Posts Tagged ‘coeliac’

Allergens in Food
Anyone with true food allergy or coeliac disease needs to be very careful about avoiding certain foods. The information given here is aimed mainly at such people, rather than those with food intolerance (see p. 74), who can usually tolerate small amounts of their offending foods. However, some of the basic information given here is relevant to those with food intolerance as well.
There are different levels of sensitivity even among those with true food allergy. The ‘exquisitely sensitive’ can react to unbelievably minute traces of the food, and for them life is especially difficult. The same is true of some coelicacs, who can be affected by the tiniest quantity of gluten.
These people are a small minority. The level of vigilance required of such people will not be necessary for most people reading this book, so don’t get things out of proportion. While it is vital to be sensible about avoiding your problem food, it is also important not to become over-anxious.
Buying basic ingredients
Cooking for yourself is the safest way to eat for those with true food allergy and coeliac disease. There are relatively few hazards, but do beware of well-meaning assistants in health-food shops who try to sell you some exotic package of grain or flour – spelt or kamut or triticale, for example – reassuring
you that it is ‘definitely not wheat’. Be well informed about the different forms of your problem food and the names under which it is sold (see pp. 172-5).
Oils made from foods such as corn or peanut sometimes cause concern. Ordinary refined oils have been so thoroughly processed that they actually contain no allergenic proteins, so you can safely use these. Bottles of gourmet walnut oil and almond oil are a different story however, and should be avoided if you have nut allergies. Sesame oil is not purified either and can provoke serious reactions. With any oil, if you are unsure how safe it might be, go by the smell. Oils that smell or taste like the food from which they are made could well contain allergens.
Those with allergy to tuna can usually eat tinned tuna because the processing makes it safe. The allergens in fresh fruit and vegetables are generally inactivated by cooking too, so jams and tinned fruits tend to be safe – but test very cautiously. Cooking does not have much effect on other food allergens, apart from eggs. In rare cases, cooking can create allergens (see box on p. 186).
If you share your kitchen with others, and are highly sensitive, check that all cooking utensils are truly clean before use. Coeliac should watch out for breadcrumbs in the butter dish, jam or toaster. Where small children are allergic to a food, it may be best to keep the culprit out of the house entirely.
Genetic engineering and food allergy
Many people with food allergies are very concerned about the possibility that genetic engineering could introduce allergens from one plant species into another. This concern seems to be shared by government officials and those in the food industry, who are being extremely vigilant and cautious at present. As long as this attitude continues, there should be little danger to food allergy sufferers.
Finding food in funny places
If you are suffering some inexplicable reactions to non-food items, it might, just possibly, be a food reaction. Some latex gloves contain the milk protein casein, for example, added as a manufacturing aid.
Buying packaged foods
There are several different issues here:
• the need to read labels carefully for allergenic ingredients described by unfamiliar names (see p. 172)
• errors in the packaging used (see pp. 174-5)
• contamination by minute traces of a food substance due to processing machinery not being cleaned adequately. Cartons of fruit drink have occasionally been contaminated with traces of milk because the same production lines were used for packaging milk drinks. Tofu desserts made in ice-cream factories can also become contaminated with milk. These tiny traces of a food will only affect the most highly sensitive individuals, but contamination by nuts can involve large pieces and affect anyone with nut allergy (see p. 174).
• foodstuffs which are used as part of the production process
and leave a tiny residue in the finished item (see p. 174).
Be very cautious indeed about ready-made food that is unlabelled, such as that from bakeries and home-made stalls. Egg is frequently used as a glaze on baked products, nuts may lurk within, and milk or wheat can turn up in the most unlikely places.
Restaurants, cafes and takeaways
The majority of fatal and near-fatal incidents involving people with true food allergy are due to restaurants, cafeterias and canteens. Takeaways can also be a problem except in the case of the large chains such as McDonald’s, where ingredients are standardised. It is alarming that highly allergenic foods (e.g. peanut) are sometimes used – yet far from obvious – in recipes and sandwich fillings where they would simply not be expected. Anyone with peanut or shellfish allergy should be ultra-cautious about Chinese, Thai or Malaysian cooking – but those with milk allergy should find a haven here, because milk is not part of these culinary traditions.
The simplest solution is to eat very plainly when you go out –steak and salad, for example. Steer clear of casseroles and thick soups, where you can’t see what’s in it (the occasional chef throws in peanut butter to thicken the mix…). Food wrapped in pastry is best avoided for the same reason. Desserts and cakes are risky for anyone with nut, egg or milk allergy.
You must insist on accurate information about the food before you taste it. If the counter staff, the waiter or the waitress
is unsure of the ingredients, ask them to check with the chef, or with the label on pre-packaged food. Be persistent and never eat anything unless you are sure. Make eye contact with the person concerned, and learn to be a good judge of character. Your life could depend on telling the difference between the waiter who knows the facts about the food and the waiter who is being blandly reassuring for the sake of a quiet life.
It is a great mistake to pick out the pieces of offending food – kiwi fruit from a fruit salad for example – and eat the rest. There is often enough allergen left behind to cause anaphylaxis in the highly allergic individual.
Those who are extremely sensitive to the offending food must also consider the problem of contamination in the kitchen. Grills and fryers in restaurants and canteens can become contaminated with fish allergens or nut allergens (e.g. from nut cutlets) and these can be transferred to fried potatoes or other foods, provoking anaphylaxis in the highly allergic individual. One person with fish allergy died in this way. Sesame seeds can also contaminate equipment, work-surfaces or bakery counters.
Parties and buffets
Milk, egg, shellfish or nut allergies can make it especially hazardous to eat buffet or party food. Regard everything with suspicion. Cocktail snacks with nuts or peanut paste hidden inside are a particular problem.
When fish allergy isn’t fish allergy
Anisakis is a parasitic worm that infests fish and can sometimes survive the
cooking process to infect humans. The worms are easily thrown off by the human immune system, but the body is primed to make IgE antibodies should
it ever encounter Anisakis again. Another meal of parasitised fish – even if the Anisakis worms are all dead this time, and only the allergens remain
will provoke a massive IgE-mediated reaction, leading to anaphylactic shock. This problem is usually misdiagnosed as allergy to fish itself.
Other inconsistent reactions to food can be due to contaminants such as antibiotics, preservatives, other food additives or (especially in the case of shellfish) naturally occuring toxins.

Skin-prick tests
This is an indirect method of detecting true allergic reactions. It is one of a family of skin tests that use a similar approach. The three different tests in this family are known as: skin-prick tests or prick tests, puncture tests, and scratch tests.
For the skin-prick test - the technique used in Britain - a small drop of liquid containing an allergen, such as grass pollen, is placed on the arm. The doctor makes a small prick in the skin, under the drop of liquid, allowing a minuscule amount of the allergen to get into the skin. A positive reaction is recorded if a red bump develops soon afterwards. For accuracy, the bump must be compared to positive and negative controls (see below).
The puncture method is very similar to the skin-prick test but uses a slightly different technique for breaking the skin. The term prick-puncture test covers both techniques.
With the scratch method, the skin is scratched lightly, and the allergen solution is then applied over the scratch. This method gives less consistent results than prick-puncture testing.
It is important to include a negative control in the test - a skin-prick test with plain salt water (saline). This should not produce much of a bump - if it does, the skin is clearly over-reactive and the tests more difficult to assess. The doctor should also include a positive control - a skin-prick test with histamine, the substance that plays a central role in allergic reactions. This should always produce a bump. If it does not, the skin is decidedly under-reactive, and the tests are invalid.
Taking antihistamines will make the skin under-reactive, and you should stop taking them before the testing, for a period ranging from a day to several weeks - it varies depending on the particular antihistamine. Ask your doctor for specific instructions about stopping these and other drugs before testing.
Skin tends to be over-reactive to testing in people with dermatographism (see p. 52). Blood tests for specific IgE,
such as RASTs (see p. 92), are needed for anyone who has this condition. Eczema sufferers with a rash over large areas of the body may also require blood tests, if there is too little clear skin for testing.
Skin-prick tests can produce both false positives and false negatives (see box below). Some allergic diseases will give a lot of false negatives and relatively few false positives, while for others the reverse is true. The allergen itself influences the rates of misleading reactions: for example, tests for soya allergy are notoriously unreliable, whereas those for peanut are far more accurate. The age of the person being tested also makes a difference. With all these influences at work, interpreting the test responses is a real art, and the doctor’s experience counts for a lot.
All sorts of people offer skin-prick tests, including alternative practitioners. Get them done by a qualified doctor, preferably by an allergist, who will know how to make sense of the reactions.
Note that the purpose of these tests, and of blood tests for specific IgE, is to identify the allergens that are bringing on your symptoms, not to predict how strongly you will react to those allergens. The tests may give some indication of the intensity of your reaction, but they cannot be regarded as a good guide to how you will respond to the allergen in the future.
The safety record of skin-prick tests is very good. Occasionally a systemic reaction (anaphylaxis) occurs with these tests, but there are no records of any deaths. Nevertheless, if you suffer from severe asthma or have experienced anaphylactic shock in the past, it is advisable for the doctor to have adrenaline and resuscitation equipment available. Those with strong allergic reactions to latex may also react badly if they are tested with an allergen that cross-reacts with latex (e.g. cypress pollen), not just when tested with latex itself. Taking beta-Mockers (see box on p. 150) increases the risk of a life-threatening reaction for anyone in these higher-risk categories.
False positives and false negatives
Apart from challenge tests, none of the tests used for allergy works with 100% accuracy. Most give both false positives and false negatives.
A false positive means that there is a positive test but no actual reaction when the allergen is encountered (e.g. eaten or inhaled). A false negative means that there is a negative test result despite a genuine reaction (as shown by a challenge test, for example).
A test that gives relatively few false positives has good positive predictive value - in other words, if it suggests you are allergic to something, you probably are.
A test that gives relatively few false negatives has good negative predictive value. If it comes up negative, you are probably not allergic to that allergen.
Some tests for allergic reactions show good positive predictive value but poor negative predictive value, while for other tests the reverse is true.
Fresh is best
The fruit and vegetable allergens that provoke Oral Allergy Syndrome (see p. 63) are chemically unstable, so commercially produced extracts for skin-prick testing quickly lose their potency and give false-negative results. Most allergists now favour using a drop of fresh juice from the fruit or vegetable concerned.
Intradermal tests
These tests (also called ‘intracutaneous tests’) put allergen more deeply into the skin than prick-puncture tests. The skin tends to react more when penetrated to this depth, so there are more false positives. There is also a greater risk of a serious reaction which may require emergency resuscitation. Don’t undergo these tests if you are taking beta-Mockers (see box on p. 150).
Blood tests for IgE
There are blood tests that look at the total amount of IgE (the allergy antibody), which is sometimes useful in diagnosis. But more important are blood tests for specific IgE – against egg or grass pollen or latex, for example. There are different ways of measuring the IgE in the blood, the most commonly used being a radio-allergosorbent test or RAST.
Research shows that RASTs are no more accurate than skin-prick tests in confirming real-life allergic reactions. However, they are useful for patients who can’t discontinue their antihistamines without developing severe symptoms, and for those with dermatographism or very severe eczema (see p. 91).
Patch tests
These tests, used primarily for contact dermatitis, are similar to straightforward challenge tests, because the suspect substances are applied directly to the skin.
The test substances are placed on the skin – usually on your back – in small chambers. They are held in place with sticky tape, and left there for several days. Ideally, the reaction of the skin should be checked three times: after two days, again the next day, and again the day after that. It really is worth going back for all these separate visits, because the accuracy of the test increases greatly with repeated checking.
The substances chosen for testing are a standard set of antigens that most commonly cause contact dermatitis. This standard set will pick up 60-80% of all sensitivity reactions in contact dermatitis. If you have substances that you suspect may be causing symptoms, such as cosmetics, the doctor can usually test for these too.
You should not be tested while you still have a rash, as the testing will probably make the existing rash flare up, even though the test patches are applied well away from the rash.
Use of steroid creams and any light treatments (including exposure of the test area to ordinary sunlight) must stop at least a week before testing starts, or the results will not be accurate.
Interpreting patch tests requires a huge amount of skill, plus extensive knowledge of the finicky details of the different test substances. You need a dermatologist with considerable experience in this area.
False positives (see box on p. 91) can occur, especially if you react very strongly to one of the substances tested – some people develop what dermatologists call an ‘angry back’, and this generates false positives to various other substances being tested at the same time. Should you be told that you are sensitive to a great many different things, you may want to query this reading of the test. Ernest N. Charlesworth, an allergist and dermatologist at the University of Texas, describes patients who ‘develop into environmental cripples’ after being told that they are definitely sensitive to multiple antigens, on the basis of misinterpreted false-positive patch tests.
False negatives (see box on p. 91) are also possible, even with very careful testing. Should this occur, a type of challenge test known as a ROAT (Repeat Open Application Test) is possible. The suspect substance is applied to the inner fold of the elbow twice a day for a week. Get your doctor’s agreement before trying this test.
Endoscopy and biopsy
Miniaturised cameras and sophisticated fibre-optics have allowed modern doctors to do something that their predecessors could never have imagined possible – look right inside the human body. This procedure is called endoscopy, and it has a useful role in a few sensitivity reactions.
Looking inside the sinus cavities can assist in understanding exactly what is going wrong in chronic sinusitis. Inspecting the digestive tract can be valuable in several of the non-IgE immune reactions to food, such as coeliac disease (see p. 70) and eosinophilic gastroenteritis (see p. 72).
A biopsy is often carried out at the same time as endoscopy.
s involves taking a small sample from the affected area, such as
I ning of the gut, and studying it in detail under a microscope.
One purpose of a gut biopsy is to look for characteristic :goes of damage to the lining of the gut – such as the distinctive charges produced by untreated coeliac disease. A biopsy can also reveal what kind of immune cells are present. Abnormal numbers of certain immune cells, for example, eosinophils (see p 19), may suggest a particular diagnosis.
Another way of looking at what kind of immune reactions are going on, used for lung diseases, is a bronchoalveolar lavage – iterally a ‘washing out’ of the airways and lungs, allowing immune cells to be collected and studied. This diagnostic technique is lased for Heiner’s Syndrome (see p. 72).
Tests for food intolerance
The only really effective way of testing for food intolerance is an el ruination diet (see pp. 194-7). This is the gold standard. However, it is neither easy nor quick – which has led to a constant search for alternative tests.
The proposed alternatives are all indirect tests, that is to say, non-dietary. The results of the tests are used as a basis for an avoidance diet. In other words, the foods that give a positive test result are avoided.
Some of these tests use samples of hair or blood, others use pulse testing, pendulums, or muscle strength tests (’applied kinesiology’). A few of these tests do show some promise. Pulse tests, and a blood test called the ‘lymphocyte transformation test’. for example, can give a general indication of sensitivity reactions – sometimes. However, even in the most expert hands, these do not give a result that is accurate enough to be useful.
Of the other tests that are available, most have not been evaluated at all objectively.
Many of them are advertised directly to the public, and one of the problems with this approach is that the testing company starts by assuming that food is the problem. The same is usually true of ‘dietary therapists’ and others in the alternative health field offering tests of this kind.
Almost everyone who undertakes such tests is given a fairly long list of foods which have come up positive in the tests. This does not fit with the evidence from medical trials in which a group of people with irritable bowel or migraine (typical food intolerance symptoms) undertake an elimination diet. A significant proportion of them always find that they do not have food intolerance. Of the rest. many find that they react to one or two foods only. The long lists of foods produced by the commercial tests are, to put it mildly, implausible.
With tests that require a sample of blood, sending off two blood samples from the same person, under different names, is a simple way of assessing the tests’ validity. This exercise has been tried several times with different testing companies, and every time two completely different lists of foods have been sent back.
Covert studies of this kind have also shown that the tests overlook genuine reactions. In one alarming case, a woman with a true allergy to peanuts was assured by a ‘dietary therapist’ that she really could eat peanuts safely.
Many people with food intolerance will tell you that they did well after following a diet based on such tests – and they may well have done. Given that common foods such as wheat and milk are regular offenders in food intolerance, and that these foods very frequently feature on the lists of positive test results generated by commercial testing companies, quite a few people should do well. The problem is that these people may also be avoiding many other foods quite unnecessarily.
Furthermore, if people have sensitivities to some other foods that are not on the list, they will be missing out. They could enjoy a far better level of health if all the foods causing symptoms were Identified and removed from their diet.
In the end, an elimination diet is both cheaper and far more likely to give the right answers.
Testing for IgG antibodies
In diagnosing food intolerance, a few doctors offer tests for a type of antibody called IgG. This antibody is formed to any food molecules that get Into the bloodstream after a meal – and some do, even in entirely healthy people. So finding IgG antibodies to food molecules is not indicative of any disease at all. It occurs in everyone and is perfectly normal.
Nevertheless, some doctors feel that by measuring the level of IgG antibodies to foods, they can get a general idea of the permeability of the gut wall (which might possibly be true) and of particular foods that could be causing intolerance reactions (very doubtful – the tests just tell you what you eat most, and you know that already).
This test does measure something real, unlike some of the alternative tests for food intolerance. But the relevance of what it measures to the health of the individual concerned is partial and indefinite. A recent study of IgG testing for irritable bowel syndrome has confirmed this view.
In short, blood tests for IgG antibodies to food molecules seem like very poor value for money, and potentially misleading, whereas an elimination diet is a far more precise way of pinpointing food intolerances.

Coeliac Disease
During World War 11, there was no bread to be had in the Netherlands and people were forced to eat tulip bulbs. ‘My mother roasted them,’ one survivor recalls, ‘and they tasted delicious then, because we were so hungry I suppose. I cooked some years later, just to taste them again, and they were absolutely disgusting.’
While most of the population was thin and unwell on this starvation diet, a few children were actually healthier than before. An observant Dutch doctor noted that these were the children who, before the war, had suffered from constant diarrhoea, fatigue, poor growth and muscle wasting. They were suddenly stronger and, his enquiries revealed, their diarrhoea had vanished. But when the food situation improved at the end of the war, all their old problems returned. By carefully experimenting with the diet of these patients, the doctor discovered that eating wheat and rye caused the symptoms. Subsequent research has revealed that both contain a collection of proteins, referred to as gluten, which are the source of coeliac disease.
Belly disease
Coeliac disease (or celiac disease) is an old name which simply means ‘belly disease’. It is derived from the Greek word for’belly’ — koilia. Once the cause of the symptoms became understood, a new name was devised — gluten-sensitivity enteropathy — but it has not really caught on. Other terms that you may come across are non-tropical sprue and coeliac sprue, based on the close resemblance of the symptoms to those of tropical sprue. This disease, found in those who live or have lived in the tropics, is probably caused by bacterial infection. There is no causal link with coeliac disease.
Symptoms
The symptoms of coeliac disease are:
• diarrhoea, with pale, bad-smelling stools
• in a few patients, constipation rather than diarrhoea, but this is very rare
• bloating and wind
• damage to the lining of the intestine. This is of a characteristic type: the complex folded structures (the villi) of the intestinal lining are destroyed. Additionally, huge numbers of immune cells are present.
• the loss of the villi results in failure to absorb nutrients from food (malabsorption) causing poor growth in babies, and weakness and weight-loss in adults.
• poor appetite, especially in babies. This can greatly reduce the diarrhoea.
Coeliac disease usually appears in babies during weaning, a few weeks after cereals are introduced, but it can also begin for the first time in adults. The tendency to coeliac disease is genetically inherited, so it runs in families.
Where coeliac disease runs in the family, another disease, dermatitis herpetiformis, is also likely to occur. Dermatitis herpetiformis has the same basic mechanism as coeliac disease but very different symptoms:
• an intensely itchy rash, sometimes with tiny blisters; the rash is symmetrically distributed on the buttocks, shoulders, scalp, and the outer surfaces of the knees and elbows
• the same characteristic damage to the lining of the intestine as seen in tests for coeliac disease, though generally less severe
• diarrhoea, in some cases, but not all. About 5% of those with coeliac disease actually go on to develop dermatitis herpetiformis. Most people have either one or the other.
Both diseases are caused by the same gene, which results in sufferers developing antibodies against one of their own proteins, an enzyme called tissue-transglutaminase. The job of this enzyme, which is found in the intestines, is to assist with the breakdown of gluten.
If no gluten is present, the enzyme does not arouse the interest of the immune system. It is the process of gluten digestion, in which a particular peptide is produced from gluten, that provokes the autoimmune reaction. (A peptide is any short length of protein chain, obtained from the complete protein chain by digestion.)
What seems to trigger the autoimmune reaction is this enzyme–peptide combination: the offending peptide, newly produced and still attached physically to the enzyme. There is something about the particular ‘chemical picture’ that this combination makes which outrages the immune system of individuals with a particular genetic make-up.
The impact of this autoimmune reaction on the intestinal lining is severe in coeliac disease, less so in dermatitis herpetiformis. What causes dermatitis herpetiformis is a particular type of antibody, called dimeric IgA, which is transported by the bloodstream from the gut to the skin. It is deposited in the skin all over the body, but for some reason only provokes inflammation in certain areas.
In rare cases, an IgE-mediated food allergy to wheat can co-exist with coeliac disease, making reactions more severe.
Secondary problems
Paradoxically, while the damaged gut lining of untreated coeliac disease makes a poor job of absorbing specific nutrients (e.g. iron and vitamins) in a form that the body can use, it also lets through far more intact, or partially digested, food molecules. These get into the bloodstream in such numbers that they can lead to idiopathic food intolerance (see p.74). Sensitivity to soya is a common problem, because it is so heavily used in gluten-free bread and other prepared food. Those with coeliac disease who have not improved fully, despite a strict gluten-free diet, often benefit from an elimination diet (see p. 194). This must be done under medical supervision.
Another possible effect of the intestinal damage is lactose intolerance (see p.79), producing a sensitivity to milk.
The frequency of schizophrenia is higher among those with coeliac disease than among the general population. Coeliacs not following a strict gluten-free diet are also vulnerable to other psychological problems. These might be linked to the effects of food-derived exorphins (see pp. 76-7) and other peptides on the brain. The increased permeability of the gut could play a part in this, allowing more exorphins to reach the bloodstream.
Diagnosis
A biopsy (see p. 92) is the only really reliable form of diagnosis. It is crucial that this is done before removing gluten from the diet, because the damage is repaired if gluten is avoided and the healing process is fairly rapid for some people (though in others it takes many months). If the intestinal lining reverts to a normal appearance quite quickly, an accurate diagnosis is never obtained, which can have serious consequences: if you or your child are coeliac, you need to know.
New blood tests can also be helpful in diagnosis, but they do not give the unequivocal result obtained with a biopsy.
Research from the United States suggests that coeliac disease is under-diagnosed in some countries compared to others – for example, Italy screens children routinely but the States does not. Some authorities suspect that there is a great deal of ‘hidden’ coeliac disease in the States, and this could be true in other countries as well. There is no routine screening of children in Britain.
The symptoms of coeliac disease are not always distinctive. Many cases are first detected when patients with rather non-specific symptoms are discovered, by a blood test, to be anaemic.
Treatment
There are no drug treatments for coeliac disease and avoiding gluten religiously is the only way to remain well. Those who are lax about their gluten-free diet may be more vulnerable to certain cancers of the digestive tract.
A strict gluten-free diet is not easy to follow (see p. 177). The most severely affected coeliacs are so sensitive to gluten that they react violently to even a tiny amount: this is known as coeliac shock and can be fatal.
A gluten-free diet is also the treatment for dermatitis herpetiformis, but at the outset the rash can be controlled with the highly effective drug dapsone.

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.

 

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

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)