used methods that have been developed in this way are Provocation-Neutralisation and Enzyme- Potentiated Desensitisation.

Although these techniques are practised by doctors with a conventional medical training, they remain ‘outside the pale’ as far as orthodox medicine is concerned. The

controversies that surround them are discussed below.
Enzyme- Potentiated Desensitisation (EPD)
This technique has been developed by a British doctor, Dr Len McEwen, who began work on it in the 1960s. It is now practised in many parts of the world, as well as Britain,

including the United States, Germany and Italy.
EPD is used for a far wider range of problems than conventional immunotherapy, being given to people with food intolerance and chemical intolerance, as well as to those with

true allergies. This — along with the fact that it is unclear how it works —contributes to the controversies that surround it, because these conditions do not have the same

basic causes.
Dr McEwen began with the observation that, when immune cells are aroused during inflammation — whether caused by allergy or some other stimulus — they release large amounts of

an enzyme called beta-glucuronidase. This enzyme increases the immune response to the allergen or antigen that provoked the inflammation.
Dr McEwen experimented with injecting beta-glucuronidase into the skin, along with very small amounts of allergen, believing that in such circumstances the enzyme might have the

opposite effect, and reduce the immune reaction to the allergen. Eventually he discovered a combination of enzyme and allergen which seemed to have the desired effect.
EPD has been tested, in a rigorous scientific manner, and the results suggest that it can work for hayfever and asthma, as well as for childhood migraine and hyperactivity in

children when these are triggered by foods.
In one trial with hayfever patients, researchers measured the levels of anti-pollen IgE following EPD treatment, and it did not rise during the pollen season as it normally does

in those with hayfever. This kind of finding is impressive because it is unlikely to be due to placebo effect. Not all studies have produced positive results, however.
In addition, doctors using EPD claim that it is very effective for patients with allergies who have not done well on the standard course of immunotherapy injections (see p.

164). This fits in with other studies suggesting that the immune changes brought about by EPD are fundamentally different from those induced by traditional immunotherapy.
Patients with true food allergy have been given EPD, and while it does not enable them to eat their culprit food, it does
seem to reduce their reaction to accidental exposures.
Doctors in the Netherlands are using EPD as a treatment for people with Chronic Fatigue Syndrome (CFS), and report that it helps about 50% of patients.
One point in favour of EPD is that it uses very small amounts of allergen, and is therefore very safe — anaphylaxis has never occurred with this technique.
Provocation-Neutralisation
‘After following conventional methods [of immunotherapy] for thirteen years, I heard Carleton H. Lee deliver a paper on provocative testing in 1965, at a meeting of the American

College of Allergists in Chicago. I was naturally sceptical, but tried his suggestions when I returned to my office. The results can only be described as astounding. Many

patients with unresolved allergic problems responded markedly and rapidly. Many with resistant asthma or perennial allergic rhinitis improved greatly or cleared completely when

food injection therapy was added to their inhalant injection therapy.’ So wrote Dr Joseph B. Miller — a distinguished allergist and paediatrician, and a Professor of Medicine at

the University of Alabama, in 1972.
The technique which he learned from Carleton H. Lee was controversial then and, although Miller developed it with great care and precision during the years that followed, it

remains controversial now.
There are two elements in provocation - neutralisation: testing and treatment. Both are used for a wide range of problems — not just classical allergic diseases, but also food

intolerance and chemical intolerance. As with EPD (see left), this is one of the controversial aspects of the technique.
Although provocation-neutralisation involves an injection technique that looks, superficially, very much like conventional immunotherapy (see p. 164), there are several

important differences. Firstly, the allergen extract used (in the case of true allergies) is a very dilute extract, so that far less of the allergen is injected than in

conventional immunotherapy. Likewise, in the case of food intolerance and chemical intolerance, the extracts of the offending substance are used in highly dilute form.
Secondly, the idea of the neutralising dose — which is the central plank of provocation-neutralisation — is quite different from anything in conventional immunotherapy. Broadly

speaking, the conventional technique (see pp. 165-6) works by slowly reeducating the immune system with a gradually increasing dose of the allergen. Only after a succession of

injections does the immune system start to behave differently on encountering the allergen. By contrast, in provocation-neutralisation treatment, the neutralising dose is

claimed to have an instantaneous and direct effect on the body, ‘turning off’ symptoms that have already begun. This is the neutralisation aspect of the technique. The doctors

who practise this technique do not claim to know how the neutralising dose might work.
According to the theory of provocation-neutralisation, the strength of the extract that acts as a neutralising dose is specific for a particular allergen and a particular

person. It can only be worked out by a rather slow procedure involving a series of injections. These are intradermal injections – they place the allergen extract in the skin, at

a slightly deeper level than a skin-prick test. (For treatment, rather than testing, subcutaneous injections are used – these go deeper than intradermal injections, placing the

allergen extract just underneath the skin. Neither hurts very much.)
Ideally, the neutralising dose should be decided on by measuring the size of the wheal (a raised area of skin around the injection site), and whether it grows, stays the same

size, or disappears. The doctor or nurse carrying out the procedure can, in theory, work out the neutralising dose just by careful examination of the skin wheals.
However, it is part of the tradition of provocation-neutralisation techniques that verbal feedback from the patient is also taken into account – so if the patient says that an

injection has turned off the symptoms, that reinforces the belief that the neutralising dose has been found.
The problem with this aspect of provocation-neutralisation is that expectations, and the power of suggestion, can become involved. So if the doctor or nurse says ‘you may find

that this next injection makes the symptoms go away’, that is often exactly what happens – because the forces of placebo effect (see p. 233) come into play. Unfortunately,

verbal interactions such as this are a key aspect of the provocation-neutralisation procedure in many clinics.
Just the same hazard besets provocation - neutralisation if it is used to test for the existence of allergy or intolerance, because it is quite common for practitioners to tell

patients which allergen (or other offending substance) is being injected and to ask if any symptoms are provoked by the injection. This is not good practice – if someone expects

to react to a particular substance, they are quite likely to produce symptoms through purely psychological mechanisms (see pp. 232-3).
Quite apart from this, the question of allergy testing with provocation-neutralisation techniques is contentious, because the pioneers of the technique, such as Professor

Miller, never advocated using provocation - neutralisation in this way. Using it as a routine test for sensitivity reactions was a later development, and there are many doctors

today who, while they practise provocation-neutralisation as a treatment, say that it does not work well as a test for sensitivity reactions. While they agree that injecting a

dose
which is either stronger or weaker than the neutralising dose may provoke actual symptoms (this is the provocation aspect of the technique) they don’t think the reaction is

reliable enough to form the basis of a test for allergies. Nor do they think that using skin-wheal measurements alone (i.e. silent testing) turns the technique into an accurate

test for allergies. That is not what the provocation-neutralisation technique was designed for – it is about treatment, not testing.
The evidence from research
Recent research from the Nova Scotia Environmental Health Centre in Canada confirms that testing by provocation injections is not reliable. The subjects in this study were all

suffering fr= multiple chemical intolerance, a condition which – for one reasor or another – makes patients liable to develop symptoms at an,, time. No less than 70% of these

patients experienced symptoms in response to a dummy injection which contained none of the offending substance. Indeed, 15% of patients also produced a skin wheal in response to

some of the dummy injections, confirming that even this reaction may be subject to the power of suggestion (see pp. 232-3).
Looking just at the patients who did not react to the placebo injection (i.e. those least susceptible to suggestion) the test still did not yield any reliable result – a person

might react to one injection with a particular substance, but fail to react to a subsequent injection with the same substance. The authors concluded that their patients were ‘in

a state of heightened sensitivity as the result of the chronic irritation by various environmental components and other external and internal stressors’. In this state of

sensitivity. patients are so close to the brink all the time that the smallest thing can trigger symptoms. So the apparent reactions to the test injections were actually

determined by other factors – some psychological factors (including a psychological response to the prick of the needle) and some external ones, such as exposure to smells or

very small amounts of airborne chemicals.
Another recent research study, carried out by scientists at the University of California, confirmed the finding of the Nova Scotia team as regards testing. Although this study

did not set out to look at the use of the neutralising dose for treatment, some of the patients were given neutralising doses during the testing process and the researchers

observed that ‘in most cases a single neutralising injection relieved the symptoms’. This casual observation clearly needs to be confirmed by more rigorous testing. Oddly

enough, despite this positive observation about the neutralising doses, the overall conclusion of the researchers was to completely dismiss all aspects of

provocation-neutralisation as ‘the result of suggestion and chance’. This conclusion has been widely publicised in the United States as part of a general campaign against

provocation-neutralisation and doctors who practise it.
Other researchers have looked at treatment with neutralising doses, using stringent scientific methods (a double-blind placebo-controlled trial — see p. 90), and found that they

do work. In one such trial, patients with asthma. and allergies to dogs or cats, were treated with injections of the neutralising dose. They showed a reduction in the

sensitivity of their airways, as measured by objective tests. In another experiment, patients with perennial allergic rhinitis and an allergy to house-dust mite were studied,

and the neutralising dose was given as drops of allergen extract placed under the tongue (sublingual drops) – an alternative to injections. The blockage of the nose, as measured

by scientific tests, was reduced by the neutralising dose.
A great many more trials of this kind would be required to convince most doctors that provocation-neutralisation works.
Furthermore, the recent study from California – which observed a number of practitioners of provocation-neutralisation at work with their patients — showed that these

practitioners need to be a lot more rigorous and objective in their approach. However, the fact that provocation-neutralisation is often practised badly does not necessarily

mean that the basic technique is without any value. There are a great many level-headed doctors and patients who, while initially very sceptical about

provocation-neutralisation, have found it surprisingly effective – just as Professor Miller did back in 1965.
Deciding for yourself
So is provocation-neutralisation an option that is worth trying for your condition?
As regards testing, the answer is probably ‘no’. The most reliable tests are skin-prick tests or FAST blood tests for true allergies (see pp. 91-2), an elimination diet for food

intolerance (see p. 194), and avoidance followed by re-exposure (a challenge test) for chemical intolerance.
As regards treatment for true allergies, conventional immunotherapy has been far more thoroughly tested and, if you can get it (not easy in Britain — see p. 164), is probably a

better bet. It is definitely the best treatment for allergy to insect stings.
The major advantage that provocation-neutralisation has over conventional immunotherapy, in the case of true allergies, is that it is far safer. Because such small amounts of

allergen are used, anaphylactic reactions (see p. 58) don’t occur.
When it comes to treatment for food intolerance, complete avoidance of the problem food(s), for a period of a year or two, is usually a very effective treatment (see p. 77).

Other forms of treatment are only needed for people who find that they have
intolerance to a great many different foods (on the basis of an elimination diet, not kinesiology, blood tests and the like — see p. 93) and cannot devise an adequate diet from

the foods they are able to eat. For such people, provocation-neutralisation may be worth a try. Many patients feel that they have gained considerable help from this treatment.

They report suffering fewer symptoms and being able to return to a more nutritionally balanced diet.
In the case of chemical intolerance, the first line of treatment should be to avoid the substances concerned as far as possible, eat a good balanced diet, and take a vitamin and

mineral supplement if nutritional deficiencies are suspected. Treating any underlying hyperventilation (see pp. 226-9) can also help considerably. Only if there are persistent

symptoms, and you are sure these are not due to psychological causes, might provocation-neutralisation be worth a try. Some people with chemical intolerance do find it is

helpful, but whether this is a real effect, or simply placebo, remains uncertain.
If you decide to give provocation-neutralisation a try, find a practitioner who has good medical qualifications, who seems objective and sensible in their approach, and who

doesn’t make implausible claims for the technique. Take note of what other treatments the practitioner offers, and whether these seem rational or not – this is often a good

guide to the care and objectivity with which provocation - neutralisation is carried out.
Ask the doctor how he or she assesses the neutralising dose. and avoid anyone who does not use the traditional method of a series of injections combined with wheal measurement.

When the neutralising dose is being assessed, say that you would like it to be done ’single-blind’ – that is, you don’t want to be told anything about what is being injected.

Reporting how you feel to the doctor or nurse during the assessment is fine, but only mention really significant symptoms, or a very definite clearance of the symptoms, if this

occurs. These precautions will help you to be sure that you are getting something which is of genuine benefit, rather than just a very expensive form of placebo treatment.
I always wanted to be a doctor, and I enjoyed
medical school immensely, but once I became a
ell GP, I no longer felt quite so sure about what I was doing. It seemed clear to me that there were a lot of people coming to my surgery who I couldn’t do much for. And there

were others who, while I could treat their obvious medical problems with some success, remained distressed and were not coping well with life. Once I became a senior partner in

this practice, I experimented with having a counsellor come in for one session a week, and then an osteopath for the bad backs. It was popular with the patients, and I saw some

people improve enormously. Now we have stress-management classes too, and one of my colleagues has trained in acupuncture, which he uses for selected patients. We also use

elimination diets for patients with a lot of long-term problems like migraine. Overall, I think of it in terms of having more tools at our disposal - being able to tackle things

from a different angle when standard medicine isn’t hitting the spot.’
Geoffrey, a GP in the north of England, is typical of the reconciliation that is now beginning to occur between conventional medicine and alternative medicine. But he also has

plenty of criticisms to make of the alternative scene. ‘The idea that alternative medicine is “holistic” while conventional medicine isn’t, really raises my hackles. Most GPs

could be magnificently holistic if they had an hour with each patient as alternative therapists usually do. We have just 15 minutes, on average, and we have to pack a lot into

that - including our basic duty to eliminate the possibility of serious organic disease such as cancer. Time pressure is everything now, and it has squeezed the humanity out of

medicine, to a very large extent. But the potential for a holistic approach is there - most doctors have a tremendous store of wisdom and life
experience at their disposal, which could form the basis of a holistic approach to treatment if only there were more time to spend with each patient.’
It is in search of a more unhurried and all-embracing approach to treatment that many people turn to alternative medicine. Frequently, what they get out of the therapy has less

to do with the actual methods used, and still less with the theories behind those methods, but everything to do with spending a quiet hour with someone supportive and caring who

listens to all the complex concerns that surround any illness, gives reassurance or advice, or just offers a `safe space’ in which to talk about life’s difficulties.
Other people turn to alternative therapies due to a more serious disillusionment with orthodox medicine. When patients with inscrutable medical problems -such as persistent

unexplained diarrhoea, joint pain or chronic urticaria - are given a succession of different diagnoses by different doctors, they often lose faith entirely in modern medicine

and reject orthodox treatment in favour of alternatives. This is a great mistake. Modern medicine isn’t perfect, but that is only to be expected, because it is not a fixed body

of knowledge but a process - a continuing journey of questioning, investigation, discovery and improvement. Scientific medicine has come a tremendously long way from the state

of ignorance that prevailed two centuries ago, and it will undoubtedly go farther.
Conventional medicine has a great deal going for it - ask anyone over 50, with severe life-long asthma, what they think of treatment now compared to treatment in the 1950s or

early 1960s. You will hear a hymn of praise to the improvements in both drugs and drug delivery systems. Asthma is just one example -conventional medicine has a lot to offer for

all the classical allergic diseases. Alternative medicine should always be regarded as an adjunct to conventional treatment, not a replacement. That is why many doctors prefer

the term complementary medicine.
A third reason for using alternative medicine is a more philosophical one, a need to understand illness in some larger sense, often part of a general search for meaning in life.

Some types of alternative treatment attempt to offer metaphysical reasons for allergy -rather than the mundane explanations of antibodies and immune cells that are given in this

book - and this can be attractive to some people. There is no harm in this approach, which can prompt you to make a critical review of your life, look at unresolved emotional

issues, or reassess choices that are making you unhappy.
But not all illness, or worsening symptoms, can be explained by emotional causes, and the rigid belief that every illness must have a meaning can be damaging. It easily

degenerates into the wholesale psychologisation of illness, the kind of blame-the-victim mentality which can attribute hayfever to ‘Emotional congestion; fear of the calendar; a

belief in persecution; guilt’ and asthma in babies to ‘Fear of life; not wanting to be here’. Both these diagnoses are taken from the best-selling You
can Heal your Life by Louise Hay, which is very influential among some alternative therapists. This compulsive psychologisation of illness can be profoundly damaging, and if

your complementary therapist is preoccupied by ideas of this kind, you could find yourself on a very long guilt trip indeed.
Apart from the psychological aspects of alternative medicine, there is the question of whether it actually works in a practical sense - whether it provides more than just

emotional support and placebo effect (the benefit that comes from any treatment which you believe in). This is always the central question for scientific medicine in relation to

its own treatments,
and conventional doctors naturally apply the same criteria to alternative medicine. Most of this chapter is concerned with trying to answer that question.
Unfortunately, there are so many different kinds of alternative therapy available today that it is impossible to cover all of them in this book. To complicate matters further,

many complementary therapists now practise two or more different techniques, mixing them to
produce their own unique cocktail of diagnosis and treatment. This eclectic approach can span a remarkable range - you may find a therapist doing distinctly whacky stuff such as

iridology (looking at the eye to diagnose all illness - it has been tested and definitely doesn’t work), combined with something perfectly rational such as an elimination diet.

(The elimination diet might be presented as a ‘detox diet’, but it is actually being used to detect food intolerances.)
With new forms of therapy springing up all over the place, a healthy scepticism is a distinct asset for the consumer. Be sceptical about any diagnostic test or treatment that is

only being practised by one person in the country, or in the world - when doctors hit on something that works, they want other doctors to try it out. World exclusives in

medicine are usually suspect.
Avoid any practitioner who tells you to stop using your drugs without your doctor’s consent. Likewise, avoid those with a messianic gleam in their eye, an evident disregard for

logic or reasonable discussion, or an amazing cure that fixes everything from acne to AIDS. Very few of those who sell bogus cures and phoney diagnostic tests are complete

rogues. Most are nice people who are quite genuinely convinced that they have indeed found the answer to people’s problems. The powers of placebo effect (see p. 233) can sustain

such a conviction for a very long time.

Acupuncture
Acupuncture shot to fame in the West in 1972, when James Reston, a correspondent for the New York Times, fell ill with appendicitis while covering President Nixon’s historic

trip to China. Following the removal of his appendix, he received acupuncture treatment for pain, and was highly impressed with its effects.
His Chinese doctor invited Reston to witness the use of acupuncture in anaesthesia, and he reported the remarkable fact that patients undergoing surgery could be free from pain

with just a few tiny needles inserted into carefully chosen points on the body. They remained alert and talkative throughout the operation.
Traditional Chinese medicine has enjoyed a good reputation in the West ever since, but what few people realise is that acupuncture anaesthesia is a very new invention. Surgery

was not traditionally practised in China and it was only in the 1950s, after Chairman Mao had urged Chinese doctors to unify Western and Chinese medicine, that the anaesthetic

potential of acupuncture was discovered.
The remarkable effects of acupuncture anaesthesia made a huge impression on doctors in the West – a high-profile success that has had both good and bad results. On the positive

side, conventional medicine has been prepared to take acupuncture seriously, and to undertake some research into its effects. On the negative side, most
of that research has concerned pain control – the effects of acupuncture on the endorphins. These are natural painkilling compounds produced by the body (their effects are

mimicked by opiate drugs such as morphine and heroin).
Western researchers have paid little attention to how acupuncture affects most other aspects of health, including the immune system and allergic diseases. One exception to this

is asthma, where certain nerves do play a large part in producing the symptoms (see box on p. 235).
Treating the person
Diagnosis and treatment are far more orientated towards the individual patient-, in traditional Chinese medicine, and diagnostic labels such as ‘allergy’ or `hayfever’ are less

important than the particular character of a person’s Qi (see box on p. 215), as detected by the acupuncturist. A traditional Chinese acupuncturist pays great attention to the

quality of the different pulses and takes them at the start of every appointment, and at intervals during treatment, to check how the Qi flow has changed. Each treatment session

is unique and tailored to the individual’s condition at that particular moment.
This makes it very difficult to carry out conventional scientific research into traditional acupuncture.
In an effort to make acupuncture accessible to research, a more Westernised and formulaic approach has been developed, using orthodox medical diagnosis and needling a set of

acupuncture points that are prescribed for that medical condition. Experts in traditional acupuncture feel that this approach – first name the disease, then apply a standard

remedy – will often fail, and is missing the whole point of acupuncture.
That is not the only problem with Westernised acupuncture, as Dr David Eisenberg of Harvard University, a leading expert on acupuncture, points out. He describes a typical

acupuncture session in China: ‘Each time the acupuncturist inserts a needle, he or she asks the patient, “Do you have it or not?” referring to the patient’s “obtaining the Qi”

(de Qi). The question asks whether the patient has felt a sensation of fullness, distension, pins and needles, or the like, from the insertion of the needle in the spot being

used… Most Chinese have experienced acupuncture and they understand the phenomenon of de Qi… By contrast, most Western patients seeking acupuncture therapy know nothing of

the phenomenon of de Qi. Not knowing what sensations they should anticipate, they cannot tell the acupuncturist whether a needle is in the right place. When both therapist and

patient know little about de Qi, as frequently occurs in Western acupuncture clinics, the result is bound to be disappointing.’ Fortunately it is possible to find acupuncturists

who have been properly trained, and the sensation of ‘obtaining the Qi’ is perfectly detectable, even to a sceptical Westerner, so look for someone who pays attention to this.
There can be emotional and psychological reactions to acupuncture, so make sure that you also feel relaxed with your acupuncturist and that there is a certain empathy between

you.
Does acupuncture work for allergies?
According to Chinese theories, acupuncture can have some benefits in any illness – if you are ill, your flow of Qi must be disturbed, and it will help to put that right. Indeed,

most people do feel a sense of well-being after an acupuncture session.
To look at this from a Western scientific perspective, acupuncture can stimulate your body to increase its production of endorphins (see p. 214). This gives you a mild high,

similar to that you’d get from running for a couple of hours. Feeling relaxed and confident helps most people to cope better, and gives them a new perspective on life’s

problems. Since the mind plays some part in almost all illness (if only to aggravate the effects of an underlying physical problem), inducing a more positive state of mind can

be of benefit.
As regards more specific effects, several studies show that acupuncture can have a small, short-term effect in opening up the airways of asthmatics. This is not surprising

because acupuncture affects the autonomic nervous system, the ‘auto-pilot’ section of the nervous system (see box on p. 235) which can tighten or relax the muscles around the

airways. A short-term effect is just that – it doesn’t treat the real problem. What matters more in asthma is the long-term impact of any treatment on the underlying

inflammation of the airways (see p. 36). Although some studies of acupuncture treatment have found a reduction in inflammation, other studies have not. However, only one study

to date used an individualised approach to acupuncture, as opposed to a same-for-everyone formula. It is interesting that this study did find good long-term effects on airway

inflammation.
The larger picture
Acupuncture is just one element of Chinese medicine, which has several other techniques available. In China (and in some Chinese clinics in the West) these techniques are used

together, as different ways of tackling the same problem. No traditional Chinese doctor would dream of trying to treat every patient with acupuncture alone and, in the case of a

patient with allergies, herbal remedies would usually be a central part of the treatment.
A recent and very careful scientific study from Germany took this combined approach with hayfever, and showed some benefit. The patients were treated with both acupuncture and

herbal treatment, using a standardised regime but with additional acupuncture points and herbs chosen to suit the individual. Those treated reported a substantial improvement in

how they felt generally –but not in the specific symptoms of hayfever.
The flow of energy
Acupuncture is rooted in ancient Chinese ideas of the human body. which are radically different from those of Western medicine:
•    Vital energy. called Oi or Chi (and always pronounced ‘thee’). is what distinguishes living bodies from dead ones. It should flow easily and harmoniously thrOLIC11011i

the body nourishing and protecting the organs. When the flow of Qi is blocked, or becomes unbalanced. then illness develops. - Channels called meridians are the conduits for Qi

in the body. They mostly run vertically (i.e. from head to toe) and the points where acupuncture needles are inserted all lie on these meridians.
•    The flow of Qi can be measured by carefully taking pulses — not just one pulse as in Western medicine, but several different kinds of pulse.
•    By detecting disturbances in the flow of Qi, and correcting them, existing illness can be cured, and incipient illness prevented, before there are any obvious symptoms.
The nature of the meridians and the acupuncture points remains a mystery to Western doctors. Some parts of the meridians run roughly along the lines of certain nerves or blood

vessels, but they do not follow them exactly. The acupuncture points have no anatomical reality — there is nothing to see either on the surface or under the skin. However, many

are located near major nerve endings or over deep pressure receptors.

Allergies and Pregnancy
Great care is taken in prescribing drugs during pregnancy. This is something that doctors are now exceedingly cautious about, but do tell the doctor as soon as you decide to try for a baby. The foetus is most vulnerable to damage by drugs during the first three months, and especially the first few weeks after conception.
Your prescription will be changed if the drugs you are currently taking could pose any threat to the unborn child. A drug that has not had sufficiently rigorous testing for safety during pregnancy, or lacks a long track record, will probably be withdrawn. New drugs are generally considered to be slightly more risky than the tried-and-true older drugs: rare side effects may not come to light during the testing which precedes release of a drug, but they do become apparent once the drug is in widespread use for a long time (see pp. 136-7).
If you are already pregnant as you read this, don’t worry too much. With a few notable exceptions – certain antihistamines and antibiotics – most of the drugs used for allergic diseases do not pose any major risk to the unborn child. There is probably nothing to worry about, but see your doctor as soon as you can – and talk to a pharmacist, in the meantime, if you are concerned. Don’t panic, and don’t stop taking your drugs unless you are absolutely sure that you can do without them. Do not stop taking your drugs if you have asthma.
Some non-prescription medicines are best avoided during pregnancy. Read the packet carefully, and talk to your pharmacist if you have any doubts.
From the moment you start trying for a baby, remember to tell any medical personnel who treat you, and any pharmacist you buy medicines from, that you could be pregnant.
Immunotherapy and skin testing
Immunotherapy should not begin during pregnancy, because of the risk of anaphylaxis (see below), but pregnant women who are already undergoing immunotherapy can continue.
The safety procedures described on p. 166-7 should be followed with meticulous care.
Most doctors continue immunotherapy at a steady ‘maintenance dose’ because there is always a small risk of anaphylaxis with immunotherapy when the dose is increased. Some doctors are even more cautious and reduce the maintenance dose during pregnancy, but give more frequent injections – this minimises the chance of bad reactions.
Many doctors do not give skin tests for allergy during pregnancy, as these also carry a very small risk of anaphylaxis. If you do have skin tests, there must be resuscitation equipment available. Intradermal tests (see p. 92) are best avoided.
Severe allergic reactions (anaphylaxis)
Special care should be taken to avoid anaphylaxis during pregnancy as this may increase the chance of a miscarriage.
Injecting adrenaline during the first three months of pregnancy may carry some small risk of malformation of the baby. But the evidence here is uncertain, whereas the danger to your own life, if you don’t use adrenaline when you need it, is both certain and substantial. If you have an adrenaline self-injection kit, talk to your doctor now about what you should do in an emergency. The best policy is to be ultra-careful about avoiding your allergen, so that anaphylaxis does not happen.
Women who suffer from exercise-induced anaphylaxis (see p. 59) generally play safe by exercising less strenuously while pregnant. The problem can get worse during pregnancy, but it does not usually do so. Labour itself is very strenuous of course, but problems during the birth are uncommon. If anaphylaxis does occur, the reaction is usually quite mild – nettle rash only – and the baby is delivered alive and well. However, many women find that the attacks of exercise-induced anaphylaxis are more frequent and severe when they start exercising again after the baby is born. It is best to resume exercise very gradually.
Eczema and other skin problems
Atopic eczema may improve during pregnancy, probably because the body produces slightly more of its own natural steroid, hydrocortisone. Contact dermatitis may either improve or flare up.
Stretch marks often itch a great deal, and widespread itchy skin, with or without a rash, is a common problem during pregnancy. These are not usually allergic reactions, and no cause can be identified in most cases. The skin tends to recover a few days after the birth.
If there is itching in the vulva) area, this could be due to a Candida infection (your doctor can prescribe a safe treatment) or it might be just another of those unexplained itches of pregnancy.
Hayfever and other nasal allergies
The natural hormone changes of pregnancy affect the nose, which can become more blocked. If you have allergic rhinitis this will add to your woes. See your doctor and make sure that your drug treatment is adequate (see p. 29). The nose-clearing exercises on pp. 230-31 might also help.
Asthma
Severe asthma can be bad for both the pregnant mother and the unborn child. Uncontrolled asthma increases the risk of the baby being born prematurely – and premature babies are more likely to develop asthma themselves. The death rate for newborn babies is also higher if the mother has poorly controlled asthma.
Treating a severe asthma attack promptly helps to prevent any damage to the baby, so don’t hesitate to call an ambulance –and tell the operator you are pregnant. The ambulance should be carrying oxygen which is particularly important for helping the unborn baby through the attack.
If you have asthma, don’t stop using your drugs or reduce the dose unless advised to do so by a doctor. Because it is so important to keep asthma under control during pregnancy, your doctor may want to add, or increase, preventer drugs such as inhaled corticosteroids or sodium cromoglycate (see p. 148). It
also makes sense to monitor your peak flow twice a day (see p. 97) so that you have advance warning of serious attacks.
Unfortunately, some asthmatics – usually those who have severe asthma to begin with – get much worse during their pregnancy. In such cases, careful monitoring and increased use of preventer medicines are essential. The symptoms usually increase from week 24 to week 36 of the pregnancy. The last four weeks tend to be much better, and things are back to normal by about three months after the birth.
Some women with asthma have fewer symptoms while they are pregnant, and for others their asthma stays about the same.
Asthma can also appear for the first time during pregnancy, and may be quite severe. However, a relatively mild breathlessness can be due simply to the fact that, as the pregnancy advances, the chest cavity, and therefore the lungs, become compressed. This is not necessarily asthma.
This simple physical effect can also add to the difficulties experienced by women who were already asthmatic before they became pregnant.
GER (acid reflux) – see p. 38 – can contribute to asthma during pregnancy, and treating this problem may help.
Asthma attacks during the birth
Severe asthma attacks very rarely occur during labour, but it is still important that all the medical staff in attendance know you have asthma. They should also be told if you have taken steroid tablets during the previous two years. A record of when you took steroids, how long for, and at what dose, will be valuable. You may need a low dose of steroid to get you through the physical stress of labour (see p. 142). Some doctors believe that patients who have been using high-dose inhaled steroids should be treated in the same way.
Smoking
Smoking is a bad idea if you have allergies or any allergic tendency in the family. Smoking is a very bad idea indeed if you are pregnant, or a parent. This is the moment, if ever there was one, to give up.
Enlist your doctor’s help, and ask if counselling, psychotherapy or other forms of support are available. If you have tried all this before, and failed, then talk to your doctor about the possibility of using nicotine patches. Some doctors believe that, for pregnant women who smoke 20 cigarettes or more a day, the advantages of nicotine patches outweigh the risks to the foetus. Nicotine levels in the blood are lower with patches than with heavy smoking, and your baby is not enduring the hundreds of other toxins found in cigarette smoke.

Drugs for Asthma
The drug treatment of asthma is far more complex than for any other allergic disease. Drugs prescribed for asthma fall into two basic categories: those that open up the airways by relaxing the airway muscles, called relievers, and those that treat the inflammation in the lining of the airways, called preventers. The former offer a ‘quick fix’ - like taking an aspirin when you have a headache. Just as the actual cause of the headache is not treated by an aspirin, so the actual cause of the asthma attack is not addressed by relievers. Preventers, on the other hand, tackle the basic problem - the inflammation that triggers the contraction of the airway muscles (see p. 36).
In the past ten years, there has been a quiet revolution in asthma treatment, with far more people being given preventer inhalers, usually low-dose steroids. The aim is to get the airways in better condition, with the inflammation thoroughly damped down, so that the airway muscles don’t go into spasm. The ultimate objective is to make people far less reliant on reliever inhalers, because the potential hazards of over-using them are now realised.
The details of modern asthma management, and the different approaches used, are described on p. 160, following the discussion of the main types of drug used for asthma treatment.
Beta-2 relievers (beta-agonists)
Our airways open up when we produce adrenaline. This is the body’s natural response to feeling angry or frightened. The adrenaline widens the airways so that we can run faster or fight more vigorously.
Adrenaline (epinephrine), given as a drug, was among the earliest treatments for asthma. However, it also stimulates the heart to beat faster and raises
the blood pressure. While it is useful for emergency treatment (see p. 155) the side effects make it too hazardous for routine use.
The beta-2 relievers work by mimicking adrenaline – they bind to the same receptors in the airways, the beta-2 receptors. Binding to these receptors stimulates the airway muscles to relax, so that the airways open up.
In other respects, the beta-2 relievers are not like adrenaline. Clever chemical manipulation has made them sufficiently different from adrenaline to have little effect on the heart and other organs, when taken at normal doses.
Beta-2 relievers are best taken by inhalation. Although tablets and syrup are available these are far more likely to bring on side effects, because the dose needed is so much bigger.
Inhaled beta-2 relievers target the drug directly on the airways, so the dose can be smaller. They also have the great advantage of taking effect soon after being inhaled, and giving full relief from airway narrowing within 10-15 minutes.
There are two different kinds of beta-2 relievers:
•    the traditional short-acting beta-2 relievers whose effects last for 3-6 hours (usually about four). The modern consensus is that these should be used only when needed, not taken routinely.
•    the newer long-acting beta-2 relievers, which last up to 12 hours. These drugs are prescribed for more severe forms of asthma (see p. 154), and are generally used routinely, twice a day.
A key question for asthma sufferers is: How often can short-acting beta-2 relievers be used? Ideas about this have changed considerably over the last 20 years, and no doctor would now want to have patients using a Ventolin inhaler five, six or more times a day - something that was quite common in the past. This level of need for beta-2 relievers indicates that the asthma is poorly controlled and requires treatment with a preventer, to quell the inflammation in the airways.
Detailed policy on beta-2 relievers still varies from one part of the world to another. British guidelines state that anyone who needs to use a short-acting beta-2 reliever more than once a day, or who suffers from nocturnal asthma, should be given a preventer as well. The international guideline is more stringent: if a short-acting beta-2 reliever is needed more than three times a week, a preventer should also be prescribed.
How safe are these drugs in the long term? The cause of the big re-think on beta-2 relievers was an epidemic of asthma-related deaths in New Zealand between 1976 and 1988. The death rate from severe asthma attacks was 2-4 times its previous level for a while, and over a thousand New Zealanders died in the epidemic.
There has been a huge controversy over what exactly caused these deaths. Most researchers now agree that the main cause was a new brand of inhaler that delivered a double dose of the drug fenoterol, a short-acting beta-2 reliever with a very powerful effect on the airways and quite high levels of side effects involving the heart. The same brand of inhaler may have been linked to increased death rates in Canada and Germany.
Research suggests that the problem was greatest in New Zealand because sales of the new inhaler were highest there, and because many patients got their inhalers through repeat prescriptions. As a result, people whose asthma was deteriorating badly were not seen by a doctor and were using large amounts of beta-2 reliever, rather than taking preventer drugs. This is now believed to be a major cause of asthma deaths. There are three separate factors involved:
•    The beta-2 reliever covers up the effects of the severe inflammation of the airways. People feel reasonably well, because the reliever is opening up their airways, and don’t realise just how bad their asthma really is. The untreated inflammation in the airways can eventually lead to a very serious, and potentially fatal, asthma attack.
•    The short-acting beta-2 reliever, used regularly, makes the airways more sensitive to exercise, and to allergens such as dust mite or pollen. This means that an asthmatic who is already allergic to these allergens reacts to them at much lower levels in the air.
•    The airways become less and less responsive to the beta-2 reliever itself, so that when a serious attack occurs, requiring hospital treatment, huge doses of beta-2 reliever are needed to open up the airways. These massive doses carry a risk of serious side effects involving the heart.
The details of the New Zealand epidemic still evoke controversy. Was fenoterol itself, which is stronger than other beta-2 relievers, the cause of the deaths? Or was it just that the inhaler delivered a double dose - would any short-acting beta-2 reliever be dangerous at twice the normal dose? Or was it over-use of all beta-2 relievers and lack of preventer drugs?
Some common brand names
Common brand names include:
short-acting beta-2 relievers in inhalers - Aerolin, Airomir, Bricanyl, Ventolin short-acting beta-2 relievers in tablets - Bambec, Bricanyl, Volmax short-acting beta-2 relievers in syrup - Monovent, Ventolin
long-acting beta-2 relievers in inhalers - Bambec, Foradil, Oxis, Serevent
Until this is resolved, safety-conscious asthmatics may want to assume that any of these possibilities could be correct. An ultra-cautious approach would include:
•    Avoiding fenoterol (it is no longer available in Britain, except in the Duovent inhaler, combined with an anti -choli nerg ic drug)
•    Not using double-dose inhalers of any beta-2 reliever (i.e. inhalers that deliver 200mcg/ micrograms per puff)
•    Not routinely taking two puffs of a single-dose inhaler (check with your doctor if you have been told to take two puffs)
•    Using any short-acting beta-2 reliever only I as needed’ – which should be once a day or less according to British guidelines. Note that, with this level of use, there is absolutely no risk from these drugs: it is only regular over-use that is damaging and dangerous.
•    Using a peak-flow meter and ensuring that you are assessed regularly by your doctor
•    Always taking your preventer medication as prescribed.
Since about 1990, the death rate from asthma has been falling, particularly in countries with a policy of reducing use of beta-2 relievers, and increasing inhaled steroids. The death rate in New Zealand is now the lowest it has been for 50 years, and at the same level as in other Western countries.
Unnecessary alarm
While investigating the causes of the New Zealand epidemic, medical researchers discovered that patients inhaling a short-acting beta-2 reliever four times a day had more irritable airways after just two weeks. Their airways were also less responsive to the drug, even after this brief period of use.
Some researchers began to ask if the asthma epidemic itself – the increasing number of cases of asthma – could actually be due to these drugs. Maybe children with mild wheezing, which might have cleared up if left untreated (and which would have gone untreated in the past) were becoming full-blown asthmatics because they were now using beta-2 inhalers?
Many doctors became very concerned about these questions, and a leading medical journal
published an article with the provocative title: ‘Worldwide worsening wheezing – is the cure the cause?’ That was in 1992. Since then, much more research has been done, and it is clear that this particular fear about beta-2 relievers was unfounded.
Unfortunately, there are a few books and other publications around that are spreading unnecessary alarm about these drugs by reporting the debate as it was in 1992. They have taken up that question ‘Is the cure the cause?’, assumed that the answer is ‘yes’, and ignored all the subsequent research, which shows the opposite.
Beta-2 relievers in severe asthma
A few patients with severe asthma remain breathless and wheezy, even though they are inhaling moderate doses of a steroid preventer every day. Increasing the dose of inhaled steroids does not make a huge difference to their symptoms, and it substantially raises the risk of steroid side effects.
Taking a long-acting beta-2 reliever often works wonders for such patients. These relatively new drugs relax the airway muscles, and go on working for 12 hours or more.
There has obviously been concern about long-acting beta-2 relievers having the same sort of insidious side effects as their short-acting colleagues (see p. 153), and so increasing the likelihood of deaths from asthma. However, studies of people taking these drugs suggest that the risks are minimal. Certainly, long-acting drugs taken twice a day are very much safer than short-acting drugs taken four times a day.
Other studies show that the chemical differences of the long-acting drugs, as well as prolonging their effects, also give them a more complex set of actions in the body. For example, they improve the effect of steroids in calming inflammation, and may even have some small anti-inflammatory effect of their own.
Doctors believe that, for patients with troublesome asthma, the benefits of long-acting beta-2 relievers greatly outweigh the risks. But they should only be used in combination with inhaled steroids. Various other options, such as allergen avoidance and the new anti - leukotriene drugs (see p. 159), should probably be investigated as well.
If you are taking long-acting beta-2 relievers, do use them regularly, once every 12 hours – the good effect gradually builds up with consistent use.
Generally speaking, you should not take additional doses in between. These are not intended for use if you have a sudden asthma attack – your doctor will prescribe a short-acting beta-2 reliever for this. This limitation on the use of long-acting beta-2 relievers is certainly appropriate for salmeterol (which was the first of the long-acting beta-2 relievers to be developed) because it is very slow to take effect on the airways. However, one of the newer long-acting beta-2 relievers, called formoterol, begins to work just as quickly as a short-acting beta-2 reliever. Formoterol could, in theory, be used on an ‘as-needed’ basis to combat asthma attacks. You may want to discuss this possibility with your doctor.
Finally, don’t stop taking your preventer drug (e.g. inhaled steroid or cromoglycate), even if you feel a lot better. Long-acting beta-2 relievers are not a substitute for preventers.
Some patients with very severe asthma need to take regular doses of short-acting beta-2 relievers as well as long-acting beta-2 relievers. You should obviously follow the advice of your asthma specialist closely if you are on this kind of drug regime, and not change anything without approval. However, it might be worth discussing other options, such as anti -leukotriene drugs. In addition, do all you can to combat your asthma in other ways – by reducing allergen exposure, avoiding asthma triggers (see p. 39), and employing various other self-help measures (see p. 41).
Immediate side effects of beta-2 relievers
Minor immediate side effects of these drugs include:
•    headache
•    nervousness, trembling, restlessness, anxiety; children may become more excitable, and some are badly behaved or even aggressive.
•    flushing
•    dry mouth
•    muscle cramps.
These side effects – all of which are due to the resemblance of beta-2 relievers to adrenaline – usually wear off relatively quickly. Some long-acting beta-2 relievers may cause nausea and vomiting.
A pounding heart is usually a relatively minor side effect, but it can be more serious, and should be reported to your doctor.
A few asthmatics find that their airways tighten up when these drugs are inhaled, rather than opening. This is called paradoxical bronchoconstriction. If this happens, stop using the inhaler and see your doctor as soon as you can.
Even more rarely, asthmatics can develop allergic reactions to the drugs, or suffer hallucinations or seizures. Obviously you should stop using the inhaler immediately if you experience side effects of this kind, and should see your doctor.
There can be an interaction between beta-2 relievers and other drugs or medical conditions. Should you need a diuretic, tell the doctor or pharmacist that you are also taking a beta-2 reliever, and ask which diuretics are safe. If you have high blood pressure, a heart problem, or a thyroid condition, make sure the doctor remembers this when prescribing beta-2 relievers.
Adrenaline inhalers
Adrenaline inhalers are for use in emergencies. Technically, they are not available in Britain, but they can be imported under special licence, and your doctor may be persuaded to obtain one for you if he or she thinks it might be useful. They are given to people who have asthma and have sometimes had attacks of anaphylaxis (see p. 58), for example in reaction to food, latex or an insect sting. The inhaler provides prompt emergency treatment for the kind of severe asthma attack that you may experience during anaphylaxis.
You should probably be carrying an adrenaline auto-injector as well, as you may need to use both (see p. 98). Those who usually have fairly mild reactions to their allergen can use the inhaler first, to treat symptoms in the mouth, throat and airways. If other symptoms develop, such as faintness or widespread nettle rash,
Asthma alert
If you ever find that your short-acting beta-2 reliever has no effect within ten minutes, or is needed more than once every four hours, this indicates a serious asthma attack and you need urgent medical help (see p. 100).
During a severe asthma attack, while getting to hospital or waiting for a doctor to arrive, up to 30 puffs of a short-acting beta-2 reliever should be taken as an emergency treatment, to get the airways open. There is a risk of death if you don’t use the reliever fully in this situation. (This emergency dose is safe for almost everyone, but there may be risks if you have a heart condition – get detailed advice from your doctor in advance.)
then the adrenaline injector can be used. Those with a history of more severe reactions should start with the adrenaline injector and then use the inhaler if there are still symptoms in the mouth or airways.
Don’t exceed the maximum number of puffs stated on the canister, as the propellant can cause problems. If you have a heart condition, your doctor will advise you about using this kind of treatment safely - adrenaline can affect the heart.
Ephedrine
Ephedrine and orciprenaline (brand name Alupent) belong to the previous generation of reliever drugs. They are chemically very similar to adrenaline and therefore cause a lot of side effects, especially involving the heart.
These drugs are no longer recommended, and will soon be phased out completely. Some older asthmatics may still be using them, just because they have been on them for years and no one has reviewed their treatment.
If you are taking such drugs, ask your doctor about switching to a newer form of reliever - it will be more effective in treating your asthma, as well as having fewer side effects.
Anti -cho linerg ics
These drugs, also known as anti-muscarinics, are relievers. However, they work in a completely different way from the beta-2 relievers. They block the action of the parasympathetic nervous system, a set of nerves that are the biological equivalent of auto-pilot - working without the intervention of conscious thought. The parasympathetic nervous system has many effects on the body, including keeping the airway muscles nicely toned (see box on p. 235). By blocking the parasympathetic, anticholinergics help the airway muscles to relax.
Anti-cholinergics are taken by inhaler, and require 30-90 minutes to achieve their full effects. They should continue working for 3-6 hours.
Some common brand names
Common brand names of anti-cholinergics include: inhalers – Atrovent, Oxivent
nasal spray - Rinatec
For most asthmatics, especially those with a strong allergic component to their asthma, anti-cholinergics are generally less effective than beta-2 relievers. But they are useful to children under one year, who may not respond to beta-2 relievers. They also have a role where asthma is combined with chronic bronchitis -here the anti -choli nerg ics can sometimes be more effective than beta-2 relievers - and they are particularly useful for asthma with a lot of mucus, because blocking the parasympathetic tends to reduce mucus production. For severe asthmatics, anticholinergics may be combined with beta-2 relievers.
Anti -choli nerg ics should be taken only when needed, not regularly several times a day. If used regularly, they can make the airways more sensitive, just as short-acting beta-2 relievers can (see p. 153).
Side effects
Minor side effects of anti-cholinergics may include a dry mouth, blurred vision, constipation, and irritation of the mouth and throat. A few people suffer nausea or difficulty in passing urine.
Serious side effects are rare. Any increase in the stickiness of the sputum coughed up may be a cause for concern, especially in children. If there is an increase in wheezing or coughing, stop taking the drug and see your doctor.
If you already have glaucoma or prostate problems you should be monitored carefully by your doctor, as these conditions can get worse with anti -choli nerg ic drugs.
When anti -choli nerg ics are used in a nebuliser, it is vital that the mask fits well (see p. 163).
Anti-cholinergics for the nose
Another use for anti-cholinergics is in nasal sprays, for the treatment of vasomotor rhinitis, a non-allergic condition that is frequently mistaken for allergic rhinitis (see p. 29). In this disorder, the constant flow of mucus is caused by a malfunction of the parasympathetic nervous system, which is why anti-cholinergics work well.

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.

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

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.