Posts Tagged ‘perennial allergic rhinitis’

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

Antihistamines and Allergy

Antihistamines were first introduced in 1947, and are very widely used, so their safety — at least in the case of the older antihistamines — is beyond doubt. Most of the antihistamines have no major ill effects, and no one should feel concerned about taking them. At worst they produce some rather annoying minor side effects, such as drowsiness, which often wear off in time.

These drugs are particularly valuable for hayfever and other allergies in the nose (perennial allergic rhinitis). They are also used for chronic urticaria, sometimes in combination with anotherhistamine-blocking drug — see p. 53.

Antihistamines are not much used for asthma. They have relatively little effect, probably because so many other messenger chemicals are involved in an asthma attack. However, doctors in Japan do use antihistamines for asthma, and it is possible that people of Asiatic origin react differently to them.

Only one antihistamine, ketotifen, is widely used for asthma in the West, and this has other effects besides blocking histamine (see p. 159). A new role may soon develop for antihistamines in thetreatment of asthma, combined with anti-leukotriene drugs (see p. 159).

If you suffer from anaphylaxis you might be given antihistamines in a liquid or chewable form, for use in an emergency. These are not enough in themselves to treat this dangerous condition - you must have an adrenaline injector (see p. 150).

In the past, some doctors prescribed antihistamines for atopic eczema, mainly for their sedative effect(see p. 139) which was thought to help children to sleep better and scratch less at night. This treatment has largely gone out of favour, because its value is in doubt. But a recent study has revealed that the non-sedating antihistamine cetirizine may be useful for very young children with atopic eczema, not only in treating their skin, but also in reducing the chance of them developing asthma (see p. 249).

Most people take their antihistamines in tablet or capsule form. Syrups and sugar-free elixirs areavailable for children.

Antihistamines can also be applied directly, in the form of nasal sprays or eye drops. These are mainlyused to treat hayfever and the conjunctivitis (inflammation of the eye) which often accompanies it.Levocabastine (brand name Livostin) is particularly effective for the eyes.

Antihistamine creams are also sold, without prescription, for the treatment of insect bites - i.e. thenormal non-allergic reaction to such bites. These creams are not recommended for atopic eczema or otherallergic conditions affecting the skin. Not only are they unlikely to help, but they may make mattersworse because, with regular use, skin sensitisation to the antihistamine occurs very readily (see pp.54-5).
Some common brand names

Common brand names include: non-sedating antihistamines - Clarityn, Semprex, Zirtek; Mistamine, Mizollen, Telfast, Terfenadine. Thefirst three are available without prescription.

older (sedating) antihistamines — Atarax, Dimotane, Optimine, Periactin, Piriton, Tavegil, Vallergan eye drops — Emadine, Livostin, Optilast nasal sprays — Livostin, Rhinolast

How antihistamines work
Of the messenger chemicals released when an allergic reaction occurs, the most important is histamine.

This does its work by attaching to specialised receptors in certain parts of the body, and so

triggering various reactions (see box on p. 12). The action of antihistamines is very simple: they bind

to the same receptors as histamine, but they do not trigger any reaction. Histamine cannot bind to the

receptor because the antihistamine is already there.
Unfortunately, the reverse is also true: if the histamine is already there, the antihistamine cannot

elbow it off the receptor, which is why it is important to take the antihistamine well before the

allergen is encountered. Taking antihistamines at the first sign of a snuffle or itch can also work,

but the effects will not be nearly as good as taking them in anticipation of an exposure.
The best approach to treating hayfever, for example, is to start taking the antihistamines at least a

week before the pollen season begins, and preferably two to three weeks before. You should then take

them continuously until it is over. This will make a huge difference to the degree of symptom control

you achieve.
Side effects
The older types of antihistamine, such as chlorphenamine (brand name, Rriton) are relatively

non-specific in their effects – they bind to several different kinds of receptors, not just those for

histamine. As a result they can have some unwanted effects, such as causing drowsiness and poor

coordination. While these sedative effects are no cause for concern in themselves, they can, of course,

be hazardous if you work with dangerous machinery or drive. Avoid both until you are sure how you react

to the antihistamine. Note that the effects of alcohol may be increased.
Very occasionally antihistamines have the opposite effect, causing stimulation rather than sedation;

this is most likely to occur in children and old people. Lowering the dose may solve the problem.
The other possible side effects of the older antihistamines –all of which are minor ones – are

headache, dry mouth, blurred vision, difficulty in passing urine, nervousness, shaky hands, upset

stomach or diarrhoea. A few men suffer impotence while taking antihistamines, but this disappears when

the drug is stopped.
The minor side effects of antihistamines, including drowsiness, often wear off after a while, although

the benefits of the drug remain. So it is worthwhile persisting with an antihistamine, even if it

causes some problems at first. Many people experience side effects from certain antihistamines but not

from others, so try several different types to find one that suits you.
The problem of drowsiness has been reduced, in recent years, thanks to the development of new drugs

that are far more
specific for histamine receptors, the non-sedating antihistamines. A few people do get drowsy even with

these drugs. Again, the effects vary from one drug to another, so if the first one disagrees with you,

try a different one.
It is worth noting – since some people may still have the odd packet in their medicine cabinet – that

two of the non-sedating antihistamines that were available without prescription a few years ago proved

to be unsafe for a small minority of people. One was astemizole (brand names: Hismanal, Pollon-eze),

which has now been withdrawn from use altogether in Britain. The other was terfenadine (brand names:

Triludan, Seldane, Terfenadine) which is still available, but only on prescription.
There are several special precautions relating to terfenadine:
• Never exceed the correct dose.
• If you have ever had any kind of heart problem, talk to your doctor before taking terfenadine.
• Stop taking the drug if you have palpitations, or if you feel faint; see your doctor promptly.
• Do not take terfenadine if you are taking the antibiotic erythromycin, or anti-fungal drugs

such as ketoconazole (Nizoral) or fluconazole (Diflucan), used to treat vaginal thrush.
• Do not take terfenadine if you have liver disease.
• Do not drink grapefruit juice while taking terfenadine: something found naturally in grapefruit

interacts unpleasantly with this antihistamine.
In addition to these special precautions concerning terfenadine, any antihistamine should be treated

with caution by those suffering from epilepsy, Parkinson’s disease, glaucoma, prostate enlargement,

kidney problems, urinary retention, a gastric ulcer, a thyroid disorder, porphyria or liver disease.

Check with your doctor before taking antihistamines if you have any of these conditions.
It may be inadvisable to use antihistamines if you are taking sleeping tablets, anti-depressants or

anti-anxiety drugs – again, see your doctor.
Stop taking antihistamines if you suffer any unusual kind of rash, or if your skin becomes more

sensitive to sunlight.
If you are breast-feeding, note that, because they go through into the milk, the older antihistamines

may make the baby sleepy. However, they do no harm.
Rescue treatment
Most antihistamines perform very badly if you take them once the allergic reaction has set in, but

acrivastine (Semprex) can be good in these circumstances and is non-sedating. No prescription is

required for this drug.
possibly identify all major side effects. We vary in our response to drugs, because we are all so

different at the chemical and cellular level. A drug might have a serious side effect that only affects

one person in 10,000, and no safety trial can hope to identify such a rare response. Only when a drug

is released, and becomes widely used, do such side effects come to light. Other unanticipated side

effects can sometimes arise when people taking the new drug are much older than those in the safety

trials, or belong to a different ethnic group with different susceptibilities. Combining the drug with

certain other drugs can also be a potential source of trouble, although pharmaceutical experts can

often predict such problems from a detailed knowledge of the chemistry of drugs and how they are broken

down in the body. Side effects that take several years to develop - more than the timespan of most

safety trials - will also fail to show up until the drug has been released.
All this may sound very alarming, but in fact severe reactions to new drugs are not that common. And

there are various safety nets in place - doctors keep a close eye on patients taking new drugs, and a

special reporting system ensures that, if unexpected side effects do show up, the information is

quickly shared with others in the medical community.
In order to relate the information here to a particular medicine that you take, you need to know what

drug category it belongs to. Does your inhaler contain a beta-2 reliever, a steroid, a cromoglycatetype

drug or an anti-cholinergic, for example? If you are not sure, ask your pharmacist.
Those are the category names for drugs: they denote families of drugs which are similar chemically
and work in roughly the same way. Within each category, or family, there are a number of individual

drugs. The individual drugs should, ideally, have a standard internationally agreed name - this is

known as the generic name. Unfortunately, a few of the drugs used for allergies and asthma have more

than one generic name - salbutamol is known as albuterol in some parts of the world, and adrenaline is called epinephrine.

Finally there are the brand names, which are the ones most patients are familiar with. These are always

shown with a capital letter, unlike the generic names. Long-established drugs are usually made by

several different pharmaceutical companies, and therefore marketed under several different brand names.

A newer drug, which is still covered by the patent of the pharmaceutical company that developed it,

will be sold under only one brand name.

The issue of brand names is important, because a different brand name might make you think you are taking a different drug, when in fact it is exactly the same drug being marketed in a different guise.If you have suffered side effects from a particular drug in the past, and wish to avoid it in future, take note of its generic name, rather than its brand name. Sometimes the generic name is used as the brand name, in what are called generic drugs. These arerelatively inexpensive copies of popular drug brands -they are just the same chemically, but they costless because there is no advertising of the brand to doctors, and profit margins have been cut to aminimum. In order to reduce National Health Service costs, doctors are now asked to prescribe generic drugs whenever possible.

Food Intolerance
The comments of those who have recovered from food intolerance after many years of ill-health are always memorable. ‘It’s like getting my life back again,’ said one woman. ‘I had actually forgotten what it felt like to be well,’ said another, ‘the effect of cutting out certain foods was just amazing.’
For most of those with food intolerance, the disease begins very subtly and gradually – first one symptom (persistent and unexplained diarrhoea, perhaps) then, some years later, another (migraine or headaches) and then, when a few more years have passed, another symptom (such as joint pain or muscle aches). Steadily increasing levels of irritability, `fuzzy-headedness’ or inexplicable tiredness may accompany this decline in health.
Most patients have no idea that all these symptoms are connected until they try an elimination diet, and everything clears up at once, quite dramatically. As one former sufferer described it: `Some of the stuff that got better – well, I’d been like that so long I thought it was just the way I was –grumpy and exhausted, and feeling terrible if I didn’t eat meals on time. It was an absolute revelation to feel completely OK again.’
What does ‘food intolerance’ mean?
In this book, food intolerance means any reaction to food where the immune system has no proven central role.
All the people I have described so far have idiopathic food intolerance, which means, food intolerance with no established mechanism – in other words, doctors can’t say exactly how it is caused. This is a highly controversial area.
The definition of food intolerance used in this book means that it also includes metabolic abnormalities, which do have a well-established cause. These are due to defective enzymes (see upper box on p. 75).
The question of what words mean is a key part of the debate over idiopathic food intolerance. At one extreme, you may come across doctors who call this problem ‘food allergy’, using the original meaning of the word ‘allergy’ (see p. 6). (Some of these doctors use terms such as delayed food allergy and masked food allergy, to point up the distinction from true food allergy, but not all do.) Using the word ‘allergy’ in this context causes a lot of aggravation and confusion, so the term ‘food intolerance’ has, for a long time, been widely accepted as a useful one that avoids unnecessary conflict.
You will also hear the term ‘food intolerance’ used to mean idiopathic food intolerance only – this is probably the most common usage. When the term is used in this way, metabolic abnormalities are being thought of as a separate entity altogether.
A new twist has recently been added to this long-standing wrangle over meanings. When mentioning food intolerance in their literature, some of the major medical organisations (those who dispute the very existence of idiopathic food intolerance) now say simply ‘food intolerance e.g. lactase deficiency’. To anyone familiar with this field, it looks suspiciously like an attempt to redefine ‘food intolerance’ so that it means nothing more than ‘metabolic abnormalities’. The idea seems to be that, if you deny a disease a name, it will go away!
In the medical wilderness
The main text of this article is about idiopathic food intolerance, a disease with a distinctly dubious reputation among doctors. Because it is so controversial, few doctors actually look at the evidence that it exists – which is in fact quite strong (see box on p. 77). Such evidence is simply ignored in most of what is written by the major medical organisations debunking idiopathic food intolerance.
This lack of medical recognition is very unfortunate for patients with idiopathic food intolerance, whose debilitating symptoms could be eliminated, rather than simply being treated (usually to little effect) with drugs.
This prejudiced attitude to idiopathic food intolerance also plays into the hands of those offering bogus diagnostic tests and phoney treatments, often at a very high price. These practitioners
– who have moved in to fill the gap left by conventional medicine
– are a considerable part of the problem, helping to give idiopathic food intolerance a bad name.
The waters are muddied even more by the fact that some people who believe themselves to have food intolerance are actually suffering from psychological problems, which they prefer to attribute to food. Many more have picked up on food intolerance as something rather glamorous to suffer from, inspired by all the media reports about food intolerance among celebrities. All these patients are a good source of revenue for the less scrupulous fringe practitioners and are unlikely, therefore, to be discouraged from their beliefs.
Fortunately there are enough conventional but open-minded doctors, often GPs, who have come to realise, through experience with their own patients, that elimination diets have a remarkable curative effect for some people. The ones who benefit are often the doctor’s ‘old faithfuls’ – those with long-term multiple symptoms, who have been referred to innumerable specialists and treated with all kinds of drugs, but who never get much better. The conventional view of such patients is that they have psychological problems that are being expressed as physical symptoms. This may well be true for some – but others have idiopathic food intolerance.
One of our enzymes is missing
Metabolic abnormalities are a distinct type of food intolerance. Unlike other kinds of food intolerance, metabolic abnormalities have a clearly understood cause: an enzyme that carries out a crucial task in the body’s metabolism is either missing or inept. The problem is generally caused by a defective gene and is therefore inherited.
The most common metabolic abnormality is lactase deficiency leading to lactose intolerance (see p. 79) — this may or may not be inherited. Other metabolic abnormalities include:
trehalase deficiency, lack of the enzyme which breaks down a substance in mushrooms and most other fungi, including yeast. galactosaemia, a defect in the enzyme which processes galactose, one of the sugars found in milk (cow’s or human). This is a serious disease and sufferers must avoid milk scrupulously.
fructose intolerance, which is extremely rare. Those affected have an unpleasant taste in the mouth on eating fruit and other sources of fructose, so avoidance is no particular problem.
phenylketonuria, also very rare. Those affected are usually identified early in life, by a routine blood test.
Is it just placebo effect?
Doctors who doubt the very existence of idiopathic food intolerance will say that people who recover on an elimination diet are just experiencing placebo effect — a psychological response that operates with any treatment, whether effective or ineffective, simply because people believe that the treatment will work. But this is to ignore certain facts:
• Placebo effect produces a fairly small improvement in most people — you have to be very suggestible to feel enormously better. By contrast, when people respond to an elimination diet (the standard method for diagnosing idiopathic food intolerance —see p. 194) they usually have a sudden and dramatic improvement.
• Most of those with idiopathic food intolerance have had it for years and tried all sorts of treatments. They have often experienced some small benefit from these, probably placebo effect. When they try an elimination diet, they have a response that is in a completely different league.
• The idea that all the different symptoms are linked has never occurred to many people who try an elimination diet — they are often trying it for just one symptom, and are staggered when everything clears up. Placebo effect relies on expectation.
• Placebo effect doesn’t last very long — it fades over the ensuing weeks and months. Avoiding the culprit food usually produces a lasting improvement for those with idiopathic food intolerance.
Symptoms
The symptoms of idiopathic food intolerance come on slowly after eating the offending food, and the foods to blame are often those eaten very regularly, such as wheat or milk. Consequently, the symptoms from one meal tend to overlap with those from the previous meal and people with idiopathic food intolerance are more-or-less unwell for most of the time. It Is usually not obvious that food is at fault.
All the symptoms of idiopathic food intolerance are common ones that can be caused in other ways. And no two patients have exactly the same set of symptoms.
(As far as doctors are concerned, neither of these attributes gives the disease a respectable air.)
These are some of the symptoms commonly reported:
• headache or migraine
•diarrhoea, sometimes with bloating and wind; this is often diagnosed as irritable bowel syndrome (IBS)
• in children, stomach aches
• occasionally constipation
• nausea and indigestion
• joint pain
• aching muscles
• a constantly runny or blocked nose (this could be perennial allergic rhinitis linked to food – see p. 68)
• glue ear (see p. 29)
• fatigue and a general feeling of vague ill-health.
Asthma and eczema, triggered by specific foods (see p. 68), can also be part of the picture.
In babies, colic is often caused by food intolerance, including foods the mother is eating which come through into the breast milk in tiny amounts (see p. 202).
Less common symptoms include:
• recurrent mouth ulcers
• stomach or duodenal ulcers
• chronic urticaria (see pp. 50-53)
• swelling (angioedema).
The following diseases have also been linked to idiopathic food intolerance in some patients:
• Crohn’s disease
• palindromic rheumatism (intermittent episodes of joint inflammation)
• rheumatoid arthritis.
Psychological problems such as depression, anxiety, or hyperactivity in children can sometimes be due to food (see p. 80) but it is rare for such psychological effects to occur without any physical symptoms.
Remember that every single one of these symptoms and conditions can be caused in some other way. However, the constellation of migraine/headache, joint pain and diarrhoea is highly characteristic of idiopathic food intolerance.
How might intolerance be caused?
No one knows how idiopathic food intolerance is caused. There are probably many factors involved, with a slightly different mix of factors in each patient. This would help to explain why the symptoms are so extraordinarily varied, with no two sufferers exactly alike.
Although symptoms accumulate over the years, some people can in fact pinpoint the moment when their problems began. ‘I had this terrible bout of diarrhoea from eating too much melon. I lived near a farm and they were free, because of a glut, so I just gorged myself on them. Although I was over the diarrhoea in a couple of days, I was never what you’d call “regular” after that, and the least thing would upset me. Eventually the doctor said it was irritable bowel syndrome. When the other problems began, ages afterwards – headaches and hypoglycaemia and fatigue – it seemed like something quite separate. I never associated them in my mind with the diarrhoea.’
Bad diarrhoea can clear the intestines of their beneficial bacteria, known collectively as the gut flora (see p. 204), and this is probably what initiates food intolerance in such cases. Large doses of antibiotics (as are sometimes given before an operation, e.g. a hysterectomy), or prolonged and repeated courses of antibiotics, given for glue ear or acne, can also disrupt the gut flora and lead to food intolerance. A study of hysterectomy patients has shown that antibiotic treatment before the operation tends to result in irritable bowel syndrome – a common symptom of idiopathic food intolerance – afterwards.
A few interesting observations suggest that minor metabolic abnormalities – a defect in certain detoxification enzymes – may sometimes play a part in idiopathic food intolerance. This is especially likely where there is intolerance to food additives, or where there are behavioural symptoms (such as hyperactivity) or symptoms involving the nervous system (such as migraine).
A third factor that could play a part for some patients are food-derived exorphins. These are fragments of proteins (called peptides) produced by the digestion of food proteins. They happen, probably by pure coincidence, to resemble the substances called endorphins that we all produce for ourselves. Endorphins
are our internal painkillers. They modify nerve impulses in the body and brain, reducing sensations of pain, and improving the sense of well-being. The receptors to which they bind are the same receptors that bind morphine and heroin - it is the intensive stimulation of these receptors that makes these drugs so effective.
Food-derived exorphins may sound like the stuff of science fiction, but they have actually been demonstrated in the digestion products of wheat and milk. They may exist for other foods as well. They are nowhere near as strong as morphine, but do seem to improve mood.
These exorphins may explain the strange observation (made repeatedly, by a great number of initially sceptical doctors) that patients with idiopathic food intolerance often eat huge amounts of their offending food, and ‘can’t live without it’. Often they eat the food several times day, sometimes at every meal. With a ubiquitous ingredient like wheat or milk, this is not particularly difficult - wheat cereal and milk for breakfast, a cheese sandwich at lunchtime, pasta with a creamy sauce for supper, a milky drink and biscuits at bedtime.
Any of these abnormalities is likely to be just one factor in a multi-factorial disease.
Diagnosis
Unfortunately there are no simple accurate tests for idiopathic food intolerance. The kind of tests you may see offered commercially (in advertisements in health magazines for example) are very inaccurate, and a waste of money. Consequently, the only way to diagnose idiopathic food intolerance is through an elimination diet, in which you cut out all the foods you commonly eat, and then -if you get better - test them one by one.
It sounds easy but it isn’t, so make sure you read all the instructions for doing the diet before you start (see pp. 194-7). You should also see your doctor and get his or her approval. Some symptoms - such as severe diarrhoea or headaches -should be investigated by conventional methods first, in case there is some serious underlying cause.
The first step in diagnosis is to decide if a food really is the cause of the symptoms, and the second step is to identify the food or foods concerned.
The first step is crucial. One of the problems with the diagnostic tests that are advertised - such as those using samples of hair or blood - is that they begin with the second step. In other words they assume that food is the problem (see p. 93).
When it comes to the second step, remember that although common foods are often the culprits, almost anything that is eaten can cause idiopathic food intolerance. Every patient with this problem is different in the foods they react to.
Treatment
Avoidance of the food is usually the best treatment for idiopathic food intolerance - however most people do not have to avoid their problem foods for ever. After a while - it could be six months or it could be three years - you can usually go back to eating it again, but in moderation. You must never start eating the food in large amounts again, and it is best not to eat it every day - certainly not at almost every meal, which is the usual pattern for cow’s milk and wheat in the Western diet.
If you find the restrictive diet too difficult, you could try desensitisation treatment (see pp. 210-13). This can work very well.
The patients who should avoid the culprit food indefinitely are those with Crohn’s disease and rheumatoid arthritis: a severe and irreversible relapse can occur otherwise.
The evidence
The evidence for idiopathic food intolerance is more substantial than its opponents would have you believe.
One very well-conducted and interesting study involved children with severe migraine who were investigated by a research team at Great Ormond Street Hospital in London. These are children who are very difficult to treat successfully by normal means. On an elimination diet, 88% of those children got better — an astonishing number. Not just their migraine, but all sorts of other symptoms as well, including aching limbs, runny noses, asthma, eczema, diarrhoea, wind, mouth ulcers and hyperactivity. Some of these children also had epileptic fits, and even this symptom cleared up on the diet, recurring when culprit foods were tested.
A notable feature of this study is that, of the five researchers involved, four were deeply sceptical at the outset. Their report notes that they ‘embarked on this study believing that any favourable response, such as that claimed to substantiate the dietary hypothesis, could be explained as a placebo response. The positive double-blind controlled trial… provides clear evidence that a placebo response was not the explanation.’
Other studies with good scientific credentials have demonstrated a role for idiopathic food intolerance in adults with migraine, and for sufferers from irritable bowel syndrome and Crohn’s disease. There are also good studies of individual patients with rheumatoid arthritis and palindromic rheumatism (an episodic form of inflammatory arthritis) who have responded dramatically to avoidance of a particular food. Some of these patients were given several double-blind challenges and showed changes in certain immunological tests, as well as joint symptoms, when challenged with the offending food. This suggests that the immune system could be playing some part in these food reactions.

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

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

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.