Posts Tagged ‘pollen’

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.

Homeopathy
`We believe that a serious effort to research homeopathy is clearly warranted despite its implausibility.’ That was the conclusion of a group of German and American scientific

researchers who, in 1997, looked at every study of homeopathy they could find. This prestigious trans-Atlantic team carefully assessed the scientific validity of each study, and

then considered the data from studies that were of reasonably good quality.
This kind of study, in which all the available research data on a topic are combined, is called a meta-analysis. There were 119 research studies which were good enough to be

included in this meta-analysis and, taken together, these studies suggested that homeopathy does indeed have some real effects. In other words, it produces significantly more

benefits than simple placebo effect – the psychosomatic improvement which tends to occur with any treatment, even a dummy pill (see p. 233).
Some of the most convincing scientific studies included in the meta-analysis were those relating to homeopathic remedies for allergic conditions (see p. 217). But what exactly

does this mean for allergy sufferers? Is homeopathy a treatment that is worth a try? Unfortunately, it is difficult to say.
Firstly, the evidence from the homeopathy meta-analysis is far from overwhelming, as the researchers themselves point out. The observed improvements – the overall differences

between the placebo and the homeopathic remedy – are not huge. Secondly, even if there are some homeopathic treatments that have real effects, it does not mean that every kind

of homeopathic treatment works. Homeopathy is a very broad field, with a multitude of different approaches. The types of homeopathy that have been tested, and appear to help,

may bear little or no relation to the homeopathic remedies that are generally available (see p. 217).
`Let like cure like’
The central idea in homeopathy – often known as the principle of similars – is that a substance which causes a particular set of symptoms can also, if handled in the right way,

cure symptoms of
a similar kind. In the words of Samuel Hahnemann, the German doctor who invented homeopathy at the beginning of the 19th century, ‘Let like cure like.’
The natural substances that form the basis for homeopathic remedies are mostly derived from toxic plants or minerals. (Sometimes extracts from diseased tissue – called nosodes –

are used instead, but this is a relatively recent development. So is the use of allergen extracts, such as pollen, described on p. 217.) Hahnemann himself began with the

standard drugs of his own day, such as belladonna and arsenic compounds. His innovation was to use them in very much smaller doses than his fellow physicians, and to apply them

to entirely different diseases.
Hahnemann worked by first discovering what the effects of the drugs were, when taken by a healthy person (he experimented on himself and his family for this). Then he tried to

match the symptom pattern produced by the drug with the symptoms of a particular disease. For example, he observed that belladonna produces hallucinations and a hot, dry skin –

symptoms that were also seen in children with scarlet fever. He claimed that, by giving belladonna in very small doses, much less than was normally used, he could stimulate the

body to heal itself of scarlet fever.
Hahnemann, unlike his medical contemporaries, also advocated a good diet, fresh air and exercise. And he was heartily opposed to the conventional medicine of his day, a brutal

business that involved a great deal of blood-letting and large doses of very toxic medicines. Considering how useless, and indeed dangerous, the orthodox medicine of the time

frequently was, Hahnemann’s successes were not really surprising.Less is more’
Homeopathy today is the ultimate version of the ‘less is more’ philosophy. A homeopathic remedy is prepared by taking the basic ingredient, dissolving it in water, and then

diluting that solution over and over again. Imagine pouring a bottle of wine into the Pacific Ocean, and you have a rough idea of how dilute homeopathic remedies are. Making

extreme dilutions was an idea introduced by some of Hahnemann’s followers, after his death.
Dilution is only part of the story, however. With each dilution, homeopaths apply a special shaking-and-tapping technique known as percussing. This was originally done by hand,

but now is often done mechanically. Homeopaths believe that percussing makes the active substance more powerful, despite the dilution. The term used by homeopaths is potency,

and a homeopathic remedy of the highest potency is the one that has been most thorDughly diluted and percussed.
In fact, a simple calculation, using the basic laws of physics, shows that there is nothing there at all but water – many homeo pathic remedies are watered down so thoroughly

that not one Jingle molecule of the active substance is likely to remain. It is  which leads medical researchers to use words such as ,nplausibility’ (see p. 216) when talking

about homeopathy.
Nhat homeopaths do
\ homeopath starts by considering all your symptoms (not just allergies, but any other symptoms as well) and various other characteristics that conventional doctors do not

usually consider, including physical appearance and psychological traits. The homeopath then chooses a substance which, if taken at full strength, would produce a comparable set

of symptoms and characteristics. This approach is called classical homeopathy.
In addition, homeopaths often give advice on diet, sleep, exercise and allergen avoidance. As in the early days of homeopathy, this may be the most important part of the

treatment.
Like many other complementary therapists, homeopaths will listen if you need to talk about personal problems and emotional difficulties, and will offer reassurance or advice.

This can be valuable, though not everyone would agree that a homeopath is the best source for such help. There are two distinct traditions within homeopathy – a scientifically

inclined tradition (represented today by experiments with homeopathic immunotherapy – see right) and a highly metaphysical tradition. Among the many ideas floating about within

the metaphysical tradition is the notion that all illness is a result of psychological or moral failings. Attitudes of this kind, which are quite common among complementary

therapists, can be very damaging (see p. 209).
Sometimes homeopaths recommend avoiding certain foods, on the assumption that the patient suffers from food intolerance, though they rarely use an elimination diet (see p. 194),

the only way to achieve accurate diagnosis.
In addition to all this, some homeopaths also give herbal remedies where they think it will help. This approach is called complex homeopathy.
A much more recent development within homeopathy is homeopathic immunotherapy or HIT, which uses an extreme dilution of an allergen (such as pollen or dust mite) to treat people

who are allergic to that substance. While homeopathic immunotherapy was inspired by conventional immunotherapy, the relationship between the two is a very distant one indeed.

The extensive dilution process means that the liquid used for homeopathic immunotherapy is unlikely to contain even one molecule of the allergen. This puts it in a completely

separate realm from conventional immunotherapy, where the presence of the allergen, and the steadily increasing dose with successive injections, is what produces the beneficial

effect (see p. 166).
Does it work for allergy?
Two scientific trials suggest that HIT makes a difference, albeit a small one, for hayfever and pollen asthma. In the meta-analysis described on p. 216, one of these trials was

given a good rating for scientific reliability, and the other was considered fairly good.
Another type of homeopathic treatment that appeared to be effective for patients with allergic asthma was one using a nosode – an extract of the asthmatic airway itself. A small

sample of the airway was taken from each asthmatic patient, diluted and per-cussed, then given to the patient as a treatment. It seemed to work, and the scientific rating of

this trial was very high.
The third homeopathic treatment that appeared to have an effect in valid scientific studies was Galphimia, used for symptoms in the eye caused by pollen allergy.
If you go to a local homeopath, it is very unlikely that you will be given either of the first two treatments – these are only used experimentally, in large research centres.
The Galphimia treatment might be available from a local homeopath, but it will not necessarily be in the same form as the treatment used in the scientific trial.
Note that all the studies described above are trials with a positive outcome. If you are trying to assess homeopathy overall, you should also consider the many trials that found

no effect. For example, a very careful study of homeopathy for children with asthma, carried out at the University of Exeter and published in 2003, found no benefit from

individualised homeopathy treatment.

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.

Let’s hope it never happens - but if it does, knowing what to do could make the difference between surviving and not surviving. The sensible thing is to read these pages - or whichever parts are relevant to you or your child - before you encounter an emergency. It is often helpful to rehearse the procedure in your mind and actually imagine yourself going through the actions described here.
Find out in advance what the local ambulance service is like, and ask your GP for advice about who to contact in an emergency. (If you have latex allergy, check in advance that all local ambulances carry a latex-free kit.) These are the options:
• Call your GP.If the doctor is nearby and the hospital or ambulance station a long way off, this may be the best decision. Doctors in rural areas may have supplies of adrenaline for emergency treatment, and oxygen for those suffering a severe asthma attack.
• Call an ambulance. Where the local ambulance service is dependable, this is always the best option. The ambulance crew will have adrenaline and oxygen.
• Go by car or taxi to the nearest hospital
emergency department. This is not usually a
good plan, because your condition may quick-
ly get worse, and you have no emergency
treatment available. But there may be situa-
tions where it is a sensible decision. Emergencies can occur when you are away on holiday or business. Never stay anywhere without a phone – check that it is working as soon as you arrive. Make sure you have the number of a local doctor and know where the nearest hospital is. A remote holiday cottage can be a dangerous place to suffer an asthma attack or anaphylactic shock.
Anaphylactic shock
This is an extremely serious emergency, requiring immediate medical help. The signs of anaphylactic shock are listed on p.58. In the case of food allergy, there are additional signs in the mouth, lips and throat (see p. 62). Use adrenaline (epinephrine) straight away if you have it – but get emergency medical help as well. With injectable adrenaline (an EpiPen or Anapen – see p. 150), remove the cap and jab firmly into the outer thigh, going straight through any clothing. Never inject into any other part of the body – this can be dangerous.
If you have an adrenaline inhaler (see pp. 155-6) you can use this first to treat symptoms in the mouth, throat and airways, and then use the injector if you still have symptoms. (Improvise a spacer – see p. 100 – if there is difficulty in inhaling the adrenaline.) Anyone whose reactions tend to be severe should use the injector first and follow up with the inhaler if necessary. Overdosing with adrenaline is possible, and can be fatal, but using the inhaler as well as the injector is safe as long as you don’t have a heart condition (see pp. 155-6).
If you do not improve after using the injector, a second one can be used, 10-15 minutes later.
In situations where medical help is not yet available and the symptoms are not abating, another shot of adrenaline can be given every 15-20 minutes. But the maximum number of shots recommended by your doctor should never be exceeded. Keep count of how many you’ve had, and tell medical staff.
An asthmatic who does not have an adrenaline inhaler can use a beta-2 reliever inhaler such as Ventolin (see p. 152) as well as the adrenaline injection, although it probably won’t help very much.
Suppose you know for sure that you have encountered your allergen, but you don’t have any symptoms yet? In Britain, the usual advice is to wait for symptoms, but doctors in the United States say go ahead and use the adrenaline injector if you have reacted very badly in the past. In general, for people with no other health problems, it is better to give an adrenaline injection which isn’t needed than to delay giving one that is needed. Delaying the use of the injector may mean that the reaction gets out of control. Some people put off using the injector because they think it should be saved for when they ‘really need it’. In fact the adrenaline works just as well if you have used it on previous occasions.
Following anaphylactic shock, you should be kept in hospital for 6-12 hours even when everything seems fine. Attacks have recurred as much as eight hours later. Corticosteroids reduce the chance of this happening – ask if these have been given. If you are discharged early and it is a long journey home, consider waiting in the hospital, or nearby, until eight hours after the original reaction.
First aid for anaphylactic shock
A badly swollen tongue or throat can cause suffocation. If there is visible swelling and the person is unconscious or turning blue, try to keep the top of the trachea (the main airway leading from the throat) open. Use the handle of a spoon – one that has very smooth edges. Slide it carefully over the top of the tongue and into the throat. Press down gently but firmly to open the airway.
Someone who is feeling faint or dizzy, or losing consciousness, or (in the case of a child) becoming very pale and floppy, may be suffering from a dangerous drop in blood pressure. He or she is more at risk of a fatal collapse if in an upright position, because not enough blood is reaching the heart. The worst thing is to stand up suddenly, or to move (or be moved) quickly from a lying to a sitting position –death can follow within seconds. The best thing is to lie down, preferably with the legs resting on cushions or a stool so that they are above the torso, and with the arms raised above the chest. Adrenaline can be given while in this position. A stretcher should be used to get the patient to an ambulance.
Latex allergy and emergency treatment
If you have anaphylaxis due to latex allergy, going to hospital can be alarming, as you may suffer further reactions to latex gloves or equipment. Some patients with latex allergy have had such bad experiences in ambulances and hospitals that they become fearful of using their adrenaline injector, since this means they must go to the hospital afterwards. They delay using the injector, which makes the situation worse. Some doctors are now giving such patients all the medicines and training they need to manage their anaphylactic shock themselves, so that they don’t need to attend hospital.
A person who has lost consciousness should be lying down on their side in case they are sick (this reduces the chance of them inhaling their vomit). The same goes for anyone who feels nauseous.
On the other hand, if the major problem at the outset is difficulty in breathing (as it generally is in children) a sitting position is better.
It is unusual for both faintness and severe breathing problems to be present at once. If this occurs, the patient should lie down, and if there is swelling in the throat, a spoon should be used (see left) to keep the airways open.
Insect-sting allergy
If you don’t have an adrenaline injector, get medical help immediately.
If you’ve had a cutaneous systemic reaction (see p. 60) in the past, use the adrenaline injector if there is any difficulty in breathing, hoarseness, stomach cramps, diarrhoea, nausea, faintness, dizziness or confusion. If you are unsure, remember that, unless you have a heart condition, it is usually better to overreact (i.e. use the adrenaline unnecessarily) than under-react.
If you’ve had a severe systemic reaction (i.e. anaphylactic shock) in the past, use an adrenaline injector at the first sign of any reaction other than immediately around the sting.
If there is a honeybee stinger left in the skin, scrape or flick it out sideways using a fingernail, knife blade or credit card – the venom sac is attached and will go on injecting venom for up to 10 minutes if you leave it there.
Don’t try to pull the stinger out – this squeezes the venom sac and pumps more venom into the skin.
Get emergency medical help, and follow the other measures for dealing with anaphylactic shock (see left).
Don’t go alone
If you suffer vomiting or diarrhoea during anaphylaxis, and have to go to the toilet, tell someone to call an ambulance and take someone else with youto the toilet. Do not go in alone and lock the door, in case you collapse.
Asthma attacks
Even those with mild asthma, who have never had a serious attack before, can quite suddenly get into difficulties and require emergency treatment. Don’t be over-anxious about this, because it is unlikely to happen – but do be prepared. Not having your reliever inhaler with you when a severe attack starts is a recipe for disaster – always take it, wherever you go.
Deal with an attack promptly. The sooner you act, the fewer drugs you’ll need in the long run to control the attack. Most asthmatics wait too long and then under-treat their asthma.
The important thing is recognising an asthma attack, and knowing when it is getting out of control. Not all attacks are the same – some come on fast, some come on slowly.
Rapid asthma attacks come on in a matter of hours. You may have been fine all day, but then start to feel very breathless and wheezy, or begin coughing badly. Less than an hour later, despite using the reliever, the breathlessness is worse and it is a struggle to speak or walk across the room. This is a severe attack: don’t delay in getting medical help.
Slow asthma attacks come on over a period of days. At first you are more breathless and wheezy than usual, and your reliever inhaler is not helping much. Asthma wakes you up at night, and you are far more breathless than usual in the morning. This could be the beginning of a severe attack, so don’t delay in getting medical help. If you get to the point where your asthma is disturbing your sleep every night, and in the morning you have difficulty in speaking or walking about, this is a very serious situation – you must see your doctor or go to the hospital now.
A few asthmatics have great difficulty recognising when they are increasingly breathless, and for them, using a peak-flow meter (see p. 97) every day is essential. Indeed, most asthmatics find
Recognising an asthma attack in a very young child
With a young child, these signs indicate a severe asthma attack:
• the nostrils are flared
• the shoulders are unusually high
• the child can say only one or two words between breaths
• the ribs are pushed out, and the spaces between the ribs, and below the chest cage, are sucked in during breathing
• you can hear wheezing (a whistling noise)
• the lips, tongue or fingernails are blue.
If wheezing stops, without any other apparent improvement, this is a very bad sign — it may mean that the airways are now so narrow that no air is passing through them. This is called a ’silent chest’, and indicates an urgent need for medical attention.
that monitoring peak flow is a valuable way of spotting attacks in advance. However, if your peak flow seems normal, and yet you feel breathless and have a tight feeling in your chest, pay attention to your symptoms and get medical help.
Your response to your reliever inhaler is another helpful sign assessing asthma attacks. Things are serious if:
• the reliever inhaler does not seem to be working at all within 10 minutes of taking a puff
• it does not work as well as usual
• it works, but the effect wears off in less than three hours. If you have an asthmatic child, give everyone who normally takes care of the child detailed written instructions for recognising and dealing with an asthma attack. People forget verbal instructions especially in an emergency. A child who is exhausted or upset c. an attack should always be given medical care.
Taking action
If your reliever inhaler is not working well (see above), take another puff to open up your airways – and then take further action. as described below.
If you seem to be in the early stages of a slow asthma attack check your management plan, and if your peak flow has fallen below the recommended level, double the dose of inhaled steroids (twice as many puffs each time) now. Add any other medicines (e.g. steroid tablets) as recommended by the management plan.
Those who don’t have a peak-flow meter or management plan should double the dose of inhaled steroids and make an urgent appointment to see the doctor.
If you are suffering a rapid attack, or a slow attack that has got out of control, you need emergency medical help. Ring for an ambulance, ring your doctor, or go to the hospital – the ideal course of action will vary, depending on where you live (see p. 98).
Use your reliever inhaler until medical help arrives. You can take a puff every 5-10 minutes if needed, but keep a count of how many puffs you’ve had and stop after 30. Some doctors suggest taking up to 30 puffs all at once. (If you have a heart condition, this dose might be dangerous: follow your doctor’s advice.)
If it is difficult to inhale, use a spacer – this can make all the difference, especially for children.
You can improvise a spacer from a plastic cup, a plastic bottle, or a paper bag. Make a hole in the bottom of the cup or bottle, or in one corner of the paper bag, and insert the mouthpiece of the inhaler here. The open end of the cup, bottle or bag goes in or over the mouth – with the bag, you have to bunch it up and hold it around the mouth. Squirt the inhaler repeatedly into the improvised spacer, while breathing steadily in and out.
The six golden rules for asthma attacks
• Breathe as slowly as possible and concentrate on breathing out, not on breathing in. Exhale as fully as you can and your in-breath will follow automatically.
• Never panic – if you do, you may start hyperventilating, and this makes matters much worse (see p. 226). Panicky parents are the worst possible thing for an asthmatic child during an attack.
• Adopt a position that makes breathing as easy as possible. Propping your arms up at about shoulder height can help – for example, sit back-to-front on a dining chair, with your arms folded and resting on the back. Or put pillows on a table, sit in an upright chair, and rest your head and arms on the pillows. Don’t lie down, as this makes matters worse. Open a window, as long as the air outside is not cold, polluted or loaded with pollen.
• Avoid factors that can make an asthma attack worse, for example, vigorous activity, cold air, irritants and allergens.
• Drink plenty of water, fruit juice or other liquids as a lot of water is lost through the surface of the airways during an asthma attack, and you can become dehydrated.
• Don’t take anything to help you sleep, even herbal pills. If your asthma gets worse during the night, you need to wake up so that you can get more air.
After an attack
Asthmatics who have suffered a severe attack are occasionally sent home from hospital before they are completely better. A few people have died as a result of being discharged too soon. So if you feel breathless or otherwise unwell after you leave hospital, don’t hesitate to go back – or seek other medical help.
See your GP or specialist within a few days of any emergency treatment. Don’t be over-confident just after a severe attack – this can be a very vulnerable time. Take more rest than usual and drink plenty of fluids, as you may be dehydrated. Keep taking your preventer inhaler at the increased dose – reducing the dose now could lead to another severe, possibly fatal, attack. Keep taking steroid tablets if you have been given them.
If you produced a lot of mucus during the attack, try to clear it, but without violent coughing. Mucus can sometimes form solid plugs which block small airways. Treatment by a physiotherapist would help, and expectorants – drugs which help loosen mucus –can also be useful (ask your pharmacist about these). Don’t take ordinary cough medicine (see box on p. 163). There are also some breathing exercises which can help to clear mucus (see p. 231).
An asthma attack represents a chance to learn more about preventing asthma – so think about what went wrong. Had you forgotten to take your preventer inhaler regularly? How long is it since you had your medicines reviewed by the doctor or asthma clinic? Have you been using your peak-flow meter daily? Were you exposed to a high dose of allergen or an irritant?
A reaction to aspirin-like drugs
Aspirin sensitivity can begin quite suddenly in someone who has previously taken aspirin without trouble. If you have unexplained chronic urticaria, or polyps in the nose, plus asthma and/or rhinitis, the development of aspirin sensitivity at some time in the future is a distinct possibility (see p. 151).
A sensitivity reaction to aspirin or aspirin-like drugs usually begins between 30 minutes and two hours after the drug is taken. You will have some or all of these symptoms:
• a runny or badly blocked nose, and red eyes
• a feeling of warmth, flushing and sweating
• a general rash
• a sensation of tightness in the chest, a dry cough, increasing breathlessness
• malaise and exhaustion
• vomiting or diarrhoea
• swelling (angioedema) and/or nettle rash (urticaria). If you have such symptoms get emergency medical help immediately because the reaction can quickly develop into severe asthma, shock, collapse and unconsciousness.
If you have asthma, use your reliever inhaler as much as required (up to 30 puffs) until medical help arrives. Anyone who has an adrenaline (epinephrine) auto-injector, or an adrenaline inhaler, can use this as well – up to 30 puffs of the inhaler, or whatever maximum dose is given in the instructions. Tell the ambulance crew and doctors exactly what you have taken.

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

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.

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.

 

Cross Reactions in Allergy

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

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

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