Posts Tagged ‘health’

Conception is a complex process that depends on everything working properly at a number of stages. Firstly, your hormone balance must be correct so that the egg develops normally. Secondly, you must be ovulating so that the egg is released. Thirdly, you must have sex at the right time in your cycle (there may be only two or three days a month when you are fertile). In addition, your partner must have a good sperm count and possess healthy sperm, which are capable of penetrating your cervical mucus to reach the egg. Then the egg has to be captured by the fallopian tube and be fertilised. Finally, once the egg has been fertilised, the embryo has to implant securely in the lining of the womb, which needs the right levels of the hormone progesterone to maintain the pregnancy. No wonder they talk about the miracle of life!
It’s daunting to think about the number of things that can go wrong. But, as we have seen, there are many simple ways in which you can dramatically improve your chances of getting pregnant.
In this section of the book I outline all the different factors that can undermine your fertility.The list may seem long but it is important to identify the particular combination of factors that may be undermining your and your partner’s health and wellbeing.
You may have been given the impression that there is no medical reason – and therefore no Solution – for your problem. But when you read this section you will realise that nothing could be further from the truth.

Nutrition
You are what you eat. Or, to put it another way, if you put poor-quality petrol in a high-performance car, like a Rolls-Royce or a Porsche, it may run for a while but eventually it will become less productive and less efficient. It is exactly the same with the human body.You need top-grade `fuel’ to function properly, and to produce healthy eggs or sperm. To a very large extent, your fertility depends on what you eat.
Food Isn’t What it Used to Be
One of the problems is that nowadays we eat a lot of convenience and refined foods that have been stripped of essential nutrients during manufacturing. For example, 80 per cent of zinc is removed from wheat during the milling process to ensure that a loaf of bread has a longer shelf life.’
The soil our food is grown on is so lacking in nutrients due to overuse and commercial farming methods, that even what we regard as ‘healthy’ foods — vegetables, for instance — may not contain the amounts of minerals we expect to get from them. If you have been dieting for a number of years (either restricting your food intake or trying different diet drinks or pills), you could well be deficient in a number of vitamins and minerals.
The well-balanced diet is a myth. We simply do not get all the nutrients we need from our food. This was confirmed by a National Food Survey conducted in 1995 which found that the average person in Britain was grossly deficient in six out of the eight vitamins and minerals surveyed. Fewer than one in ten people received the RDA (Recommended Daily Allowance) for zinc, which is the most important mineral for both male and female fertility.

Put this lack of nutrients together with all the additives, preservatives and pesticides (see Chapters 4 and 5) in your food and you can see that your fertility may well be compromised on a daily basis. Chemicals like pesticides are known to affect fertility, others will affect your general health, and this in turn can reduce your ability to conceive. Scientists may know the toxic effects of one particular chemical but what they don’t and can’t know for certain is the effect of being exposed to a cocktail of these substances.
Balancing the Scales
Your weight is crucial for your fertility. Being very underweight or very overweight can make conception difficult or impossible. So it’s important that your weight is within a certain range in order to give you the best chance of conceiving.
Nature gave women proportionately more body fat for a specific purpose, in order to reproduce and then feed our young. That is why fat accounts for 27 per cent of an average woman’s body weight, while it is only 15 per cent for a man.
Fat is essential to fertility and it is necessary in order to ovulate.Young girls do not begin to menstruate until their bodies are composed of at least 17 per cent fat.
Underweight
If a woman’s body fat drops too low, then her periods can stop. This low level of body fat may be caused by excessive exercise, as sometimes happens with ballet dancers or athletes who have very tough physical regimes.’
Infertility can also be caused by excessive dieting. When a woman is anorexic, for instance, her periods stop.’ With so much publicity about anorexia and an increasing number of young women falling victim to the ,slimmer’s disease’, the long-term damage to fertility caused by drastic weight loss is well-known. But not so many people realise that being overweight can also affect fertility.
Overweight
If a woman is overweight it can stop her ovulating. Studies have shown that just losing a small amount of weight, 10 per cent, for instance, can be enough to increase fertility by stimulating ovulation, improving hormone balance and making periods more regular.”‘
In another study, on women who previously did not ovulate, 11 out of 12 conceived naturally after exercising and dieting over a period of six months to get their weight down.”
Fortunately your dietary intake is fully within your control, and eating the right food may be the single most important thing you can do to achieve a successful pregnancy. Later (in Chapter 7) I will explain how the right  fertility. -Ig it nutrition can give you and your partner optinitini health and fertility.

Alcohol, Smoking and Drugs
Most of us know that smoking and drinking alcohol when pregnant can be very harmful to the baby. But what most couples don’t realise is that smoking and alcohol could actually be stopping them conceiving a baby because it reduces their fertility. The good news is that the negative effects are not permanent and simply stopping will dramatically improve your chances.
Alcohol
Research has shown that drinking alcohol causes a decrease in sperm count, an increase in abnormal sperm and a lower proportion of motile
sperm.12
Alcohol also affects a man’s fertility by changing his hormone levels because it can alter the way testosterone is produced and then released.” Because alcohol affects the liver (the organ which normally clears out any excess hormones), a man who drinks alcohol may accumulate small amounts of female hormones (men produce `female’ hormones, just as women produce testosterone). These female hormones can lower sperm production and potency.
In addition, alcohol stops absorption of nutrients like zinc which is one of the most important minerals for male fertility. Zinc is found in high concentrations in the sperm. Adequate levels of zinc are needed to make the outer layer and tail and are therefore essential for healthy sperm. If you reduce the amount of zinc in a man’s diet, his sperm count goes down.”
Finally, alcoliol reduces fertility in nianirrials, and studies show that women who drink heavily may stop ovulating and menstruating, and take longer to conceive.”

How Much is Too Much?
A study of 430 women demonstrated that drinking more than 5 units of alcohol (equal to five glasses of wine) a week could stop women conceiving. Researchers discovered that the women in the survey who drank less than 5 units a week were twice as likely to get pregnant within six months compared with those who drank more. A study published in the British !Medical Journal concluded that women should be ‘warned to avoid alcohol when trying to conceive’.”
The fact is that drinking any alcohol can reduce your fertility by half— and the more you drink, the worse the impact on your chances of conception.”
Studies have also shown a strong relationship between alcohol and miscarriages. Women who have a drink every day have a much higher risk of miscarriage (2.5 times more) than non-drinkers.” The same study found that if the woman was a drinker and a smoker her chance of a miscarriage was four times higher.
Smoking
There is so much information available nowadays about the risks of lung cancer, emphysema and other life-threatening conditions and most people are aware of the detrimental effects of smoking when pregnant. I know how shocked many of us feel when we see a heavily pregnant woman standing with a cigarette in her hand.Yet most people are not aware of the impact smoking can have on a couple’s fertility. It’s not surprising that tobacco has such an effect — it contains more than 4,000 compounds, including carbon monoxide, oxide of nitrogen, ammonia, aromatic hydrocarbons, hydrogen cyanide, vinylchloride, nicotine, lead and cadmium.
Although many women smokers resolve to give up when they get pregnant, they don’t realise that by smoking they are reducing their chances of getting pregnant in the first place. Not only that but you don’t usually know that you are pregnant for the first couple of weeks and the baby will be taking in all that tobacco smoke in the meantime.
The man’s fertility is also affected by smoking — it decreases his sperm Count, makes his sperm more sluggish, increases the number of abnormal sperm and reduces his testosterone levels.
In addition, smoking reduces the level of vitamin C in the bloodstream. Lack of vitamin C encourages sperm to clump together (a process known Alcohol, Smoking and Dru
as agglutination) instead of moving forward to fertilise the egg. One study showed how male fertility was improved by giving men 500mg of vitamin C twice a day.”
Smoking has definitely been linked with infertility in women.” It can even bring on an early menopause, which is an especially important consideration for older women trying to conceive who may be racing against time.” If you are a smoker, you should ask yourself why you are taking something into your body that is bringing you nearer to the menopause
—and infertility?
Recreational Drugs
The use of marijuana and cocaine has increased steadily over the years to the point where, for some people, it is part of everyday life. Although still illegal, recreational drug use is increasingly socially acceptable. That does not mean it is healthy or safe. The fact is that these drugs can compromise both your and your partner’s fertility. But, as with alcohol and tobacco, you can stop using recreational drugs and negate the damage to your fertility in a relatively short space of time.
If you continue to use them during a pregnancy, of course, it can have disastrous effects on your developing baby.
The Effects of Some Common Recreational Drugs
•    Marijuana can lower a man’s levels of FSH and LH, two hormones needed to produce sperm. It can also lower his libido.” For the woman, marijuana can lead to irregular periods, reducing fertility and sometimes even stopping ovulation.”
•    Cocaine users will have a lower sperm count, poorly moving sperm and a high rate of abnormal sperm.21
•    Heroin can cause a decrease in testosterone levels.2`
•    Cocaine and heroin, taken together, will make it harder for a woman to conceive and she is more likely to have a miscarriage, a stillbirth or a baby born with a malformation.21

Medicines
If you or your partner are taking medication while you are trying to conceive you should speak to your doctor about which drugs are medically essential and which are not. Some drugs have a direct effect on fertility and you do need to discuss this with your GR
Many drugs can affect not only the man’s sperm but also his ejaculatory function and libido. Some medicines may even cause impotence. These drugs can include sulphasalazine (used to treat irritable bowel), nitrofti•antoln, tetracyclines, cimetidine, ketoconazole, tricyclic antidepressants, monoamine oxidase inhibitors and propranol.”
In addition, medication given for conditions like gout or high blood
pressur can interfere with fertility. And non-steroidal anti-infianiniatory drugs (often used for arthritis) can stop ovulation.”

Suffering from a long-term illness, especially if it is severe and sometimes limits activity, can easily make a child feel different from other children, and ‘not good enough’. Children with allergies, especially those with severe asthma or food allergies, may also be very frightened and anxious. At the same time, such children often feel that they have to protect their parents by not revealing their fears.
Children may also think that their illness is a punishment for something they have done wrong. Their guilty feelings can be so powerful that they may not confide in you unless you spend time talking with them about their illness, and encourage them to share their feelings with you.
One of the most valuable things you can do for children with allergies is to build up their self-esteem. This is especially important when they first start school, because they have to adjust to other children there, and learn how to deal with questions about their illness, as well as some unkindness.
For children whose allergies limit what they can do physically, or restrict some normal activities, try to find other interests and hobbies that the child can do well. When talking with the child, always emphasise the positive things – the difficulties that you have overcome together in the past, the measures that the child can take to keep the symptoms under control (such as stopping scratching, applying creams, or using a preventer inhaler) and the areas of Iife where he or she is particularly successful. As the child gets older, introduce the idea that coping with illness makes you a stronger, kinder and more resolute person, one who can cope with any of life’s challenges. Show the child how much you value their maturity and perseverance.
Pay attention to what the child’s friends are
saying – a bit of eavesdropping is allowed – and be prepared to counteract any negative messages. Teach your child to be strong and self-confident about choosing their friends, and to prefer those who are sensible, understanding and supportive. Ask casually about what schoolteachers and other adults say when you are not around, because they can, without meaning any harm, undermine a child’s confidence with thoughtless remarks.
For children with problems that are potentially life-threatening, such as true food allergy, your natural anxieties as a parent can lead you to be overprotective. This can make the child feel smothered, but letting go is far from easy. You somehow have to find a middle path that works for you both.
With asthmatic children, focus on letting them live as normal a life as possible. Avoid saying ‘no’ automatically to things that might induce an asthma attack – such as running around outdoors in cold weather. Take some small risks, and let the child make the decision sometimes – he or she will gain a lot from taking the responsibility, especially if the decision is the wrong one.
This is the only way for children to learn how to manage their own condition. The sooner you can begin letting go, the better the child will cope in his or her teenage years, when it really will be necessary to make some difficult decisions without your help.
A pitfall for parents
In bringing up a child with allergies, remember that there should never be any ’secondary gain’ from illness – absolutely no advantages to having the eczema get worse (easily done by scratching) or starting an asthma attack (some children can bring one on by breathing in a particular way).
If your child has to take time off from school because of ill-health, ask the teacher for work that can be done at home, and check that it really is done. Children who are allowed to benefit from being ill can establish an unhealthy pattern for dealing with life’s difficulties (see pp. 94-5), which may be long-lasting. Such a mind-set can seriously limit a child’s development.
Incidentally, the ’secondary gain’ from illness may be quite altruistic in nature. It can include stopping parents from arguing, or from nagging a naughty brother or sister, as well as more obvious things such as getting a parent’s attention – so be aware of all the circumstances in the family that are affecting the child.
Sometimes a child realises, unconsciously, that attending to illness gives a parent welcome distractions from emotional problems and a comforting feeling of being needed and useful. The allergies can become part of the structure of a family, the glue holding everyone together.
Conversely, long-term illness can tear families apart: according to recent research carried out in the United States, divorce is more common in families where a child suffers from severe asthma.
Doctors frequently notice that severe eczema also can create a lot of tension in the home.
If you feel that a child’s illness is affecting the family badly – in whatever way – talk to your doctor, or someone else who you trust. You may need the help of a counsellor or family therapist to sort things out.
Children and medicines
Parents often feel very anxious about all the medication an allergic child uses. On the whole, the drugs prescribed for allergy are very safe, and only children with severe disease are at risk of significant side effects. These children will be carefully monitored by the doctor.
Needless to say, if you can cut down on the drugs by reducing allergen exposure, avoiding irritants (e.g. tobacco smoke) and implementing some of the other measures described in this book, you should do so. But if the child still needs drugs to control the symptoms, it is far better to accept them than to let the child struggle with all the discomfort, limitations and distress that the illness imposes.
Parents who are very concerned about drugs should talk openly to the doctor about their fears. If there are differences of opinion about drugs within the family, try not to expose the child to the disagreements. Sort out a joint policy in advance and always present a united front to the child. Be consistent and reassuring about drug use, otherwise the child may feel confused and anxious about the situation – or may even learn to manipulate it.
The asthmatic child
Children with asthma should have a management plan (see p. 96) and may benefit from using a peak-flow meter (see p. 97). Once your child is old enough to comprehend the difference between preventers and relievers, explain that using the preventer regularly keeps asthma under control, which means no sudden attacks and less need to use the reliever in public — something which most children find intensely embarrassing. You should oversee the child’s treatment closely until the age of seven or eight, then gradually let the child take over some of the responsibilities.
Coping with food allergy
The following concerns true food allergy (see p. 62), which can be life-threatening, not idiopathic food intolerance (see p. 74).
Protecting a child with severe food allergies is a major task. You will find it enormously helpful to be in contact with other parents who are facing the same challenge. The practical details are everything here, and you can benefit from other people’s ingenuity in solving day-to-day problems. Several support groups exist (see p. 255), offering a wealth of advice.
For very small children, the main task is to ensure that everyone who looks after the child understands exactly what can and can’t be eaten. Child-minders and baby-sitters should spend time with you as ‘apprentices’ seeing what is involved in preparing food for the child – this is far better than just giving verbal instructions. Also make sure that everyone knows how to use the adrenaline auto-injector (see pp. 98-9).
Once children start going to parties, you should always stay at the party for the whole time, and supervise your child closely. Take food that your child can safely eat, but which other children can also share. Some parents put a label on toddlers warning other adults that certain foods are taboo – for children under reading age this is probably acceptable, and does allow you to relax a little, but with older children the dangers of being teased or stigmatised should always be borne in mind.
Plan ahead all the time. Keep a snack box in the car containing food that the child can safely eat. Whenever you go on a trip, however short, have some safe foods with you, in case you get stuck somewhere and the child gets hungry. If you go out to eat, exert maximum caution about the restaurant food (see p. 111). Some parents take along a guaranteed-safe, but super-delicious sandwich or burger, and ask the restaurant to warm it up in a microwave (where appropriate) and serve it at the same time as the other food. If you do this, be sure the staff understand that the food must not touch any other food.
At home, some parents opt for everyone eating the same allergen-free food, on the basis that this makes for being ‘a real family’. Others, finding this too problematic or expensive, make a virtue out of the allergic child having a different meal. ‘I try to make her feel special about having her own food. The allergen-free dinner or cake always looks and tastes really good.’
As children get older, and more independent, you need to educate them thoroughly about avoiding the offending food. Equip them for difficult situations by role-playing. Act out being offered a tempting item of food by another child, and being jeered at for refusing. Act out suffering an allergic reaction to food and getting help quickly, even though people around don’t understand and are uncooperative.
Allergies and schools
When your child starts at a new school, creche, or kindergarten, request a meeting with staff and teachers to talk about the child’s allergies if there is any likelihood of these becoming a problem. Do this well before your child starts at the school, so that any necessary changes can be made. If your child has a serious food allergy or severe asthma, you may have to make several visits because there are usually a number of different people you should meet, and follow-up sessions may be needed with some staff. If all this sounds daunting and ‘not my style’ then you need, for the sake of your child, to develop your skills in dealing with people and being assertive. Talk to a counsellor, or look for suitable training courses.
In addition to ensuring that the school takes good care of your child’s health (see below), you should also discuss wider issues of adjustment to school life. Teasing or bullying can be a problem for children with any kind of health problem. Ask the teacher to keep an eye on your child and ensure that he or she is coping well – for example, that there is no difficulty about using an inhaler in front of other children when necessary.
Eczema
Ensure all staff realise that the skin rash is not infectious, and that they are aware of the need to communicate this to other children. The appearance of the skin can create a lot of problems with class-mates, and teachers need to be alert for taunting remarks or hurtful nicknames.
Unfortunately, children with eczema are very susceptible to infections caught from others, such as impetigo (see p. 44), but you can’t really protect children from such infections without isolating them socially. The best way to tackle this problem is to deploy all the available treatments so that your child’s skin becomes stronger and more resistant.
Food allergy
If your child has food allergy, go and see the catering manager personally. It may be helpful to take some printed material on food allergy with you, plus lists of synonyms for food ingredients (see pp. 172-4) where appropriate. Concentrate on building up a good relationship with catering staff, while ensuring that they understand how dangerous certain foods can be to your child.
Many parents feel more relaxed if they supply their child with a packed lunch that they know is allergen-free. This is often a good strategy, but don’t be complacent. Most allergic reactions in schools involve food given or traded by another child with entirely good intentions. Some schools with food-allergic children have set up a ‘no trading food’ policy, which seems to work well. Other schools establish milk-free or nut-free tables in the canteen, so that friends can sit together and trade food safely. (The mothers of the other children sitting at these tables need to be well versed in food avoidance, of course, so that their packed lunches are as safe as your own.) In the United States, schools have sometimes tried banning nuts or peanuts altogether, where there is a nut-allergic student, but this does not work well.
Some parents prepare a printed information sheet about their child’s food allergy, with a photograph of the child, and put these up at strategic points around the kitchen and canteen area. This information can include instructions on how to deal with anaphylactic shock (see below) and who to contact in an emergency.
Finally, include the art teacher in your rounds – foodstuffs are often used in art and craft projects.
Anaphylaxis
For children with severe food or insect-sting allergies which can lead to anaphylaxis, check that everyone at the school understands the potentially fatal nature of this condition. Key staff must know how to recognise anaphylactic shock and exactly what to do: show them how the adrenaline injector kit works. You could take along an old one, so that they can practise (see p. 150). Injector kits and adrenaline inhalers must be within easy reach, never locked in a cupboard.
Repeat this educational process at the beginning of each new school year, and before school trips. As an additional precaution, your child should wear a bracelet or pendant (see box on p. 95) that informs medical personnel about his or her allergies –this is also vital for children with latex or drugs allergies.
Asthma
If your child has asthma, ask what arrangements are made for inhalers. Children who can take responsibility for their own treatment should keep their inhalers with them. For younger children, the inhaler should be in the classroom, somewhere that is easily accessible (never locked away) and should be taken along during breaks and mealtimes. The child must always be able to get to the inhaler quickly: even a small delay in using it when an attack occurs can have dire consequences. Make sure everyone at the school understands this, that they know how to recognise an attack, and how to react. Assure the teacher that there is little danger of an asthmatic child overdosing, and if other children take a few puffs they will come to no harm.
If the teacher seems to believe that asthma is a psychological problem (some still do), go and see the head. Suggest that a local asthma nurse or doctor comes in and talks to the staff and pupils about asthma.
Ensure that the teacher knows about the effects of cold air and exercise on asthmatics. Talk to the games teacher or sports coach, and the playground attendants. It is vital that the games teacher is encouraging but understanding towards asthmatic children. They should never be told to continue exercising if they feel breathless.
Allergens and irritants in school
Schools today often have soft furnishings and carpets – these may be full of dust mites. If your child is allergic to mites, and if allergy symptoms are frequent at school, have a look around the classroom and see if this might be the cause. Before discussing the problem with the school, learn all you can about dust mites (see p. 114-117) so that you can assess whether proposed solutions to the problem would actually work.
Pets are common in classrooms and they can cause allergic reactions in sensitised children. Moulds flourish in many school buildings, and will affect a child with mould allergy. Poor ventilation is sometimes a major problem in school buildings, especially those where windows cannot be opened.
Irritants in school air include glue, paint, the solvents from felt-tip pens, disinfectants, air fresheners and the fumes produced during science lessons. Make sure the science teacher is aware of the risks and always uses a fume cupboard if irritant gases such as nitrogen dioxide or sulphur dioxide are likely to be given off during an experiment.
Applying sunscreens to children’s skin is now routine in many schools and preschools. Teachers probably won’t think to ask permission, so if your child is sensitive to any common ingredients of creams or sunscreens, let them know in advance.

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

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.

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

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

What is Allergy?
Words matter, particularly in medicine. Using the same words to mean different things is a major difficulty for patients when discussing allergies with a doctor. Unfortunately, few patients realise this, and doctors are frequently too busy to explain what they themselves mean. The result can be a great deal of misunderstanding, confusion and mutual irritation.
Unclear meanings can also create problems if you start exploring other treatment options. The word `allergy’ is like one of those cats that eat at six different houses in the neighbourhood: everyone feels as if they own it exclusively. A conventional allergist will understand one thing by ‘allergy’, while a more unorthodox doctor may have a broader definition, and a herbalist or naturopath may be using the word in a completely different way again.
This is an absolute jungle for the medically unqualified, and it can be an expensive jungle if you are looking around for an answer to your health problems. With the help of this book, you should be able to make sense of all this, and understand the seemingly contradictory advice on offer.
The word allergy was coined in 1906 when it was used to mean altered reactivity - any change in the way the body responds to the environment, whether immunity to a disease already encountered, or a sudden fit of sneezing from pollen. Immunity to disease was soon shunted off into a separate category
altogether, leaving allergy with a narrower meaning:
any adverse reaction to substances that are normally harmless - definition 1. In this book, that meaning is covered by the word sensitivity.
One group of American doctors, who later became known as clinical ecologists, stuck with this definition. Their broad view of allergy is still found among some other doctors today, generally those whose approach to medicine is fairly unorthodox. It is a concept of allergy that is also shared by most practitioners of alternative medicine or complementary therapists.
The rift between the clinical ecologists and mainstream medicine came in the 1920s when the definition of allergy used by conventional doctors was narrowed further to mean reactions to harmless items where the immune system is definitely involved -definition 2. The term immune sensitivity is used in this book to convey that meaning.
In the 1960s, conventional allergists narrowed the definition of allergy again. It was an exciting time because the antibody known as IgE (sometimes called the allergy antibody - see box on p. 12) had just been discovered. The new, tighter meaning of allergy was
reactions to harmless items where IgE is involved -definition 3.
If asked to define allergy, most doctors would give the second of these definitions.
However, when they talk of ‘a tendency to allergy’, ‘allergy treatment’ or `the allergy epidemic’, doctors are generally using the third definition, and just mean IgE-mediated allergy. They may not be conscious of the fact that they are switching from one definition to another. This is not an ideal situation but, generally speaking, it does not create too many problems.
This book deals with ‘allergy’ in the very broadest sense of the word - all kinds of sensitivity. However -and this is purely for the purposes of clarity - where the word allergy is used in the text it always means IgE-mediated allergy (definition 3).
Other immune-mediated problems are called non-IgE immune sensitivity in this book.
Finally, any reaction where the immune system has no proven central role is called an intolerance. (As for other technical words, if you want to find the full definition, look in the index and turn to the page number shown in bold type.)
If you are reading widely on this topic, you may come across sensitivity used either according to definition 1 above, or as another name for intolerance. You may also encounter the word hypersensitivity. This is actually a precise medical term,
but be warned that some writers use ‘hypersensitivity’ very loosely to mean just ’sensitivity’ (definition 1).
Remember that medical politics and economics are powerful forces in all this debate over meanings. Words are quite often redefined by medical interest
groups (such as professional associations) with the clear intention of staking out territory and claiming sole access to medical truth. What is at stake, ultimately, is the right of different doctors to treat patients with certain conditions - and the right of patients to choose for themselves. To add to the longstanding battle over ‘allergy’, there are now rival claims about the meaning of intolerance (74) which have distinctly political overtones.
When you talk with doctors, using the most appropriate terms will help enormously. Talking to a mainstream doctor about ‘food allergy’ when the symptoms suggest food intolerance, for example, is very likely to cause annoyance. This is not unreasonable because IgE-mediated food allergy, unlike food intolerance, is a disease that can very suddenly kill an otherwise healthy person. Using the term `food allergy’ for a headache or mild bowel symptoms is, doctors feel, trivialising a potentially fatal condition.
The important thing is to get along well and communicate clearly with doctors, not to get into a battle about what words mean (in that sense, words don’t matter - they are just labels). Avoid using the word ‘allergy’ unless you are sure it fits in with your doctor’s perception of what is wrong. Just describing how you react - the actual symptoms - is usually the best approach. If you need a general word for your condition, ’sensitive’ is usually a much more diplomatic choice than ‘allergic’.