Posts Tagged ‘IgG’

A-Z Principal Drugs (antidepressants - astemizole)
antidepressants The drugs used in the treatment of depression fall into two main groups, the so-called tricyclic antidepressants and the monoamine oxidase inhibitors (MA01s). (Unrelated drugs include lithium carbonate, used only for the prophylaxis and treatment of manic depressive illness.) The tricyclic group, which also includes sonic other compounds with a similar action, appear to act by blocking the neuronal uptake of central transmitters such as noradrenaline and serotonin. They are more widely used than the MAOIs because they are more generally effective, and interact less extensively with other drugs and certain foods. The tricyclic drugs are widely used in endogenous depression, particularly when sleep disturbances are present, but the onset of action is slow, and improvement may not commence until after 2-4 weeks of treatment. Extended therapy is usually required to avoid the risk of a relapse, and patients should be advised accordingly. Sonic tricyclic antidepressants, such as amitriptyline, have a sedative action of value when anxiety is a complicating factor, whereas a less sedating drug such as imipramine may be useful in patients exhibiting apathy and withdrawal. Some of the side-effects, such as dryness of the mouth, are linked with their anti-
cholinergic activity, but tolerance may develop with continued treatment. They also influence the cardio-vascular system and may cause arrhythmias, tachycardia and hypotension, and may interfere with the action of some antihypertensive drugs, although the response to beta-blocking agents is unaffected. Care is necessary in cardiac disease, and with the elderly initial doses should be low. The use of tricyclic antidepressants in epileptic patients may result in a lowering of the convulsive threshold. See page 128 and Table 11.
antidiabetic agents Diabetes mellitus is a deficiency disease due to a lack of insulin, and is characterized by an excessive level of glucose in the blood and urine. Treatment is either replacement therapy with daily injection of insulin, or orally by hypoglycaemic agents such as chlorpropamide. Such agents act by stimulating insulin secretion and release by the beta-cells of the pancreas, and are ineffective in the absence of such cells. See page 132 and Tables 12 & 13.
anti-D(Rh.) immunoglobulin An ininiurioglobulin that is given to a rhesus-negative mother to prevent her forming anti-bodies against fetal rhesus-positive cells which may pass into the maternal circulation during childbirth or abortion and which, in a later pregnancy, could cause haemolytic disease.
Dose: 504) units Lin. within 60-72 hours of delivery or abortion. Doses of 1250 units are given prophylactically. It is of no value it’given after anti-D antibodies have been formed. The inimunoglobulin has also been given after the transfusion of rhesus-incompatible blood. (Partobulin).
antiemetics Nausea and vomiting may be due to several causes, including stimulation of the chemoreceptor trigger zone in the reticular formation of the brain. Man), antiemetics have some degree of central activity, and in some cases their action may be mediated by blocking the effects of dopamine on the trigger zone. Effective drugs include some antihistamines and sonic phenothiazine-based tranquillizers such as prochlorperazine. The alkaloid hyoscine is widely used in travel sickness. More powerful drugs such as domperidone, metoclopramide, nabilone and ondansetron, are of value in the control of the severe nausea and vomiting induced by cytotoxic drugs. The use of antiemetics in early pregnancy requires great care, and is seldom essential.
antiepileptics See anticonvulsants, page 136 and’] able 15.
antihistamines Drugs such as promethazine are of value in conditions associated with the release of histamine from mast cells, such as hayfever, rhinitis, urticaria, pruritus, insect bites and stings. They are also useful in drug allergies. Some antihistamines also have antienietic properties, and are useful in travel sickness. Although all antihistamines have the same basic action, the degree and duration of response and the severity of side-effects may vary. Some antihistamines pass easily into the central nervous system arid are more likely to cause drowsiness. Others may have reduced anticholinergic properties, and cause less dryness of the mouth and blurring of vision. Care is necessary in epilepsy, glaucoma, hepatic disease or prostatic enlargement. See page 110 and Table 2.

antihypertensive agents See page 148 and Table 2 1.
anti-inflammatory agents See non-steroidal anti-inflammatory drugs (NSAIDS) and page 165 and Table 29.
antimetabolites Cytotoxic drugs that appear to act by combining irreversibly with cell enzymes, and so prevent cell division. Methotrexate and mercaptopurine are examples. See page 122 and Table 8.
dermatology and pruritus as oily calamine lotion. Arachis oil enema is used to soften impacted faeces.
argipressin A synthetic form of vasopressin.
artificial tears Some chronic sore eye con clitions may occur in rheumatoid arthritis, and may be due to tear deficiency. Solutions of itypromellose or polyvinylalcohol, sometimes referred to as’artificial tears’, are useful as a bland lubricant to replace the tear deficiency. (Isopto; Hypotears).
antimuscarinic agents See anticholinergic agent” page 160 and Table 26.
antineoplastic agents Anti-cancer drugs. See page 122 and ‘rabic 8.
antipsychotic agents See pages 117 & 1(,8, and Tables 5 & 30.
antitetanus immunoglobulin aulloglobulin obtained from plasma is used in injured patients who have not previously been immunized, and when tetanus is a definite risk. Dose: 250 units jan. A course of tetanus vaccine should also be commenced,
antitubercular agents See rifampicin, page 170 and I able 31.
antiviral agents See page 144 and Table 19.
anxiolytics See page H 7 and Table 5.
apomorphine A morphine derivative formerly used as a powerful emetic, but now considered to be too toxic. Occasionally used in the hospital treatment of parkinsonism. (Britaject).
apraclorildine A clonidine derivative used as eye drops I 9A, to control intraocular
pressure during ophthalmic surgery. Some absorption may occur, so care is necessary in severe cardiovascular disease. (lopidine).
aprotinin An inhibitor of the proteolytic enzyme plasmin, obtained from bovine lung tissue. It is used in the severe haemorrhage due to hyperplasminaemia.
Dose: 500 000-1 000 000 units by i.v. infu.ioll. (Trasylol).
arachis oil Groundnut or peanut oil. It has
emollient properties, and is used in
ascorbic acid (vitamin C) Present in many citrus fruits. Deficiency is not uncommon in the elderly receiving inadequate diets. Severe deficiency causes scurvy, once the bane of seafarers.
Dose: for prophylaxis 25-75 mg daily; therapeutic dose 200-500 mg daily. Doses of 4 g daily are given for acidification of the urine. Claims that vitamin C prevents colds are unproven.
asparaginase Crisantaspase. See page 122 and Table 8.
aspirin (acetylsalicylic acid) Widely used as a mild analgesic and anti-inflammatory agent, often in association with other drugs such as paracetamol and codeine. Dose: 1.2-4 g daily, but in acute rheumatoid conditions doses of 4-8 g daily have been given. Long-term treatment with (loses of 75 mg daily are given liar the prophylaxis of cardiovascular disease. Side-effects include gastric irritation with some blood loss, hyperventilation, and bonitos, with the risk of deafness, may occur with high doses. Aspirin may cause rash and bronchospasm in asthmatic and other sensitive patients. As aspirin is now thought to be associated with Reye’s syndrome, the drug should not be given to children under 12 years of age unless specifically indicated. Aspirin may increase the effects of certain hypoglycaemic and anticoagulant drugs.
astemizole An antihistamine with an extended action and reduced sedative effects.
Dose: Wring once daily before food, and must not be exceeded. Higher doses may cause cardiotoxic side-effects such as ventricular tachycardia. Arrhythmias may follow combined treatment with many other drugs. (Hismanol; Pollen-ese). See page 110 and Table 2.

Air Pollution and Allergy

Air pollution plays a variety of roles in allergic reactions. Some pollutants irritate the nose and airways (and sometimes the skin) making them more sensitive to allergens. These pollutants can worsen existing allergic symptoms and may promote the development of allergies in children, by making the airway membranes more permeable. Other chemical pollutants may affect the immune system directly, increasing any existing tendency to allergic reactions.
Indoor pollution
For many of us, the air in our houses is much more polluted than any outdoor air. Several of the indoor pollutants irritate the nose and airways, and some can trigger asthma attacks. A few of the pollutants found indoors can also make allergies and asthma more likely to develop in young children.
Background pollution
One of the worst irritants in indoor air is tobacco smoke. Other people’s cigarette or pipe smoke can trigger asthma attacks in the short term, and makes asthmatics generally worse in the long run. Passive smoking might also affect the immune system making allergies more likely to develop, though this is not proven. Do whatever you can to eliminate tobacco smoke from your home.
Everyone is different
This article considers air pollution from the point of view of someone with classical allergies (e.g. hayfever or asthma). Those with chemical intolerance (see p. 84) may well be more severely affected by air pollution.
If you smoke yourself, there are many good reasons for giving up:
• If individuals from atopic families (see p. smoke, they have a far greater chance of developing allergies and/or asthma when exposed to an allergen in the air.
• For those who had asthma as children and have since grown out of it, cigarette smoking doubles the chance of it coming back.
• Parents of asthmatic children who smoke indoors make their children’s asthma worse. Teenagers can be just as badly affected by passive smoking as young children.
• Smoking during pregnancy significantly increases the risk of a woman’s baby developing allergies and asthma. (Smoking also leads to more prematurity, still-births and cot deaths.)
If possible, have an electric cooking stove rather than a gas one –or fit a powerful extractor fan. Cooking with a gas stove generates a lot of nitrogen dioxide, a gas that you can’t smell or see but which affects the airways. This same gas also comes from motor traffic, but peak levels of nitrogen dioxide in kitchens with gas cookers are often ten times the average level on city streets, and frequently exceed standards for outdoor air set by the world Health Organisation. Other sources of nitrogen dioxide include cigarettes, gas fires and kerosene-burning stoves.
For some people with allergies, nitrogen dioxide enhances their response to the allergen. So if you inhale dust-mite allergen together with nitrogen dioxide, it may have more effect than the Smoke screen
Smoke particles from coal or wood do not seem to make allergies more likely to develop - in fact, quite the reverse. In rural areas of Germany, researchers have found that children with coal or wood stoves in their homes were less likely to have allergies or asthma. An Australian study made a similar finding. Bronchitis and pneumonia are more common in those children with wood and coal stoves and these infections may stimulate the immune system in such a way that allergies are less likely to develop later. However, wood smoke may be a cause when asthma begins in an adult.
allergen alone. Breathing sulphur dioxide (see below) and nitrogen dioxide together boosts the reaction to allergen more powerfully than either gas alone.
Nitrogen dioxide might also make asthma attacks more likely, but the evidence on this is conflicting.
For young children, a high level of nitrogen dioxide at home may make the development of allergic reactions more likely. A recent Canadian study showed that children exposed to high levels of nitrogen dioxide in the home - usually from gas cookers - were ten times as likely to develop asthma as those breathing low levels of nitrogen dioxide. If a dog, cat or other furry pet was kept, and there were high nitrogen dioxide levels, the risk of developing asthma shot up even higher, to 25 times that of children with low nitrogen dioxide and no pets. (Other studies have not produced the same spectacular results, but their methods of measuring nitrogen dioxide exposure were less precise.)
Try to eliminate materials that produce formaldehyde fumes, or seal the items with a good coat of paint. Formaldehyde is given off by chipboard and to a lesser extent by MDF (medium-density fibreboard). Injected cavity wall insulation can also produce persistent formaldehyde fumes, and is very difficult to get rid of -moving out is often the only option. A recent study from Australia showed that children exposed to formaldehyde, especially in the bedroom, were more likely to develop allergic reactions: the higher the level of formaldehyde exposure, the more severe the child’s allergic sensitisation.
Those with asthma have more frequent symptoms if exposed to high formaldehyde levels. A recent study from Finland shows that easy-to-clean plastic wall-covering and flooring increases the risk of asthma in children.
A Canadian study found that children whose first home was less than 20-30 years old were 50% more likely to develop asthma than children living in older houses. One possible explanation for this lies with the materials used in the construction and fitting of new houses, especially the plastics, wood preservatives and insulation materials. Solvents, and chemicals such as formaldehyde, are still being given off by these materials some years later.
Air fresheners provoke asthma attacks in some people. For a few individuals they can cause general symptoms of ill-health that are similar to those described for mild chemical intolerance (see p. 84). Those affected generally don’t realise that the air freshener is the source of the trouble. This malign effect is not entirely surprising, since air fresheners work by giving off a chemical that targets part of the brain - the part involved in processing sensory input from your nose. The chemical ‘freshens the air’ by partially disabling your sense of smell. Better to open a window.
Cleaning products, furniture polish and deodorant were never intended to go into the nose and airways, but that’s what happens when they are sprayed from an aerosol, and they can trigger asthma attacks. Steer clear of aerosols as much as possible - there are usually alternatives.
Pollution peaks
Read the instructions and ingredients lists on all products carefully. It is not just a question of what’s in them, but also what gases they might give off when used. One asthmatic died within minutes when the de-rusting agent she was using on her dishwasher produced a large amount of sulphur dioxide gas: her airways tightened up so much that she couldn’t even use an inhaler to save herself. ‘Sulphuric’, ’sulphate’ or ’sulphite’ in the list of ingredients should ring warning bells if you have asthma: sulphur dioxide gas could be given off by this product.
Bleach, and other chlorine-based cleaning products, such as toilet cleaner and scouring powder, should be used sparingly, and with plenty of ventilation. These products release chlorine gas which, in large amounts, can irritate the airways of asthmatics. Never allow bleach or toilet cleaner to become mixed with any other product. Take care with any product containing hypechlorte, chloramine, ammonia, acids or morpholine and with the chemicals used for swimming pool water. All these can trigger asthma attacks.
If doing repairs or DIY work about the house, take special care. Always ventilate the work area well, and wear a dust mask if sawing or drilling.
The smell of paint is due to solvents, and these can act as irritants to the nose and airways. When decorating, ventilate well, and use low-odour water-based paint. Some of the best low-odour paints, tested and shown to be safe for paint-sensitive asthmatics, are only available by mall order: see p. 255.
‘Instant foam’ kits sold for DIY insulation can provoke asthma in those who were not asthmatic previously. Two different substances are mixed to create the polyurethane foam, and during the mixing process, isocyanate is released – this is one of the most powerful asthmagens known (see box on p. 132). The level of isocyanate can breach the safety limit set for factories.
Avoid using fly spray or other insecticides: look for other methods of pest control. A study from Ethiopia showed that people using an insecticide in their houses were twice as likely to develop allergies. A study of Canadian farmers suggested that asthma might be linked to the use of carbamate insecticides (e.g. carbofuran). The sprays used for cockroaches can act as irritants for those with allergic rhinitis or chronic sinusitis.
If advised that your house needs spraying with insecticide, for woodworm or other wood-boring pests, ask for more information before you go ahead. Is the spraying really necessary? What will happen if the house isn’t sprayed? How quickly will it happen? Is there any other method of eradicating the pest? Spraying is often done when it is not really essential – houses remain standing even with woodworm holes all over them. Unless you have a heavy infestation that is threatening the structure of the house, you are probably better off not having the house sprayed. The heavy and ongoing exposure to insecticide that spraying of a house involves is something you and your family should avoid if at all possible. All the sprays used are toxic to some extent – don’t believe those who tell you otherwise. A heavy exposure to pesticides can sometimes make allergic symptoms worse or precipitate chemical intolerance (see p. 85).
The garage, workshop or garden shed can also be very polluted. Petrol, kerosene and paraffin can affect some people with rhinitis or asthma, and can bring on their symptoms. These fuels should always be kept in airtight containers. Paints sold for cars often contain isocyanates, among the most common causes
of work-related asthma (see box on p. 132). If using such paint, wear a mask with an activated carbon filter and make sure the area is well ventilated. Avoid prolonged or repeated exposure.
Outdoor pollution
Some of the pollutants in outdoor air can make allergic reactions worse and can trigger asthma attacks in people who are already asthmatic. A study of hospital admissions in London, Paris. Barcelona and Helsinki found that high levels of pollution increased hospital admissions for asthma by about 3%.
The pollutants that matter to those with allergies are:
• ozone, which soars to high levels on sunny days, mainly in country areas that are near large cities. The reason for this is a chemical reaction which occurs when car exhaust fumes are exposed to sunlight, producing ozone, a highly reactive form of oxygen. Further chemical reactions, involving another ingredient of exhaust fumes, then break the ozone down again. Thanks to this second reaction, there is usually little ozone in city air. But in a relatively rural area 20 miles or so upwind of the city, the pollutants are too dispersed for the second reaction to occur, and the ozone from the urban traffic can accumulate.
Ozone levels in the air tend to peak in the late afternoon and early evening – but it takes 4-24 hours for ozone to produce its effects on the airways. Indoors, ozone breaks down very quickly because of contact with other gases inside the house.
Ozone can increase the effects of allergens, such as pollen, on the nose and airways.
In addition, ozone makes the airway muscles contract, even for people without asthma. Healthy people tend not to notice these effects, whereas some asthmatics may have more symptoms, and may need more drugs, on days when ozone levels are unusually high.
• diesel particulates, which can become a problem in town centres, and close to main roads used by vans and lorries. Unlike ordinary petrol, diesel fuel contains oil, so when it burns it produces tiny black particles. These consist of flakes of carbon (soot), coated with complex chemicals that are produced by the
But what about the ozone layer…?
Is ozone good for us or bad for us? People often get confused about this, because of all the discussion about
‘the destruction of the ozone layer’. But that ozone layer (which screens us from harmful ultraviolet light) is a natural phenomenon and it is thousands of feet up, well away from our lungs. At ground level, in the air we breathe, ozone is unnatural and potentially damaging .
The size of the particles
Diesel particles are 1-10 microns in size, with most smaller than 2.5 microns. Tobacco smoke, coal smoke, fumes from oil-burning boilers, and the smoke from frying food all contain very much smaller particles, down to a hundredth of a micron (.01 microns) in size. (A micron is a thousandth of a millimetre.)
In pollution reports, counts for particles in the air (mostly diesel particles these days, except in heavily industrialised areas) will often appear as ‘PM1 0′, meaning ‘Particulate Matter less than 10 microns in diameter’. This particle size is chosen because larger particles tend to settle in the nose and throat, and not reach the airways of the lungs. The term ‘Small Particles’ is sometimes used to mean PM10.
To deal with air pollution, you need a really good mask with two filters: a dust filter that can take out very small particles and an activated carbon filter that absorbs irritant fumes and gases. Note that while activated carbon filters remove most pollutants, they do not take out nitrogen dioxide unless they have been specially treated.
partial combustion of the oil. It is probably these surface chemicals, rather than the soot particles themselves, that have such bad effects on the nose and airways.
Some research suggests that diesel particulates might increase the risk of allergies developing – to pollen for example. Additionally, when levels of diesel particulates are high, asthmatics tend to have more symptoms. If levels rise above 50 micrograms per cubic metre there is a sharp increase in asthma attacks – and a recent study in Birmingham showed that such levels are regularly reached at roadsides.
• sulphur dioxide, which often reaches high levels in areas of heavy industry, particularly near coal-fired power stations and coking plants. It acts as an irritant to the airways and can trigger attacks in asthmatics, who are far more sensitive to sulphur dioxide than healthy people (see box on p. 207). However, at the sort of concentrations normally encountered, even in quite polluted air, sulphur dioxide does not have any effect on most asthmatics.
• nitrogen dioxide, which is produced by all types of vehicles, and by power stations and some factories. In towns and cities with heavy traffic, nitrogen dioxide can build up to high levels. This gas is also found indoors (see p, 128) – often at far higher levels.
Oil refineries and cement works
In addition to these widespread pollutants, there are localised areas of air pollution, around industrial sites, that are frequently accused of causing health problems, including high rates of asthma. The kinds of industrial sites regularly mentioned include:
• oil refineries and oil-burning power stations
• cement works that use waste solvents for fuel
• dock areas where oil is loaded into tankers.
None of these accusations has been investigated in any detail, so it is impossible to say if there is a real link with asthma.
Avoiding outdoor air pollution
If you live in the kind of area that experiences high levels of ozone (see p. 130), plan your outdoor activities, especially jogging or playing sport, to avoid summer afternoons and early evenings.
Those who live very close to a main road, with a lot of lorries going past, would probably improve their own health, and reduce the chance of their children developing allergies and asthma, by fitting air conditioning or high-quality HEPA air filters – or by moving house. However, the benefits, in terms of decreased risk, are not enormous, and it is important to take other preventive measures as well (see Chapter 8).
When driving, if you stop behind a lorry or bus, keep your distance, close the window and turn off the fan. Diesel vehicles often emit a thick cloud of particles as they set off, and this can come straight into your car, setting off severe attacks for some asthmatics.
A car with air conditioning will reduce your exposure to diesel particulates while driving. When buying a new car, you can make a contribution to air quality by choosing a non-diesel vehicle, preferably one with a catalytic converter fitted. Alternatively, buy a diesel vehicle with a particle filter on the exhaust (now fitted as standard in Germany).
In Britain, the Vehicles Inspectorate of the Department of Transport encourages the public to report lorries and buses seen pumping out black smoke (look in the phone book for the number).
If you are asthmatic, breathing through your nose may help as this can filter out some damaging pollutants before they reach the airways in your lungs. (If your nose is usually blocked, try the exercises on pp. 230-31).
When levels of ozone or sulphur dioxide are high, taking a supplement of Vitamin C and eating plenty of foods that contain Vitamin E and beta-carotene (see p. 207) can protect your airways.

Pollen

Do you ever wake up in the middle of the night with an attack of hayfever or pollen asthma? And do you ever wonder why this should happen? The explanation is that warm air, rising up from ground level on a summer’s day, takes pollen with it high into the Earth’s atmosphere. When the air cools down after sunset, this pollen slowly descends again — an invisible ‘pollen shower’.
This pollen shower falls quite quickly in the countryside, reaching ground level between 8 p.m. and 10 p.m., but hot city pavements and buildings keep upward air currents going, and pollen stays aloft for longer. Most pollen lands on the city between about midnight and 2 a.m. That’s why you wake up sneezing or wheezing – especially if you sleep with the windows open.
Understanding facts like these about pollen can help you to reduce exposure substantially. Pollen is by far the most difficult allergen to avoid, but don’t believe the defeatists who tell you ‘You can’t do anything about pollen.’
Pollen counts and forecasts
Pollen counts are based on the amounts of pollen collected at specific sites earlier in the day, or on the previous day.
Forecasts for the coming day are really just informed guesswork, based on the present pollen count, the time of year, the temperature and rainfall over the last few days, and the weather forecast for the next day. At best, pollen forecasts are only as good as the weather forecast.
Forecasts of pollen can be useful in deciding when to start taking antihistamines for hayfever or when to Increase your asthma preventer drugs (steroid or cromoglycate inhalers). The start of the grass-pollen season is now predicted quite accurately.
Avoiding pollen outdoors
One thing that really can help here is an air-conditioned car. In an ordinary car, closing the windows (and perhaps fitting a filter to the air intake) helps a lot, but the heat is terrible.
The size of the allergen particles
The pollen grains that cause allergies are between 10 and 40 microns in size, with the majority between 20 and 35 microns. An ordinary dust mask takes out particles larger than 5 microns, so it will be adequate for most pollens. However, a few plants — including rye grass — produce tiny allergenic fragments, some no bigger than half a micron. These are about the same size as cat allergen and will therefore need much better masks. For these fragments, it is worth using a HEPA air filter, and getting a high-quality vacuum cleaner.
A cycle mask, or special nose filters sold for hayfever, will keep out pollen at peak pollen times. Just wearing a scarf over the mouth and nose will also give some protection. Another option is to smear a little Vaseline just inside each nostril and breathe through your nose only. Much of the pollen coming into your nose will stick to the Vaseline. If you ’suffer symptoms in the eyes, sun- glasses will keep some pollen out. Even better are wrap-around shades, or safety goggles with side panels sold in DIY stores.
Pollen release occurs at different times of day for different plants. Grasses release pollen from about 7.30 a.m, onwards, but if the ground is damp the release will be delayed until the moisture has evaporated. Unfortunately, a few grass species wait until the afternoon, so there will be some pollen entering the air all day. If you get up at 6 a.m. for a walk or run, you can be safely home by 7.30 a.m. Alternatively, go out In the early evening, after grasses have finished releasing pollen, and before the ‘pollen shower’.
Birch is an afternoon pollen: release peaks between noon and 6 p.m. Unfortunately, there is no information at present for other types of plants.
All types of plants favour warm sunny days for releasing pollen, and they all avoid rainy weather. On cloudy days there is a build-up of pollen in the flowers, so a massive release of pollen occurs on the next day of good weather.
Avoiding pollen indoors
Pollen grains have one huge point in their favour: compared to other allergenic particles, they are big and heavy. This means that they settle more quickly from the air. In a room with 3m- (1 Oft-) high ceilings, all the pollen will settle within four minutes, as long as the air is completely still. In other words, if you close all the doors and windows, block off any draughts, and sit fairly still, within four minutes you will be breathing pollen-free air.
This does not mean that all your symptoms will instantly vanish, because the ‘Late Phase Reaction’ (see p. 13) can go on for up to 24 hours. But you should feel better and, by not starting a new cycle of allergic reaction, you are improving the prospects for the next day. Escaping from pollen for a few hours every day should produce a general improvement in the long run, with your nose and airways becoming less inflamed.
The bad news is that some plants produce allergenic fragments much smaller than the pollen grains themselves. Various grasses do this, as do birch trees and certain plants not generally found in Britain, such as ragweed. These tiny particles take much longer – up to six hours – to settle from the air.
Some plants even produce ‘volatiles’ – airborne chemicals that provoke symptoms. Birch trees release volatiles from their buds in early spring, weeks before the pollen itself is released, and they affect a great many people, including some who are not allergic to birch pollen. Volatiles can only be removed by masks or air filters if they contain an activated carbon filter (see p. 109).
The notorious effects of oil-seed rape on the nose are also due to volatiles, not pollen. These volatiles are simply irritants and there is no allergic reaction.
To cut down on the amount of pollen you inhale at home:
• Dry all your laundry indoors during the pollen season, to stop it collecting pollen.
• Pets bring in pollen on their fur, so keep them outdoors during the pollen season, and avoid stroking them or getting too close. Brushing them thoroughly before they come in is another option, but the allergic individual should not do this.
• Close the windows when your offending pollen is being released, and during the evening ‘pollen shower’ (see p. 126).
• Change your clothes when you arrive home, since they will be coated with pollen, and wash or rinse your hair. Keep some clothes for indoor use only.
• Aim for still air (no draughts, no fans and no vigorous movement) in the rooms where the allergic individual studies, sits or sleeps. Air currents stir up pollen from the floor and furnishings. (No draughts means poor ventilation, of course, which is acceptable during the pollen season – but ventilate again afterwards, to discourage moulds and dust mites.)
• If tranquil air is an impossibility, consider getting a high quality air cleaner, or air conditioning. Alternatively, wet-dust and vacuum every day (using a vacuum cleaner that keeps allergen particles in – see pp. 116-17) to reduce the amount of pollen residue. Those who are very sensitive may need to do this as well as having an air cleaner.
• Cover your armchair and bed with a dust sheet during the day. In the evening, fold this up very gently and wash it. This removes the layer of pollen that accumulates on furniture during the day, before it is disturbed and inhaled. If you are studying, cover your desk and books when not working.
Places to go, places to avoid
• For the grass-sensitive, mown grass is usually fine (it won’t flower) although some people react to skin contact with grass (see p. 43). Unmown grass does flower, and will cause symptoms. Wheat, barley and oats, although they are grasses, release little pollen and rarely cause problems. Rye and sugarcane do release pollen, and may affect some people, but maize (corn) has heavy pollen that does not travel far, so it rarely causes much trouble.
• The levels of most pollens do not differ much between town and country. In fact, high up in a tower-block may be one of the worst places, because of pollen rising on warm air.
• The seaside is often pollen-free thanks to onshore breezes. Mountain peaks and ridges are also good, but deep mountain valleys can be pollen traps.
Roses are not the problem
The pollens that cause allergic reactions almost all come from plants with inconspicuous greenish flowers. These plants are pollinated by the wind, which is why there is so much of their pollen wafting about in the air. Colourful and scented flowers are pollinated by insects and have big sticky pollen grains that don’t float about and rarely cause allergies. However, strong scents can irritate the nose of those who already have hayfever, and make their symptoms worse.

Because house-dust mites are a major source of allergic reactions they have been studied intensively, and various ways of killing them devised. But simply killing the mites is not enough. Their allergens will remain, and continue to cause allergic reactions for years. The allergens have to be either removed or inactivated — that is, changed chemically so that they are no longer recognised by the immune system.
Tackling dust mite is easier if you know certain key facts:
1 Dust mites prefer humid conditions. They do not drink, but absorb water from the air. When the relative humidity falls below 50%, the mites gradually dry out and are killed.
2 Mites feed on our skin scales, but only if they have been broken down first by moulds. High humidity (70-90% relative humidity) is a particular problem, for anyone with an allergy to house-dust mites, because it favours the mould that suits dust mites best.
3 Dust mites live inside mattresses, pillows, upholstery, cushions and soft toys. The allergens are blasted out when you settle into an armchair, get into bed, or turn over in the night.
This is when you inhale the biggest dose of allergen, or get the maximum dose to your skin. Carpets also contain dust mites, but the numbers are generally lower.
4 Dust-mite allergen is relatively heavy, compared to cat or mould allergens for example. Little of it floats around in the air, and the most significant exposure is inhaling it close to the source — from a pillow, mattress or teddy bear. This is why air filters are of little value for anyone with dust-mite allergy.
5 Dust mites are everywhere, and are carried around in clothing. Even if you could eliminate all the mites from your house, new ones would soon appear. A new mattress will usually be colonised by dust mites within four months.
The size of the allergen particles
The droppings of the dust mite, not the mites themselves, are the main cause of symptoms. The droppings are 4-20 microns in size, but they can crumble into fragments of 1-3 microns, and the tiniest bits are only 0.5 microns across. The pores of mite-proof covers (which really means mite-allergen-proof) should be less than one micron across, and preferably less than 0.5 microns. Dust masks (see p. 109) should also filter out particles of this size to be effective. The mites themselves are much bigger, 200-300 microns long, (A micron is one thousandth of a millimetre.)
The basics of mite warfare
• A temperature just above boiling point kills dust mites and inactivates Der pl, which is the troublesome allergen for most asthmatics. However Der p2, the other mite allergen, is not affected by heat. (Note that the carpet treatments advertised as ’steam cleaning’ generally just use hot soapy water, not steam. Because they leave the carpet very damp, they can increase the numbers of dust mites.)
• Washing with detergent at 55′C (130′1 or above (i.e. a 60′C wash cycle) kills mites and removes the allergen.
• Cooler washes will not kill mites, but will remove the allergen. This can be useful if the mites have already been killed by some other means. Regular cool washes of clothing or sheets will also remove human skin scales, reducing the mites’ food supply. (This is beneficial if you have eczema, because flaking skin adds to the problem by giving dust mites even more to eat.)
• You can buy mite-killing substances (see p. 255) to add to cooler washes, so that the mites are killed - the chemicals are rinsed out at the end of the wash, so are pretty safe.
• Dry-cleaning kills mites and it removes some of the allergen, but the amount removed is variable (20-70%).
• Freezing for more than six hours kills mites. Three hours’ strong direct sunlight in dry air will kill mites living in rugs and blankets. Neither treatment removes allergen.
• Mites hang on to the carpet fibres when the vacuum cleaner passes overhead, and about 65% of them remain afterwards. An ordinary vacuum cleaner sprays mite allergen into the air as it goes. The amount in the air - and therefore available to be inhaled - is three times higher after vacuuming.
Combating mites
Bear in mind that mites are the enemy - not dust itself. A house may be thick with dust but, because the windows are open a lot and the air is dry, it will have few mites. Another house may look perfectly clean, but be seething with mites because it is thoroughly draught-proofed, warm and slightly humid. The mites will be thriving in the carpets, beds and upholstery. Vacuuming and dusting every day, if done with an ordinary type of vacuum cleaner and a dry duster, will stir up the allergens and ensure that the air is full of them. So a person with mite allergy would feel far worse in the apparently very clean house than in the dusty one.
One crucial aspect of a mite-reduction programme is making the air drier - see p. 119 - so that mites no longer flourish.
Most of the other measures - described below - will involve stirring up dust-mite allergens, so the allergic person should not do the work, nor be in the house (see p. 109).
Too dry or too moist?
It is a well-established fact that the air in most modern houses is too humid, encouraging dust mites and moulds. Yet many people fit humidifiers because they believe that the air is ‘too dry’ and that this irritates the nose. Some very good scientific studies have shown it is indoor pollutants plus overheating that is the problem here, not dryness - even very dry air is not irritating as long as it is clean. Should your nose feel dry and ticklish, try to reduce indoor pollution (see pp. 128-9).
It is true that during an asthma attack, dry air does make matters worse, and very moist air helps. Inhaling steam from a bowl of hot water can be used to ease the attack.
The bed
Begin with the bed because this is the main exposure zone. A Danish study showed that just fitting mite-allergen-proof covers to the mattresses and pillows of dust-allergic children worked well. After a year the children had much less asthma at night, used half as much inhaled steroid, and gave better peak-flow readings.
The best approach is to buy a new mattress and new pillows before putting anti-mite coverings on them. These covers keep skin scales and mites out, which should prevent a new mattress or pillow becoming recolonised. The modern covers have tiny pores which allow perspiration to evaporate - this makes them comfortable to sleep on.
These pores are small enough (see box on p. 114) to keep any mite allergens inside, so they will also work with an old mattress, keeping the existing allergen inside. But the mites themselves will also thrive inside (there’s enough old skin there to keep them in business for years) and there is always the risk that, if a small tear develops, the stores of allergen in the mattress will come pouring out again. So start with a new mattress if you can.
Another possible option is to arrange for a contractor to heat-treat the bed, the mattress and all bedding. This is a new specialist treatment (see p. 255), where the bed is enclosed in a plastic tent and heated to very high temperatures. It is designed to kill all mites, even those right inside the mattress, and inactivate the allergen. (The contractor can also do your living room suite.)
If the covers are for a small child, check with the manufacturer that they pose no threat of suffocation. Mattresses and bedding with built-in covers may be safer.
Buy a new duvet (or wash or dry-clean your existing one) and put an anti-mite cover on it. Alternatively, buy a duvet and pillow that can be washed at 60′C (130′F), and wash them once a month. You must have the use of a tumble dryer, because mites will flourish if bedding is not completely dry.
An upholstered bed base will have its own (much smaller) population of mites. Buy a simple wooden or metal bed frame if possible. Or you could enclose the upholstered base in a mite-proof cover, or in plastic sheeting completely sealed with heavy-duty tape.
Wash all sheets and blankets at 60°C or more, or have blankets dry-cleaned – or buy new ones. From now on, wash sheets once a week and blankets once every two weeks.
Get rid of any other bedding such as patchwork quilts or fleecy underblankets. Alternatively, you can wash or dry-clean them regularly.
Electric blankets can be cleared of mites by washing them, and are very useful in keeping the bed free from moisture. This prevents mites from setting up home in the outer surface of your new mite-proof covers, so that you don’t need to wash the covers, sheets and underblankets so frequently. Leave the electric blanket on at a high setting, with the bed made, for at least twelve hours (check that there is no fire risk first). Note that some mite-proof covers might be damaged by this procedure – check with the manufacturer. If you have not yet purchased mite-proof covers, there are some made from Egyptian cotton which can tolerate this level of heat without damage (see p. 255).
Children’s beds and toys
Where children share a room, all the beds and bedding should be dealt with. Even then, an asthmatic child should never sleep in the lower half of a bunk bed, because mite allergens will shower down from the bed above.
Ali soft toys should spend at least six hours in the freezer once a week, to kill the mites. The first time, wash the toys
immediately afterwards to remove any existing allergen and dry thoroughly in a tumble dryer.
A hot wash, or the freezing/washing treatment, should also be used for ‘comfort blankets’, dressing-up clothes, dolls’ clothes and any other fabric items.
Sheepskins, sometimes used for babies’ cots, especial,. New Zealand and Australia, contain huge amounts of dust-mite allergen. It is advisable to discard these.
The next steps
Clothing is often full of mites, especially sweaters, coats and woollen trousers. Dry-clean all such items, or wash using a m –e-killing wash, then store them in a well-heated place so that they are always very dry.
Dandruff consists of skin flakes, and may help to feed mites Using an anti-dandruff shampoo may help. Semen also gives mites nourishment.
From now on, be careful about exposing your airways to dust. Get someone else to empty the vacuum cleaner bag – and they should, of course, do it outdoors. If you are stripping wallpaper, wash it down first to remove dust. Moving house, going into the attic, spring cleaning, turning out cupboards or moving furniture should all be avoided – unless you have a good mask on.
Do not use fan-heaters or convector heaters which churn up mite allergens from the carpet. Seal off any hot-air ducts from centralised heating systems, as these blow mite allergens around the room.
If possible, invest in a vacuum cleaner that keeps in all the allergens, or vents them outside, rather than spraying them out into the air. Make sure that the vacuum cleaner you buy really
What about sprays?
Chemicals that kill mites (known collectively as acaricides) are sometimes useful but have various limitations. They do not penetrate inside upholstered furniture, cushions or mattresses, so make little difference to the total population of dust mites. Even on carpets, sprays won’t reach most of the mites unless you rub the spray in really hard. (And ‘anti-mite’ carpet shampoos are completely ineffective.)
The safest chemical is benzyl benzoate — so safe that it is used directly on the skin for treating scabies infections. It can cause skin irritation at these doses, but rarely does so at the concentrations used in anti-mite sprays.
However, the idea of constant spraying, over a period of months or years, is worrying. Doctors generally advise against spraying bedding, and carpets or furniture where babies or small children play, to avoid close and prolonged contact with the spray residue.
Even more alarming are sprays containing a pyrethroid (pyrethrum) compound. The latter is derived from a plant and is therefore sold as ‘natural’, but pyrethroids are potentially toxic with prolonged exposure, and they quite often provoke allergic reactions too. They should definitely be avoided.
Sprays that inactivate allergen (rather than killing mites) sometimes have their uses. There are two kinds and both should work against a variety of allergens, not just dust mite. Polysaccharide sprays stick the allergen particles together, so that they don’t float about and get inhaled. Tannic acid sprays change the allergen chemically, making it non-allergenic. Because tannic acid is found in tea it is assumed to be harmless, but the sprays available vary a lot and often contain many impurities, so it is hard to be sure about their long-term safety. Don’t use these sprays on bedding.
Carpets and bedding covers with built-in pesticide are also on sale, but are probably best avoided.
does its job well – a lot of machines now claim to be ‘allergy’ vacuum cleaners but they are not all equally good. Very few have been adequately tested (see p. 255). Alternatively, cover the bed with a clean sheet and open the windows whenever you vacuum, leaving them open for half an hour afterwards. After closing the windows, allow the dust to settle for another half hour, then carefully remove the dust-cover from the bed.
For dusting, use a damp cloth and add a few drops of eucalyptus oil which deters mites. Alternatively, use a special anti-mite duster with an electrostatic charge that holds the dust.
Above all, keep the moisture levels in your house down. Ultimately, this is the key to eliminating dust mite. Look at p. 119 and check you are doing everything possible.
The bedroom in particular should be kept dry. Air your bedroom whenever it’s dry and sunny. Remove pot plants and fish tanks. Don’t dry clothes in the room and don’t shampoo the carpet. Avoid using Calor gas heaters, as these produce a lot of moisture. If your bedroom has an en suite shower, fit a powerful extractor fan, or open a window wide during and after showers – or just stop using this shower. En suite basins may also generate moist air.
Do you need to do more?
Give it some time before deciding if you have done enough. In one study, it took eight months for the full benefits of an anti-mite campaign to be seen.
If you are still not as much improved as you hoped, then you could try a more drastic mite-elimination programme.
Thoroughly clean the bedroom, getting rid of any dust along skirting boards or picture rails, on top of wardrobes or behind furniture. Remove anything stored under the bed, so that vacuuming is easier in future. During this cleaning operation, completely cover the bed.
Get rid of the bathroom carpet, if you have one. In the bedroom, either remove the carpet or buy a special anti-mite steam cleaner that kills mites in the carpet and inactivates the allergen. To work properly, the device must produce steam at a temperature above boiling point, by means of high pressure. Make sure you are buying the right kind of device.
If you take out the carpet, you will need to mop the floor, with a wet or oiled mop, several times a week, as the dust will quickly build up, and is easily made airborne from an uncarpeted floor. One of the advantages of carpet is that it ‘holds’ dust at floor level.
Wash the curtains, or dry-clean them, or replace them with blinds of a kind that can be easily wet-dusted. If you have bought an anti-mite steam cleaner for the carpet, use this on the curtains every 2-3 weeks.
Remove dirty clothes from the bedroom, clean out drawers and shelves, and dry them thoroughly. Only store freshly laundered clothes in the room.
Remove all upholstered items from the bedroom, such as padded headboards, cushions, armchairs, or stools with padded seats. Draught excluders, fabric lampshades and anything covered in velvet should also go.
A different approach
If you are even more allergic to housework than you are to dust mites, consider buying a really powerful dehumidifier, designed for killing mites. This makes the air too dry to breathe (its relative humidity or RH goes down to 25%), so you leave it on in the bedroom during the day, with the bedroom door closed. You must eliminate all sources of moisture that will counteract the dehumidifier, and have fairly tight seals around your windows and doors for it to work. In the evening, turn the dehumidifier off and leave the bedroom door open for an hour or so before going to bed.
Of course, all the allergen which was already there in the bed, carpet, curtains, clothes and soft toys will still be present. You need to either eliminate or inactivate this allergen using the methods described above. But once you have got your daily dehumidifier routine going, you do not need to rewash everything regularly because mites will be a thing of the past, so no new stocks of allergen will be produced.
The rest of the house
A completely mite-free house is hard to achieve, but if you are determined, you can come close. Everything so far described for the bedroom, such as reducing moisture in the air, and dealing with carpets and curtains, is applicable to the rest of the house.
The exception – and the toughest nut to crack – is the upholstered furniture in the living room. Fixed upholstery (i.e. everything other than removable cushions) is a safe haven for mites that is especially hard to deal with.
One option is to give all such furniture a specialist heat-treatment, if this is available locally (see p. 115). The mites inside will be killed, and the allergen inactivated. If you drastically reduce moisture levels at the same time – with a powerful dehumidifier used at night, perhaps – you should avoid serious reinfestation.
Alternatively, you could replace all your existing upholstered furniture with leather-covered or vinyl-covered furniture. Both are impenetrable to mites. Furniture made of wood or bamboo with loose cushions and no fixed upholstery can also work. Fit the cushions with tailor-made mite-proof covers (hard to get, but ask around) when new. Then put the ordinary covers on top, and wash these regularly.

Moulds and Other Fungi

The air around us is full of bits and pieces that are mostly too small to be seen without a microscope - pollen grains, mould spores, fragments from plants, fibres from clothing, specks of ash from smoke, skin flakes and diesel particles. Of these, mould spores are by far the most abundant.
Except in very dry climates, there are more mould spores in the air than anything else. In Britain the record count is over 160,000 spores per cubic metre of air, compared to a record pollen count of only 2800 grains per cubic metre. Luckily, mould spores are not particularly allergenic or even more people would be suffering as a result of inhaling such huge quantities of them.
Spores are produced by moulds and other fungi, and they are to the fungus what seeds are to a plant – they can grow into new fungi. Doctors generally speak just of ‘mould allergy’ because moulds are the most common offenders, but larger fungi – mushrooms and toadstools – also produce allergenic spores. For example, a bracket fungus called Ganoderma, that infests dead trees and produces spores prolifically in mid-June, has been found to affect 16% of asthmatics in one part of New Zealand. Bracket fungi occur all over the world, but until recently no one had suspected them of causing allergic reactions, so the extent to which they cause allergies has not been investigated. The same is true of other large fungi.
Yeasts (single-celled fungi) are also found in the air, and it is possible –though this has not been investigated – that people with an allergy to yeast in food would also react to inhaled yeasts.
Indoors and out
Mould spores are a particular nuisance because they can be produced both indoors and out. There are different species of mould in different places, and you may be lucky and only react to one or two uncommon species. But many moulds grow in a very wide range of situations, both indoors and outdoors. There are also cross-reactions (see p. 14) between some of the moulds, unfortunately, which means that people generally react to a great number of different moulds. You will probably need to reduce mould growth inside your home as well as avoiding mould-rich places outside. Changes to your garden that eliminate havens for moulds, such as leaf piles, may also be helpful.
Moulds may only be growing in one part of a house – the cellar perhaps – but can be carried all around the house on air currents.
The size of the allergen particles
Most mould spores are between 2 and 10 microns in size. A few species have spores that are smaller than 2 microns.
(A micron is one thousandth of a millimetre.) Some people with mould allergy may be protected by an ordinary dust mask (see p. 109), but most will probably need a better-quality mask.
Avoiding outdoor moulds
Moulds live in the soil, and grow on any decaying plant matter, such as dead leaves, dying plants, fallen trees, hay and straw. Spore counts are highest in the autumn. A thick covering of snow reduces the numbers of mould spores in the air dramatically. Once the snow melts in spring, moulds flourish on the plants killed by the cold, so spore counts soon rise again.
The effect of the weather on spore release is very complex. Some moulds like to release their spores when it is dry and windy, but others favour fog, mist or dew. Rainfall washes a lot of spores out of the air, but it stimulates the release of some small spores.
A few pollen information services also give current mould-spore counts, but predicting spore counts for the following day is well-nigh impossible.
Drastic avoidance measures, for those who are severely sensitive, include moving to a desert or semi-arid area where there are far fewer mould spores in the air.
Listed below are the mould-rich situations and activities which could provoke your allergy symptoms. If they do, you should avoid them, or wear a mask that will prevent the spores being inhaled (see box on p. 120).
Places
• Near fields of cereal crops in late summer, because of moulds growing on the cereal leaves. Symptoms are likely at harvest time, when combine harvesters disperse the spores.
• In forests and old orchards, in gardens with compost heaps or piles of dead leaves, and in greenhouses.
• Near springs, waterfalls, and other damp, shady places.
Times
• During late summer and autumn, when moulds flourish outdoors on fallen leaves and fruit.
• Following the first frost of autumn, which triggers spore release by fungi in the soil.
Activities
• Disturbing compost heaps, damp straw or hay, piles of grass clippings or heaps of fallen leaves, all of which are absolutely full of moulds.
• Collecting up fallen leaves or fruit.
• Watering the garden because mould spores are released when water hits the dry soil.
• Mowing grass, if the clippings were not cleared up after the last mowing. Unless the weather is very dry, the clippings tend to go mouldy.
• Removing dead leaves or flowers from plants.
A dangerous mould allergy
Anyone with asthma who also has allergy to the mould Alternaria should –with their doctor’s agreement – increase their dose of preventer inhaler (e.g. steroid or cromoglycate) during the spore-producing season. Research shows that severe near-fatal asthma attacks often occur during the Alternaria spore season among those allergic to this mould.
Spore release by Alternaria usually occurs in the summer or autumn, but the timing varies from one part of the world to another, so check with your doctor or a local pollen/spore monitoring service. Alternaria can live outdoors in soil, and on seeds and plants. Indoors, it is a denizen of window frames, carpets and textiles.
Indoor moulds
These are the indoor situations that can be difficult for mould-sensitive people. You should either avoid these, wear a mask, or tackle the problem at source – for example, by reducing dampness (see p. 119).
Places
• Buildings that are damp, because moisture encourages mould growth. Never sleep in a room which has mould growing on the walls or window-panes. In addition to damp houses – now very common – you may encounter moulds in old churches and church halls.
• Buildings that are near lakes, rivers or the sea, because of the dampness of the air. Rooms with humidifiers.
• Bathrooms and shower rooms, unless well ventilated, owing to the steam and condensation.
• Rooms that are generally left unheated, and are therefore colder than the rest of the house, as these tend to suffer from condensation.
• Buildings with dry rot or wet rot. Not all mould-sensitive people react to the spores of these dreaded timber-rotting fungi, but some do.
• Buildings where old timbers are being removed, as this stirs up huge numbers of spores.
• Buildings where central heating has recently been installed, as the warmer temperatures in the building stimulates the existing moulds to release their spores.
• Buildings with lots of indoor plants. There are moulds you cannot see growing on the surface of the soil around a potted plant.
• Cellars and basements. Conservatories can also be full of moulds if not well maintained.
• Antique shops, farms, mills, holiday cottages.
On the first day of Christmas…
Christmas trees usually have moulds (which you can’t see) growing on the needles. When the tree is brought indoors, the warmth encourages these moulds to shed their spores.
Times
• During the winter, when there are usually more moulds growing indoors due to condensation.
Activities
• Handling clothes, curtains or furnishings that smell mildewy: they may be dry now but they will still be full of mould spores.
• Handling vegetables or fruit that have been stored a long
time, or in damp conditions (e.g. in plastic wrapping). Note
that this can include mushrooms – they often have white
moulds growing on them, which can be quite inconspicuous. If looking around your house for moulds, bear in mind that they vary a great deal in colour. Bread, vegetables, cheese and other foods that are past their best grow green, grey or white moulds, often furry, and these are the ones most people are familiar with. But the black stuff on the walls of bathrooms and in the door seals of refrigerators is also mould. In some situations it takes a practised eye to spot this type of mould – around window frames for example, or in the patterns of bathroom-window glass, it can easily be mistaken for ordinary dirt. On shower curtains and cubicles you may find pinkish-red moulds as well as these black kinds. Garden plants and crops can have bright orange moulds (called ‘rusts’) on their leaves, as well as the more familiar grey or black kinds.
Combating indoor moulds
The crucial task here is to reduce dampness and condensation in the house – see p. 119 for the details – as this encourages mould growth on all kinds of surfaces, including walls, ceilings, windows, bathroom tiles, shower curtains, and even carpets. Once you have reduced the humidity, then you can have a big clean-up and remove the spores that have been left by moulds.
If your allergy symptoms are very bad, and you need some immediate relief, then you could get someone to clean away the mould growth and spores first, then tackle the damp problem, then repeat the cleaning operation. Obviously, this is less efficient, but it may be the best approach if you are severely affected.
Note that the cleaning will, in itself, stir up a massive but unseen cloud of spores, so the allergy sufferer should not be at home during this work (see p. 109).
Cleaning away moulds and stopping regrowth
There are two aspects to this task:
• a one-off effort to clear the accumulation of mould growth and old mould spores – trillions of them are probably lying around your house – since these spores are the cause of the allergic reaction
• an ongoing effort to prevent the regrowth of moulds in problem areas such as the bathroom.
Get rid of any furniture that smells ‘mildewy’: it is packed with old mould spores. Fabric items that have this smell should be washed thoroughly. Old clothing, books and newspapers may also be a source of mould spores.
Any carpets or other porous materials (e.g. ceiling tiles, wall panels) that have ever been soaked by flood or storm waters should be disposed of now – and, unless everything can be dried within 24 hours, this should be always be done if there is water penetration in the future. Research shows that such materials quickly become infested with moulds. Check above the flood line, as water can seep upwards through the walls or panelling.
On fridges and freezers, clean out the rubber seals around the doors, going into all the crevices to get out the black mould that lives there. Also clean out the drip-pans of fridges, freezers and dehumidifiers. Keep shower heads and air conditioning equipment (including the filters) very clean. This all needs to be done regularly from now on.
Clean off all the mould growing around windows, or on walls and ceilings, tiles or other surfaces. Alcohol (e.g, white spirit or surgical spirit) kills it very effectively, without the use of water, and it takes a long time to grow back again. You could, alternatively, wash down the walls with a mix of one part bleach to two parts water. (But note that chlorine fumes may be irritating to the airways of those with rhinitis or asthma.) Special anti-mould sprays are also available, but try them out cautiously as they too may be irritants. Do not brush mould growth off with a dry cloth, as this simply disperses the spores. In the future, keep an eye out for new mould growth, and remove it promptly.
Buy a new shower curtain and replace it regularly, or clean it thoroughly with an anti-mould spray.
Can foods and mould spores cross-react?
Some people with mould allergy appear to be affected by eating mushrooms, or foods that contain yeasts or other fungi, e.g. certain well-ripened cheeses, dried fruit, soy sauce and vinegar. There has been little scientific investigation of these claims.
No cause for concern
The drug penicillin – which can cause severe allergic reactions – comes from the Penicillium mould. Fortunately, there appears to be no cross-reaction between the drug and the spores of Penicillium.
Cut down on the number of houseplants, and find a new home for any that need constant moisture. With the remaining plants, take off dying leaves and flowers promptly, and remove the top layer of soil occasionally, replacing it with fresh soil or – even better – sand or grit. Pot-pourri should also be evicted, as it can be full of mould spores.
Use vegetables and fruit promptly, and do not allow bread to go stale, or jam to go mouldy.
What to do if these measures fail
Where there is an invincible damp problem, a really powerful dehumidifier used during the day in bedrooms, and at night in the sitting room, will kill off most moulds and defeat their efforts to regrow. Close all the doors and windows in the room where the dehumidifier is operating, and shut off air vents. Note that air conditioning will also reduce the humidity of the air, but not as much.
Keeping mould spores out of the airways
Ordinary house dust can contain a lot of mould spores. The allergic individual should not dust, vacuum clean, sweep floors or make beds until the anti-mould measures have begun to bite. Ideally the allergic person should go out while housework is done, and the house should be thoroughly aired before their return. If this is impossible, then wearing a good mask all the time is essential. A special vacuum cleaner that retains allergens, or vents them outside. may be helpful in addition to the mask.
Even though you have cut down on moisture and condensation, and tackled mould growth, there could still be a lot of mould spores around, especially in an old house, one that has been very damp in the past, or one that is close to water. If symptoms persist, then think about hiring or buying a high-quality HEPA air filter (see p. 108) to take mould spores out of the air.
Do not use fans or fan heaters, as these churn up mould spores from the floor and other surfaces.
Beating athlete’s foot
Allergenic fungi can grow on your body, as well as in your house (see pp. 16-17). If athlete’s foot is playing a part in your allergies, it is vital to treat the infection thoroughly with drugs, because the fungus grows deep into the skin and can quickly stage a come-back if not completely destroyed. You should also be careful not to reinfect yourself:
• always dry your feet very thoroughly, especially between the toes; kitchen roll does a better job than towels, and can be discarded, reducing the risk of re-infection
• wear cotton socks and shoes made of leather or canvas, which allow sweat to evaporate; only wear trainers or gumboots, or any other footwear that makes your feet feel sweaty, when you really need to
• when your feet get wet, change your socks and shoes promptly
• launder all towels and bath mats at high temperatures when you start the course of anti-fungal drugs, and again when you complete it
• never share towels, bath mats, socks, sandals or shoes
• wear flip-flops at the swimming pool or sauna, and in changing rooms; if any other member of the household has athlete’s foot, take the same precautions in the bathroom at home – and make sure they seek treatment.
Occasionally athlete’s foot is a misdiagnosis for atopic eczema of the feet, which is a common problem among allergy-prone children (see box on p. 45). If the skin between the toes is not affected, it’s unlikely to be athlete’s foot and more likely to be eczema.

Allergy and Your Immune System
`The summer used to be such a miserable time for me because I’m allergic to grass pollen. For most of

my life I have had dreadful hayfever, and my asthma would get worse during the summer as well.

Antihistamines knocked me for six, and although there were nose drops that helped a little, they

certainly did not resolve the problem completely. Exam time was always a nightmare when I was a student

- then, as now, it coincided exactly with the pollen season.’
‘Getting a job in Chicago was a turning point in my health. My colleagues were amazed to see me

snuffling through the summer and just accepting that nothing could be done to improve matters. The

whole approach to treating allergies is different there. Eventually someone marched me off to see her

allergist, who said that I should have “allergy shots” and that my health insurance would cover it. The

process was very time-consuming at first, and it took a while to work, but the change is remarkable.

I’ve never regretted having the treatment. Summer is a time I can actually enjoy now.’
Not everyone responds this well to immunotherapy, but for those allergy sufferers who do benefit, this

is an excellent treatment. It tackles allergies right at their source, by teaching the immune system to

react differently to the allergen.
Also known as Specific Immunotherapy (SIT), Incremental Immunotherapy (11T) or simply as

hyposensitisation, this form of treatment was devised by two English medical researchers, Leonard Noon

and John Freeman, who reported their successes with hayfever patients in 1911. Ironically, their

treatment is now less readily available in Britain than in any other industrialised nation. Only a

small minority of British allergy patients receive immunotherapy. The cause of this strange situation

is a ruling made in 1986 by the Committee on the Safety of Medicines (CSM). This states that

immunotherapy must only be given where there is resuscitation equipment available, and that all

patients must wait for an hour after each injection, in case of
side effects. In addition, immunotherapy cannot be used for severe asthma.
The requirement for resuscitation equipment rules out most GP surgeries, and this effectively puts

immunotherapy beyond the reach of many allergic individuals in Britain, owing to the extreme shortage

of allergists and hospital allergy clinics (see p. 89). (In the past, the lack of allergy specialists

meant that most immunotherapy in Britain was given by GPs.)
The CSM ruling was triggered by a number of deaths due to immunotherapy: there were eleven fatalities

between 1980 and 1986, with five of these in the eighteen months just before the report. But almost all

these deaths were due to very basic errors in the way the injections were given – tragic as the deaths

were, the official response to them was inappropriate. Fatal reactions to immunotherapy can be avoided

with close attention to ordinary safeguards (see p. 166-7).
Allergen immunotherapy is still freely available elsewhere in the world, and is regarded as a key part

of allergy treatment. Britain is now out of step with all other developed countries, and most doctors

feel that British restrictions are far too strict.
There are hopes that this situation may change within the next few years, and that more allergy

sufferers may be able to take advantage of this valuable treatment. This could be achieved, in part, by

investing more National Health Service money in allergy clinics and allergy specialists. In addition,

there should be a relaxation of the regulations, so that properly trained GPs can give immunotherapy to

patients who are not at high risk of a fatal reaction. For people whose lives are affected by

allergies, the reintroduction of this treatment (with appropriate safeguards) would be a huge boon.
The uses of immunotherapy
Immunotherapy is mainly used for airborne allergens such as pollen, house-dust mite and mould spores.

Allergies to animals can also be treated with immunotherapy, but the treatment cannot work miracles –

if a cat-allergic person decides to keep the cat, the high dose of allergen inhaled every day limits

the impact of immunotherapy treatment.
People with straightforward allergic reactions affecting the nose and eyes (allergic rhinitis and

conjunctivitis) respond well to immunotherapy. In patients with hayfever, for example, the success rate

(patients showing some degree of improvement) is about 80-90%. When nasal allergies are complicated by

chronic sinusitis or nasal polyps, the chance of success is a little lower.
Some studies of the long-term effects of immunotherapy suggest that, if it is given to children with

hayfever or perennial rhinitis, those children are less likely to develop asthma.
The benefits of using immunotherapy to treat established asthma are less certain. Asthma is a more

complex disease than hayfever, and allergies are only one factor among many (see p. 36), which may

limit the impact that immunotherapy can make. Experience suggests that immunotherapy can be a great

help for an asthmatic with a strong allergic reaction to a single airborne allergen, such as grass

pollen or house-dust mite, but not for other asthmatics. Asthmatics with aspirin sensitivity or chronic

sinusitis are unlikely to benefit.
The value of immunotherapy to children with asthma is a subject of great debate among doctors in the

United States. Some studies suggest that it is of little real benefit, while others are more positive.

One interesting study, that followed asthmatic children for 15 years or more, found that if they were

given a full five-year course of immunotherapy when young, they tended to have fewer asthma symptoms

and need less medication in their late teens and early twenties.
Chronic urticaria (nettle rash) is occasionally due to airborne allergens, in which case immunotherapy

may help. However, immunotherapy is not recommended for atopic eczema. When people with both eczema and

rhinitis try immunotherapy for their nasal allergies, some find that their eczema gets worse.
Insect-sting allergy is a prime candidate for immunotherapy (see pp. 167-8) but food allergy is a

different matter, and is not treated with immunotherapy at present (see p. 168).
Who can get immunotherapy?
As a result of the CSM ruling (see p. 164) remarkably few allergy sufferers in Britain receive

immunotherapy.
Those with insect-sting allergy, who have suffered anaphylaxis (see p. 58), are the most likely to be

offered this treatment. However, even with this frightening and life-threatening problem, which can be

treated with almost 100% success by immunotherapy (see p. 167-8), such treatment is not automatically

available.
A few people with severe hayfever that does not respond well to drug treatment may also be given

immunotherapy. It is worth asking your doctor about such treatment if you feel you would benefit.
How immunotherapy works
Immunotherapy consists of a series of small injections, just under the skin. The liquid that is

injected contains an extract of the offending allergen, for example house-dust mite. The injections are

given at regular intervals, usually once a week, although other schedules are possible (see p. 167-8).
At the outset, a very dilute version of the allergen extract is used, way below the threshold for an

allergic reaction. People who seem highly sensitive, on the basis of their skin tests, start on an

extract that is even more dilute.
For the next injection, a slightly higher concentration of the allergen extract is used, and the

concentration goes on increasing with each successive injection. The idea is to habituate the immune

system to the offending allergen, by very gradually raising the dose. Eventually, when the dose reaches

a level which generally gives beneficial effects, no further increases are made.
If an allergy sufferer reacts badly to immunotherapy injections (see p. 166) on several successive

occasions, the dose may be levelled off before the ideal maximum dose is reached. However, a good

allergist will persist for some time in trying to increase the dose because stopping at a lower level

often results in the treatment being ineffective.
The first stage of immunotherapy, when the concentration of allergen is being increased week by week,

is referred to as the build-up stage. The second stage, when the dose is being kept at the same level,

is called maintenance therapy, and the dose used is the maintenance dose.
There is sometimes an obvious improvement by the time the build-up stage is complete, but not always.

The benefits of the treatment generally appear within six months of reaching the maintenance dose, but

some people have to wait a year or even two before things improve. As the immunotherapy begins to take

effect, symptoms decline and there is often less need for drugs.
A great deal of research effort has gone into finding out what lies behind these changes – in other

words, what is actually happening to the immune system when immunotherapy is effective. The answer is

that a surprising number of different changes may occur and no two allergy sufferers react to

immunotherapy in quite the same way. Frequently there is a shift in the kinds of antibodies the body

produces against the offending allergen. Levels of IgG antibodies (which help to block the allergic

reaction) go up, while levels of the allergy antibody, IgE, tend to stabilise and eventually go down.

The numbers of mast cells (see box on p. 12) may also decline, and they can become less responsive to

the allergen. The balance of power between Th1 cells and Th2 cells may also shift, with the pro-allergy

Th2 cells (see p. 11) becoming less influential.
What can go wrong
The secret of safe immunotherapy is to go at exactly the right speed for the immune system of the

individual being treated. The doctor should look for feedback from the immune system – signs that show

how well it is coping with the steadily increasing dose of allergen – and use these to pace the

immunotherapy schedule.
Going too fast – getting ahead of the immune system’s ability to cope – is hazardous. A major allergic

reaction, called anaphylaxis (see p. 58), can occur, and this is the cause of deaths during

immunotherapy. However, as long as there is injectable adrenaline (see p. 150) and resuscitation

equipment available, even such an extreme crisis can be dealt with safely.
Serious reactions to immunotherapy usually occur:
•    during the initial build-up phase; maintenance therapy is much safer
•    during the pollen season, for those with pollen allergy
•    when a new vial of allergen extract is first being used, because of variations in concentration

(see p. 168-9).
Those most vulnerable to severe reactions are:
•    people with asthma, especially severe or unstable asthma
•    those who have experienced systemic allergic reactions in the past
•    anyone who appears to be extremely allergic, on the basis of skin tests
•    anyone taking beta-Mockers (see box on p. 150).
With care, these fatalities can be avoided. Patients who are given immunotherapy can ensure their own

safety by being well informed about the procedure (see p. 167).
The timing of immunotherapy
There are various different approaches to the timing of immurotherapy. The basic method (which has a

good safety record in the United States where it is very commonly used) starts with injections once a

week. After the maintenance dose has been reached, maintenance injections are given once every 2-4

weeks. The frequency of these may be increased during the pollen season, for people with pollen

allergies.
It is the regularity of the injection schedule that gradually creates, and then sustains, immune

tolerance, so the treatment is only of value to patients who can reliably keep their appointments.
When immunotherapy is successful, it can eventually be discontinued without any reappearance of the

allergic reaction. It usually takes 4-5 years of regular therapy, from the time of the first injection,

to get to this point. The benefits then persist for many years, perhaps indefinitely in some people,

even without any further injections.
Rush immunotherapy
Trying to speed up the process of immunotherapy greatly increases the risk of a severe reaction

(anaphylaxis). However, there are some situations where fast results are needed, and in such cases rush

immunotherapy, also called accelerated immunotherapy, may be used.
During the build-up stage of rush immunotherapy, injections are given every day, or even several times

a day. All the usual safety procedures (see below) are observed with particular care, to reduce the

chance of a severe reaction.
In semi-rush immunotherapy, the build-up injections are given twice a week, and the risks are lower

than with daily injections, but still higher than with weekly injections.
Minimising the risks
If you are lucky enough to be offered immunotherapy treatment under the National Health Service, you

should not feel concerned about accepting the offer. There is very little risk of a bad reaction

because safety procedures are now so stringent.
To minimise the risk of suffering a severe reaction, the doctor will ask you, at each visit, about any

reactions that occurred after your previous injection. Reactions might include redness, itching or

swelling around the injection site, or (more seriously) symptoms elsewhere on the body, such as nettle

rash (urticaria), itchy skin, sneezing, a runny nose, red or itchy eyes, tightness in the throat or

chest, coughing or wheezing. Always make a note of such symptoms, so that you don’t forget to mention

them at the next visit. This is crucially important, as such reactions can indicate that the immune

system is being hurried along too fast.
The doctor will also ask if you have an infection of any kind, as this can alter your reaction. You

should also tell the doctor about any new medicines being taken, as some, such as betablockers (see box

on p. 150), can make a bad reaction to the injection more likely to occur.
Asthmatics can expect the doctor to ask about current asthma symptoms, and to check their peak flow

both before and after an injection. If there are any symptoms, or if the peak flow is less than 70% of

the best-ever value, the injection won’t be given.
Severe reactions can sometimes begin several hours after the injection, so stay within reach of a phone

for about 24 hours. Among United States allergists (who don’t require their patients to wait after the

injection for more than 20-30 minutes) there are some who believe that everyone undergoing

immunotherapy should carry an adrenaline (epinephrine) auto-injector (see p. 150) on the day an

injection has been given, for use in the event of a severe reaction. Anyone who has suffered

anaphylaxis in response to an insect sting will probably have an adrenaline auto-injector anyway, and

this can certainly be used to treat anaphylaxis following immunotherapy. Note, however, that using the

adrenaline is just the first step in treating anaphylaxis (see p. 98) and you must then go back to your

allergist, or to the nearest hospital emergency department, without any delay.
It is sensible to avoid exercise for two hours after an injection. Be extra-cautious during the pollen

season if you are receiving immunotherapy for pollen allergies.
Immunotherapy for insect-sting allergy
`Our daughter has had two really bad reactions from being stung by a wasp. After the second one, the

doctor at the accident and emergency department told us that she nearly died. We got so anxious about

it that we worried every time we left the house in the summer, and it was even worse if she went out

without us. My wife got so upset about it that she wasn’t sleeping well. It was affecting the whole

family badly.
‘Then we heard about desensitisation treatment, and asked our GP, but he said he couldn’t do it.

According to him, they might be able to do it at the hospital, but it might not work, and it was risky

too. We accepted that at first, but then I started doing some research on the Internet, and discovered

that in America and Germany this treatment is absolutely standard – someone like our daughter would

automatically be given it. We felt very angry when we found this out, and went back to the doctor.

Eventually Ann was referred to the allergy department at a hospital, and now she is getting this

desensitisation treatment. I’m pleased about that, obviously, but I still think it shouldn’t have been

such a fight to get it.’
Immunotherapy provides highly effective protection for those with insect-sting allergy, and should be

given to anyone who has had a severe systemic reaction (see p. 60). Some United States allergists also

recommend it for adults who have had a cutaneous systemic reaction (see p. 60), on the basis that they

may well progress to a severe systemic reaction with the next sting.
Studies of people who have suffered severe systemic reactions, and are then treated with immunotherapy,

show that 97% have no systemic reaction to future insect stings. For the 3% who are not fully

protected, the severity of the reaction is much reduced and far less likely to be life-threatening. In

other words, this is an excellent treatment which can save lives.
Targeting the treatment
Choosing the right venom for immunotherapy can sometimes be difficult. Not everyone with insect-sting

allergy sees the insect that caused the reaction. Skin tests may not give the answer either, because

there are often positive reactions to several different venoms. Some of these may be false positives

(see box on p. 91) and it is impossible for the allergist to say which one(s) are actually relevant.

Most allergists will recommend immunotherapy for all of them, using a mixture of venom extracts.
Where the guilty insect was seen and identified, but other venoms also give positive skin tests, a more

difficult decision has to be made. Many allergists carry out immunotherapy for all the venoms that gave

a positive skin test, on a ‘better safe than sorry’ basis. Since there are cross-reactions between

venoms (see box on p. 113), there is some sense in this. Other allergists just give immunotherapy for

the insect that did the deed.
Will immunotherapy against one insect protect against a related insect? With two closely related

insects such as wasps and hornets, which have many allergens in common, it might do – but there is no

guarantee. The problem is that, as well as the shared allergens, each venom also has its own unique

ingredients. It’s impossible to say, with the kind of tests available at present, if an allergic

reaction was to shared allergens or unique ones. So immunotherapy against wasp venom may give

protection against hornet venom, but it will not necessarily do so – and vice versa.
In the case of bumblebee allergy (seen almost exclusively in those, such as horticulturalists, whose

work involves handling bumblebees) a more definite answer can be given – honeybee immunotherapy does

not work. Immunotherapy with bumblebee venom does work, fortunately. The bumblebee extract has to be

obtained from specialist sources.
Injections are given weekly during the build-up phase, unless protection is needed urgently, as with

work-related sting allergy, in which case rush immunotherapy may be used. Once the maximum dose has

been reached, a maintenance injection is needed every four weeks. After a year, this maintenance dose

can be given every 6-8 weeks.
After 3-5 years of immunotherapy, skin tests with insect venoms are usually tried again. If the results

are negative, the immunotherapy will stop. Research now shows that, even if skin tests are still

positive when immunotherapy ends, there’s an 8090% chance that no systemic reaction will occur to

future stings. Some people are not reassured by this, and prefer to continue with immunotherapy for

their own peace of mind. Indeed, research shows that a near-fatal systemic reaction has a long-lasting

psychological impact, and that many people continue to feel anxious despite completing immunotherapy

and reacting negatively to skin tests.
At one time, challenge stings with live insects were given to check whether immunotherapy had actually

worked. Few doctors do this now, but your allergist may be prepared to do a challenge test if you ask.

Adrenaline and resuscitation equipment would be available if a challenge test were used, so any severe

reaction could be dealt with promptly and effectively. The fact that the psychological consequences of

insect-sting allergy are so persistent suggests that challenge tests with live insects may have a

particular value, in demonstrating that immunotherapy has worked. Challenge tests are also helpful for

those who work with stinging insects, such as honeybees and bumblebees, and who need to be sure that

they can go back to work safely.
Immunotherapy for food allergy?
Attempts to use standard immunotherapy for food allergy have been made repeatedly, but without success.

The process of giving the injections is nerve-racking because of the constant risk of a severe

reaction. The risks prevent the dose of allergen being increased very much, so the beneficial effects

are small. While there may be some reduction insensitivity, it is not enough – or not reliable enough –

to be of any practical value.
What doctors are aiming for here, incidentally, is simply to protect against the effects of

accidentally eating a tiny amount of the food – no one is expecting that someone with peanut allergy

will be able to eat peanut butter sandwiches as a result.
Some of the new developments in immunotherapy may be useful for food allergy, as described in the next

section.
The future of immunotherapy
Many different research teams are working on ways of improving immunotherapy – making it more

effective, safer to give, and less time-consuming.
One approach involves altering the allergen, so that it only interacts with those parts of the immune

system whose job is to control allergic reactions (and therefore bring about tolerance). The changes

made to the allergen are designed to make it ‘invisible’ to the parts of the immune system that

actually attack the allergen. The idea is to inject something that can’t cause a bad reaction, and is

therefore 100% safe.
The modified allergens are called allergoids. Another term often used is peptide immunotherapy – this

describes a technique in which the allergens are chopped up into small pieces to make them safe

(allergens are proteins, and a fragment of a protein is called a peptide).
Already, researchers in Germany have made an allergoid from birch pollen that can reduce hayfever

symptoms with a series of just seven injections given before the pollen season.
Meanwhile, a research team in London is working on peptides made from cat allergen, with encouraging

results so far. In a group of asthmatics who were allergic to cats, a series of 4-10 injections, over a

period of 2-8 weeks, produced benefits in about half those treated. The researchers believe that they

can improve on this and help the majority of people with cat allergy, at least enough to survive

temporary exposure to cat allergen (when visiting cat-owning friends, for example). They hope to refine

the treatment sufficiently to enable some cat-allergic people to keep their pet, rather than finding it

a new home. This is a relatively safe treatment that might be given by a GP, rather than only by

specialists. The research team hopes the treatment will be available by about 2009.
Could this kind of technique work for food allergy? Doctors believe that it can, and a great deal of

research work is being done, in both Britain and the United States. A major focus of this effort is

peanut allergy, since this puts so many young lives at risk. Even if the research is successful, It

will be several years before such treatments become available.
Researchers are also working hard to produce standardised allergen extracts – in other words, allergen

extracts that always contain a standard amount of the allergen. The aim is not only to reduce the

number of treatment failures (which can occur if the extract does not contain enough allergen) but also

to avoid mishaps when a new vial of allergen extract is used (differences in strength, between one vial

and another, are sometimes a cause of anaphylactic reactions).
Standardisation is difficult, because the starting materials –skin particles from horses, for example,

or dust-mite droppings –are natural materials and therefore variable. Some samples contain far more of

a particular allergenic ingredient than others.
One way around this problem is to develop accurate methods of measuring the amount of allergen in the

extract. Another approach is to abandon the whole business of making extracts, and produce allergens

artificially, in a laboratory. This is done by inserting the gene for the allergen – the gene for the

Der p1 allergen of house-dust mite, for example – into bacteria. These bacteria then act as production

units, manufacturing large amounts of the allergen every day. With this high-tech approach, the exact

content of the allergen preparations can be controlled.
These high-tech allergen preparations are extremely pure, and therefore very effective – as long as the

person receiving immunotherapy really is sensitised to the particular allergen that is included.

Unfortunately, most natural allergenic materials contain two, three or even more separate allergens. In

house-dust mite droppings, for example, while Der p1 is the allergen that affects most people, there is

also an allergen called Der p2, and a few people are more sensitive to this than to Der pl.
Artificially produced allergen preparations usually include the main allergen only. For the minority of

people who are more severely allergic to one of the other allergens, this extract will not work.

Eventually this problem will no doubt be circumvented by means of more precise skin testing before

immunotherapy begins – skin tests with individual allergens, rather than with allergen extract

containing a mix of allergens.
A third approach is to change from injections to oral immunotherapy – giving the allergen extracts by

mouth. The best results are obtained when the allergen is held under the tongue for a while and then

swallowed. This is known as Sub-lingual immunotherapy or SLIT, and has become very popular in Italy and

France, where it is a common treatment for hayfever. A recent pilot trial among GPs in Britain suggests

that it may be useful, but is not a miracle cure. Overall, the group treated with SLIT had fewer

symptoms during the pollen season, but antihistamines were still needed. There is some evidence from

Italy that SLIT might reduce the likelihood of children with hayfever going on to develop asthma, and

reduce the chance of new sensitivities.
Side effects are unusual with this treatment, and those that do occur are mostly mild – itching in the

mouth, for example. The treatment is safe enough for routine use in children.
Might oral immunotherapy work for food allergy? Other Italian studies suggest that it could. The

objective of these studies is to reduce the risk to children with cow’s-milk allergy from accidental

encounters with ‘hidden milk’ in prepared food or drink. The immunotherapy treatment begins with

miniscule amounts of milk – the doctors start with a single drop diluted in water, each day for a week

– and increase the dose extremely slowly. Antihistamines are given to minimise the risk of a reaction.
The whole process requires enormous patience, but after seven months, the majority of the children

involved can tolerate some milk – between three tablespoonfuls and a small cupful each day.
This is a very encouraging study that should be repeated by doctors in Britain. Because of the risks of

anaphylaxis – which can, of course, be fatal – it does require full medical supervision, and you should

not attempt it at home. Whether this method would work for allergens other than milk is something that

nobody has yet investigated.
A great many other approaches to immunotherapy are currently being tried for food allergy. Many of the

new techniques are highly experimental, and some show great promise, but it will be many years before

they are in use.
One innovation that is closer to being in general use in the United States involves giving the anti-IgE

drug omalizumab (see p. 149) alongside immunotherapy injections. The drug maximises the benefits from

the immunotherapy, and may make the build-up stage (see p. 165) safer, by lowering the risk of

anaphylaxis. For British allergy sufferers, who cannot yet get omalizumab, and whose chances of getting

immunotherapy are vanishingly small, it may seem unkind even to mention such treatments, but we can

only hope that things will improve here in the near future. You might take some comfort from the

thought that, by the time immunotherapy is available again in Britain, there will be a whole host of

highly effective new techniques available for doctors to try.
All the methods described above are forms of specific immunotherapy – they treat an allergy to dust

mites or to grass pollen or some other specific allergen.
A far more radical and ambitious approach to immunotherapy is now the aim of some medical researchers:

blocking the tendency to allergies as a whole.The underlying idea here is to reverse the basic shift in

the immune response, from Th1 cells to Th2 cells. It is this shift to Th2 cells which produces the

allergic tendency (see pp. 11 –13).
Some interesting findings have already been made in this area, including the surprising discovery that

the balance of Th1 cells and Th2 cells can be adjusted even in people with longstanding allergies.

Inspired by discoveries about hygiene and allergy (see p. 21), British researchers have made a vaccine

containing inactivated cells of a harmless bacterium found in the soil, Mycobacterium vaccae. This is

given as a single injection just under the surface of the skin. It has been used for adult patients

with asthma, and for children with severe atopic eczema, with some improvement in both groups. If the

treatment proves as useful as the preliminary studies suggest, this could be a common treatment in a

few years’ time.

Using inhalers
The value of using an inhaler rather than taking tablets or syrup is explained on p. 141 for steroids. The same principle applies to all drugs.
The oldest type of inhaler is the ‘puffer’ or aerosol inhaler, properly called a ‘pressurised metered-dose inhaler’ or MDI. It delivers the drug as a fine, moist, spray. In addition, there are now many devices that deliver drugs in dry-powder form.
If you or your child find the aerosol inhalers difficult, you may do better with a dry-powder inhaler. Your doctor should have several different inhalers available for you to try out, to see which one suits you best.
When you are given an inhaler you must be shown how to use it by a doctor or asthma nurse. A great many asthma patients have a ‘poor inhaler technique’, and get too little of the drug as a result. This often leads to their asthma getting out of control. The advice given here for using inhalers is no substitute for proper training, and should only be used to supplement what your doctor or asthma nurse has told you.
When using an aerosol inhaler or MDI, remember to shake the inhaler well or you will not get the right dose. Your in-breath must coincide exactly with pressing the canister down: this is the part that many people find difficult. You must breathe in slowly and deeply, otherwise you do not get much of the drug into your airways.
Many asthmatics stop inhaling the moment the
spray from the aerosol inhaler hits the back of the
throat. The spray contains a propellant, which
makes it very cold, and there is a natural reflex
response to this cold liquid which stops inhalation.
This response may be impossible to control. If so,
you need a dry-powder inhaler (see right), or a
spacer to use with your aerosol inhaler (see p. 162).
Breath-operated aerosol inhalers such as the
Autohaler can be useful for those who find ordinary
aerosol inhalers too hard to use. With these devices, you do not have to push the canister down because your in-breath triggers the release of the drug. Take care not to block the air-intake holes with your hands and don’t stop breathing when you hear the inhaler click. (If there is no click, start again and breathe in more forcefully this time.)
One hazard with aerosol inhalers is that, when almost empty, they produce no drug – just the propellant. Although they still ‘puff’ normally, they are not effective. It may be hard to tell when your inhaler is running low. Ask your doctor or asthma nurse for advice about this.
Many asthmatics find dry-powder inhalers such as the Spinhaler, Rotahaler, Diskhaler, Accuhaler, Clickhaler and Turbohaler are the easiest to use. They have no aerosol device, so none of the problems associated with the coldness of the propellant.
On the other hand, nothing pushes the drug into your mouth and lungs with a dry-powder inhaler: you have to do all the work yourself. This means you have to breathe in quite hard and fast. During a severe asthma attack you may not be able to breathe in hard enough to get a good dose of the drug. Some asthmatics have an aerosol inhaler as well, often combined with a spacer (see p. 162), for use during severe attacks.
For the parents of asthmatics, who want to keep an eye on how much of a drug is being used, most of the dry-powder inhalers allow you to do so.
Arthritis and inhalers
Those who suffer from arthritis in their hands often find inhalers difficult to use. There are several aids now available to help with this problem – ask your doctor or asthma nurse about these.
Do hold your breath
Whichever type of inhaler you use, it is important to give the drugs a chance to do their work. After inhaling, and when your lungs are full, you should hold your breath for at least ten seconds. Then breathe out, but wait at least another 30 seconds before breathing in again.
Side effects from non-drug ingredients
There are other ingredients in inhalers, besides the drug, and they occasionally cause side effects.
Aerosol inhalers are the worst offenders. They can contain up to five non-drug ingredients, such as propellants and surfactants. Some asthmatics are sensitive to one of these, and respond with coughing or bronchospasm when they inhale them.
If inhaled in large amounts, the propellants in aerosol inhalers can give a mild ‘high’, and asthmatic teenagers and their friends may - very rarely - begin abusing inhaled beta-2 relievers. Parents should be alert for the possibility of such problems, but not worry unduly.
Dry-powder inhalers do not need propellants or surfactants, so they are suitable for anyone who develops a sensitivity to these. However, they may contain lactose, or milk sugar, in addition to the drug. Enough lactose is deposited in the mouth and swallowed to provoke symptoms, such as diarrhoea and wind, in people who suffer from severe lactose intolerance (see box on p. 79). Trace amounts of milk proteins in the lactose may be a problem for people with severe milk allergy.
CFCs and inhalers
Aerosol inhalers have long contained CFCs, which are very inert gases (at ground level) and perfectly safe to inhale. Unfortunately, they cause serious damage when they reach the ozone layer high above the earth, so they are being phased out in asthma inhalers, as they are in all aerosols. Other propellants, called hydrofluoroalkanes (HFAs), are being introduced to take their place. The spray from an HFA inhaler may taste and feel different, but it should do exactly the same job as a CFC inhaler: the drug it contains remains the same. Research suggests that these new propellants are very safe, but tell your doctor if your reaction to your inhaler seems to change suddenly.
These new propellants deliver medication more efficiently into the lungs, so that usually only half the previous dose is required. Unlike CFC-type inhalers, they will deliver a constant dose until empty. In addition, they are not affected as much by below-freezing temperatures.
Inhale - then clean your teeth
Asthmatic children are more prone to dental decay than other children, and inhalers are suspected of causing the problem. No one knows, as yet, exactly which ingredient of the inhalers is the culprit - it could be a drug, or a non-drug additive such as a propellant. Alternatively, the fact that the spray from some inhalers is slightly acidic could explain this side effect. Brushing the teeth after using the inhaler, or just rinsing out the mouth with water, is recommended as a preventive measure.
Using spacers
A spacer is a large empty chamber that can be fitted to an aerosol inhaler (a puffer or MIDI). to make it more effective and easier to use. The aerosol spray goes into one end of the spacer, and the asthmatic breathes it in from the other end.
When using a spacer, you can breathe normally: you don’t have to take all the drug in at once. or hold your breath after you’ve inhaled. But you should try to breathe as deeply as possible, and hold your breath for up to ten seconds if you can.
Note that spacers are for use with aerosol inhalers only. Spacers allow the aerosol propellant (see p. 161) to evaporate, leaving tiny airborne droplets of the drug to be inhaled. Once the propellant has evaporated, these droplets are no longer cold, so the reflex response that stops inhalation is avoided.
During an asthma attack, spacers are immensely valuable because they allow you to get some of the drug into your airways even though you are unable to take a deep breath. There is a collapsible spacer, called the E-Z Spacer, which folds up into a plastic case small enough to be slipped into a pocket. In a severe asthma attack, having such a spacer could save your life.
In an emergency, if no spacer is available, you can improvise one (see p. 100).
Babies and small children, who cannot yet coordinate the in-breath with pushing the aerosol canister down, need spacers for everyday use. There are spacers designed for children under two years, with masks that fit over the nose and mouth.
When using a spacer, shake the inhaler and then spray it into the spacer once only. Inhale within five seconds. During an asthma attack, you can add another dose from the inhaler every ten seconds, until the attack begins to subside, but keep a count of how many puffs you use (see p. 100).
For a young child, shake the inhaler well, and fit it to the spacer. Put the mouthpiece into the child’s mouth, or put the mask on. Tell the child to breathe in and out steadily. Listen for the clicking of the valve on the spacer - this shows that it is opening and closing. When the child’s breathing is regular, puff a single dose into the spacer. The child should breathe in and out 5-8 times.
Priming a spacer
Prime a new spacer, or one that has been washed, by firing the inhaler into it about five times. Do this before you actually need to use the spacer.
The drug will coat the spacer walls, due to an electrostatic charge on the plastic. You won’t be able to see the drug as it forms a very thin coating.
When you come to use the spacer, no more of the drug will stick to the spacer walls, because they are already coated, so the full dose will be available for you or your child to inhale.
Priming new spacers is particularly important when the asthmatic is a young child, because there may be some delay between firing the inhaler and the child actually getting a proper lungful of the drug. The longer the delay, the more chance the drug has to stick to the unprimed spacer walls.
A spacer can be used on a baby while it is asleep, which may make life easier for you both. If you need to use the spacer while the baby or toddler is awake, stroke the mask against the child’s cheek first. Keep smiling and talking so that the situation doesn’t seem so frightening. If the baby does start to cry, keep the mask in place: crying will bring on a deep in-breath which is just what is needed.
For an older child, decorating the spacer with coloured stickers can make it appear less daunting. Try to make using the spacer seem like a game. If this fails, don’t get into a battle with the child – leave it a while and try again later.
Playing with the spacer when feeling well will help the child to see it as something familiar, not as a frightening piece of equipment associated with asthma attacks.
Nebulisers
A nebuliser delivers high doses of asthma drugs in an easily inhaled form. It is generally used for severe asthma only, or in an emergency to relieve asthma attacks.
A nebuliser can be attached to an oxygen cylinder, which enriches the air–drug mixture with oxygen. This is useful in severe asthma.
The only people who need to have a nebuliser at home for emergencies are those with brittle asthma, whose condition can deteriorate very suddenly and sharply.
For routine use, only a very small minority of asthmatics require a nebuliser. They include:
• Those with such severe asthma that they depend on large doses of drugs to control their symptoms
• Very small children or elderly people with severe asthma, who have difficulty using inhalers. For them, a nebuliser may be the easiest way to take their drugs.
The fact that the hospital’s nebuliser is so effective in an emergency gives it a special mystique for many people, who assume that nebulisers are a magical cure for asthma. Nebulisers are widely advertised in specialist publications for asthmatics and, while they are expensive, they can look like the answer to a prayer. Many asthmatics, or their parents, mistakenly believe that owning a nebuliser would be the answer to all their problems. In fact the nebuliser only works so well because it delivers a much higher dose of the reliever drug – a dose which also carries a higher risk of side effects. This high-dose treatment should not be used on a regular basis unless it is absolutely essential. No one should buy a nebuliser without first discussing the matter with their doctor.
Asthmatics who own a nebuliser should have detailed written instructions from a doctor about when and how to use it, and how much of the drug to put in. One hazard of owning a nebuliser is that it may give you a false sense of security during emergencies, and delay you from getting expert medical help when you need it. If the nebuliser is for emergency use you should be told the exact signs that indicate a need to use it and – no less important – the signs that show the attack is out of control and needs hospital treatment.
Take care, when using a nebuliser, not to allow the mist to escape and settle on the face or eyes. Regular exposure to steroid mist can cause cataracts in the eyes, and thinning of the skin on the face. Anti-cholinergics (see p. 156) can cause glaucoma if they come into contact with the eye. The mask must fit very tightly. As an additional precaution, place a scarf around the upper edge of the mask to cover any gaps. Wash the face after using the nebuliser for steroids.
Keep off the cough mixture
Coughing can be a useful reaction in asthma, evicting mucus from the lungs. But in some asthmatics the cough does not produce mucus and seems to be no more than a reflex reaction to the airway inflammation. This type of cough can be debilitating, but it is not a good idea to treat it with cough mixture which has no benefit and may mask the seriousness of the asthma. Tackling the airway inflammation with preventer drugs such as steroids is the best course. Simple expectorants, which loosen mucus, may be of value – ask your pharmacist about these.

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

Candidal Spores of the Fungus, Candida Albicans.
`As a small child Jason was plagued with ear infections which led to many courses of antibiotics,’ Hannah Mitchell recalls. ‘Eventually he started to get symptoms such as an upset stomach, itchy bottom, flu-like symptoms and extremely itchy eyes. The GP prescribed eye drops and when I put them in Jason screamed his head off. In the morning every single eyelash had fallen out. Jason’s health deteriorated and a few months later his eyebrows started to itch. Within two days every single eyebrow hair had fallen out. His eyes were worse and I was offered steroid eye drops again. Reluctantly I accepted.’
‘Putting the drops in caused Jason extreme pain. The red patches of skin around his eyes spread and the itching increased. I was at the end of my tether when I came across a book in the library about food-related illness…
What Hannah discovered from her reading was that, for many with diarrhoea, bloating, wind and an itchy bottom, the cause can be an overgrowth of yeasts in the gut, caused in part by repeated courses of antibiotics which kill off friendly gut bacteria in the gut flora (see p. 204) and allow yeasts to flourish. This is not mainstream medicine, which is why none of the doctors who had seen Jason mentioned the possibility of yeast overgrowth.
Yeasts are microscopic fungi, so anti-fungal drugs are needed to kill them. However, reducing the intake of sugar in the diet is also very effective because yeasts living in the gut thrive on sugar. Hannah took matters into her own hands, and tried out a diet containing no sugar and no yeast. (The reason for avoiding yeast in food is discussed below.) There was some improvement and, encouraged, she went back to the doctor and asked for anti-fungal drugs.
The doctor agreed, and to Hannah’s immense relief, the combination of diet and drug treatment worked for Jason – it cleared the diarrhoea, wind and itching, and eventually allowed his eyelashes and eyebrows to grow back. (Note that few other patients with yeast problems suffer hair-loss – this is a very exotic symptom – but yeast overgrowth can produce some other quite unusual reactions.)
The elusive culprit
So far, you will notice, I have not mentioned Candida. Among those doctors who study and treat this condition, this particular yeast was once considered the prime suspect. Indeed, the disease itself was called ‘candidiasis’. But the role of Candida is now considered doubtful by many.
Researchers such as Dr John Hunter, of Addenbrooke’s Hospital in Cambridge, have tried to find Candida in their patients without success. ‘I think now we have to reject the idea of Candida causing the symptoms,’ says Dr Hunter. ‘But I do believe that there is an imbalance in the gut flora – the micro-organisms that live in the gut. I believe that’s at the root of so-called “candidiasis”.’ This new evidence has not yet affected beliefs about candidiasis’ and ‘Candida’ in the complementary health field.
The fact remains that anti-fungal drugs have proved very helpful to many patients with the typical cluster of symptoms –diarrhoea, wind, bloating and an itchy anus – that were previously attributed to Candida. Given the effectiveness of these drugs, it seems probable that yeasts of some kind are playing a large part in this condition. So the term ‘yeast overgrowth’ is being used, rather tentatively at the moment, as a label for this condition. The yeasts concerned have not, as yet, been identified.
The facts about Candida
This box is about Candida as understood by conventional medicine, rather than ‘Candida’ and ‘candidiasis’ as understood by alternative medicine.
The yeast known as Candida lives naturally in the gut, usually causing no trouble. Problems are usually caused by Candida only when it sets up home in the throat, vagina or penis (’thrush’ infections). Such localised infections have well-defined symptoms and, in most cases, are easily treated with anti-fungal drugs. Patients with damaged immune systems, caused by anti-cancer drugs or AIDS, often develop more widespread Candida infections, but this never happens to people with a normal immune system.
Inhaling steroids and not rinsing out the mouth afterwards can make asthma sufferers more susceptible to Candida infections in the throat (see p. 145).
Other symptoms that have been linked to yeast overgrowth are:
• fatigue
• poor concentration
• irritability, depression and confusion
• headache or migraine
• severe premenstrual problems
• recurrent cystitis
• skin rashes
• aching muscles
• chronic urticaria.
Sometimes there is constipation rather than diarrhoea. Recurrent thrush – a genuine Candida infection in the vagina – can also be a feature of this problem. Occasionally allergic symptoms such as asthma seem to get worse with yeast overgrowth.
Is there an allergic reaction to the yeast?
Those with symptoms typical of yeast overgrowth may give a positive skin-prick test to Candida, but what this means is debatable. For one thing, not everyone with this condition gives a positive test. For another, some entirely healthy people give a positive skin-prick test to Candida. To complicate matters, there are a lot of cross-reactions (see p. 14) between different kinds of yeasts and moulds, due to similarities in their chemical constituents. So the positive skin-prick test does not mean that Candida itself triggered the original IgE-response.
The question of whether some kind of sensitivity reaction to yeasts is occurring in those with yeast overgrowth, and contributing to their symptoms, is an interesting one. The benefits from avoiding yeast in food (see Diagnosis and treatment) suggest that it may be – but this is a question that cannot be answered at present.
Diagnosis and treatment
Unfortunately, this is one of those ’suck-it-and-see’ conditions, where diagnosis and treatment are the same – you try the treatment for yeast overgrowth, and if it works you assume that the disease is, or was, yeast overgrowth. This is far from satisfactory, but is the best that can be done at present.
It is only worth trying this treatment if you have quite a number of the symptoms listed. Bowel problems and an itchy anus are characteristic, and if you have neither of these it is unlikely the treatment will help you.
A key part of the treatment is a no-yeast-no-sugar diet (see p. 205). This diet has been developed on a largely pragmatic basis, and seems to work – but why? The rationale for cutting out sugar is clear – it feeds yeasts in the gut. But why avoiding foods containing yeast should help is uncertain. Possibly the yeasty food supplies some special nutrient that benefits the yeasts living in the gut. Alternatively, there might, for some people, be a sensitivity reaction to the yeast in food (see left).
If it seems that you are on the right track, because there is some improvement with this diet, ask your doctor for anti-fungal drugs. You should take these in addition to the diet. Nystatin (see box below) is very safe for most people, since it is not absorbed from the gut. Bacterial replacers (see p. 205) may also be useful.
You may need a referral to a doctor who is knowledgeable about yeast overgrowth but try to avoid those doctors and alternative therapists who are part of the ‘Candida’ craze, and think that ‘candidiasis’ explains a huge variety of illnesses. You may not have yeast overgrowth at all, so you need someone with an open mind.
Eczema and yeasts?
Doctors have found that some children whose eczema looks very red, and is not responding to treatment, have IgE in the blood against a range of yeasts and other fungi (Candida, Trichophyton, Saccharomyces and Pityrosporum). Given the tendency to cross-reactions among fungi (see main text) it is not clear exactly what these reactions indicate. A proportion of these children get much better on anti-fungal drugs, including a drug called nystatin, which is not absorbed through the gut wall – so cannot reach the skin. The eczema improves, and at the same time there is a fall in levels of anti-fungal IgE in the blood. In other words, a treatment that can only affect fungi living in the gut benefits the skin. Exactly what is going on here is unknown, but the important point is that the treatment seems to work. This is a controversial topic, but since nystatin is an extremely safe drug, your doctor may be prepared to try it out. A course of 3-4 weeks is the minimum needed.

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.