Friday, August 7th, 2009
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.”
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Monday, May 18th, 2009
Atopic eczema
A Greek word meaning ‘to boil over’ or ‘to erupt’ is the source of the medical term ‘eczema’. It refers, of course, to the way in which the skin erupts into a rash, but it could equally well describe the eruption of controversy around this disease. No other allergic disease is quite such a cauldron of dissent - indeed, even the question of whether it is an allergic disease remains unresolved. These controversies directly affect the treatment of atopic eczema, so it is useful to understand them if you or your child have eczema.
The disagreement begins with the question of what causes atopic eczema.
Let’s start with the one point that everyone agrees on: dry skin plays a fundamental role. Those with atopic eczema have dry skin, not just in the eczematous areas, but in other parts as well, sometimes all over the body. The skin cells are less efficient than normal skin cells at retaining water.
Everyone would also agree that there is inflammation of the skin – a reaction that is produced by the immune system. But when it comes to the question of what starts off the inflammation there are huge differences of opinion among specialists treating atopic eczema – these specialists include dermatologists, allergists and paediatricians.
Since people with atopic eczema are atopic (allergy-prone), and most have
huge amounts of the allergy antibody, IgE, going round in their blood, it might
seem plausible that an allergic reaction to some external item kicks off the
inflammation. And when skin-prick tests (see p. 91) to common allergens such
as house-dust mite are tried, there are usually a large number of positive results.
But many of these turn out to be false positives – when tested more directly,
the allergen concerned does not actually play a part in causing the skin symptoms.
This has led some specialists working with eczema, mainly dermatologists, to
What the words mean
Eczema is not a disease in itself. The word refers to a certain type of reddish rash — a rash which can be caused in a variety of ways. The type of eczema that affects people of an allergic disposition (atopics), is called either atopic eczema or atopic dermatitis.
The word dermatitis just means inflammation of the skin. Most doctors consider it to be synonymous with eczema, but some give it a slightly broader meaning.
believe that allergic reactions play little part in either initiating or perpetuating atopic eczema. In their view, the basic cause of atopic eczema is dry skin and a generally overwrought immune system, not specific allergic reactions.
To some of these doctors, positive skin-prick tests are all false positives in atopic eczema – that is, irrelevant to the disease process. A positive skin-test result, in their opinion, simply indicates that the skin of atopic eczema sufferers is in a highly sensitive state, not that the allergen concerned plays any causative role.
Allergists tend to take a different view of this, as you might expect. And recent research shows that they are correct – allergens often do play a significant part in provoking atopic eczema.
Research using direct challenge tests (see p. 90) has identified some of the things that could provoke such sensitivity reactions:
• house-dust mites, pollen or moulds
• cats, dogs, rabbits and other furry pets
• cow’s milk or other food – a prime suspect in babies and young children (see p. 68). The response to food is usually delayed, occurring some hours after the item is consumed.
With mite, pollen and pet allergens, the eczema symptoms can be provoked either by allergens falling on the skin, or by direct contact (e.g. mite allergens in the bed, skin contact with pets, or lying on grass for those with grass-pollen allergy).
The rash tends to occur on skin not covered by clothes, as you would expect. But it can sometimes occur only on particular exposed areas – usually the most sensitive areas of skin. For example, there are people who react to house-dust mite but have eczema on the eyelids only.
Additionally, experiments show that even when an airborne allergen is only inhaled it can sometimes provoke eczema symptoms. The allergen probably reaches the skin in the bloodstream. (Alternatively, it might provoke an immune reaction in the airways which generates chemical messages of the kind that promote inflammation – these then reach the skin in the blood.) This means that the skin reaction could occur anywhere on the body, not just on exposed skin.
In the case of food, the molecules of food that cause the trouble are probably being absorbed from the stomach without being completely broken down. They then reach the skin via the blood to provoke a reaction there. (Or, again, it could be an inflammatory messenger chemical travelling from the gut to the skin in the blood.)
When food gets directly onto the skin – which it frequently does with small children, of course – it can provoke a reaction that way too. This may be a slow eczema-causing reaction, or a much faster reaction known as contact urticaria (see pp. 50-51). Reacting to food with contact urticaria is quite common in children with atopic eczema – but the same food doesn’t necessarily provoke atopic eczema when it is eaten. (However, eating these foods can sometimes trigger anaphylaxis – see pp. 58-9. They should therefore be treated with great caution.)
At the same time as all this research – which shows for sure that allergens play a part in atopic eczema – others have been asking what actually happens when skin reacts to an allergen. Their studies have turned the accepted understanding of allergies upside-down. They show that when something like egg or pollen provokes atopic eczema, what is occurring isn’t necessarily an allergic reaction of the usual sort, with IgE and mast cells (see
box on p.12). Instead, other immune cells are causing the trouble. Sometimes IgE is involved, but without mast cells. Sometimes neither is involved. These revolutionary discoveries are described in more detail on pp. 18-19. One interesting realisation from this research is that in different eczema sufferers, different immune reactions may be producing the rash – even if they are reacting to the same allergen! This helps to explain why the results of skin tests are so inconsistent and puzzling.
The wandering rash
For a baby with atopic eczema, the face, and especially the cheeks, are commonly affected, but there may be a rash all over the legs, the backs of the arms, and the back. As the months go by, the rash settles on the lower legs, and spreads to the fold of the elbow, and then the fold at the back of the knees — by about three years of age, this flexure eczema is the main problem for most children.
In adults, eczema is often found in quite restricted areas, such as the hands, scalp, lips, eyelids or chest. It may be located around the nipples — a sensitive spot where rubbing by clothing is enough to initiate a rash.
Atopic eczema is always in a process of change, and different parts of the body may display different stages of the rash:
• The rash is red and usually dry at first, and there may be not a great deal to see. In this early stage the visible signs may be minimal, while the itchiness can be colossal. Sometimes there is oozing of clear fluid.
• Occasionally the first phase is more marked, with dense patches of small red bumps or tiny blisters. On the hands, these may merge to form larger blisters.
• Infections tend to change the appearance of the rash (see p. 44).
• With time the skin becomes thicker, paler and scaly. It may form leathery patches (called lichenification), especially if there is habitual scratching or rubbing. This is chronic eczema.
• When the eczema clears, there may be an area of skin that is lighter in colour, or darker, than the surrounding skin.
The next step
Whatever causes atopic eczema, it provokes the most horrendous itching, as every eczema sufferer knows. The itch cries out to be scratched, and scratching is the major cause of the visible rash. If left untouched, the skin does not erupt into eczema, although it may well turn red, and there are still distinct changes in the skin that can be seen with a microscope.
Once eczema has erupted, the skin is no longer an intact protective layer that neatly separates ‘in-here’ from ‘out-there’. The skin becomes more permeable and loses its own natural moisture far more readily, so the dryness gets worse. At the same time allergens and irritants penetrate far more easily, causing yet more inflammation.
Something else compounds the damage: once atopic eczema is established, the immune system starts making IgE antibodies to the body’s own proteins, especially those found in skin cells. This helps explain why atopic eczema can become so severe and so entrenched.
Infections — another vicious circle
When eczema erupts and the skin barrier is breached, infections often become a problem. A regular source of trouble is the bacterium Staphylococcus aureus, a cause of the infection impetigo. This microbe invades eczematous skin far more readily than healthy skin, causing a prolific ooze with golden-yellow crusting.
Staphylococcus aureus produces a toxin known as a ’super-antigen’ which revs up the immune system to even more furious effort. This effort does not, unfortunately, oust the bacteria, but it does make the skin inflammation even worse. To add to their woes, many who are afflicted with atopic eczema start making IgE antibodies against Staphylococcus aureus toxins.
Infection with fungi (yeasts and moulds) is also a problem in atopic eczema (see p. 49), and there may be sensitivity reactions to these fungi.
The herpes virus, responsible for causing cold sores, can also invade eczematous skin, though this is much rarer. It worsens the eczema and produces fever and general weakness. There may also be flocks of small red bumps, each with a tiny dimple or blister at the centre. Any symptoms of this kind indicate that the patient needs urgent treatment.
Irritants and stress
People with atopic eczema are far more susceptible to everyday irritants such as wool and rough synthetic fabrics, soap, and traces of detergent left behind in clothes. Chlorinated water, either in swimming pools or from the tap, can also aggravate the skin, and even ‘hard’ water (found in areas with chalk or limestone bedrock) may be a factor.
Some air pollutants may play a part in atopic eczema. Researchers in Germany have found that children living close to busy trunk roads, or in homes with a gas cooker and no extraction hood (see pp. 128-9), were more likely to develop eczema. Formaldehyde fumes, often found in modern houses (see p. 129), are sometimes a factor when eczema affects the face and hands.
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Monday, May 18th, 2009
Cross Reactions in Allergy
For the rabbi’s doctor, discussing the results of the allergy tests with his patient, it was an embarrassing moment. An allergy is not inborn, it is an acquired reaction — a response by the immune system to a substance it has already encountered at least once. So, in theory, nobody can be allergic to a food they have never eaten.
Naturally enough, the rabbi had never eaten shellfish - like pork, it is a forbidden food in Judaism. But the nurse carrying out the skin-prick tests was unaware of this, and she had been told to test for all the common food allergens, so shrimp allergen was included. The test came up positive.
Fortunately, the rabbi had also been tested for inhaled allergens and had given a very strong positive reaction to house-dust mite. The likely explanation was clear: the rabbi had formed antibodies to a muscle protein of house-dust mite called tropomyosin, which is also found in shrimps and prawns. His antibodies against house-dust mite had cross-reacted with shrimp tropomyosin.
This does not mean that everyone who is allergic to house-dust mite will also react to shrimp. Firstly, they must have made antibodies to tropomyosin, rather than some other dust-mite antigen. Secondly, the antibodies must be recognising a particular feature of dust-mite tropomyosin that closely resembles (chemically speaking) a particular feature of shrimp tropomyosin.
The important point about antibodies is that, on the one hand, they achieve results by being specific for their antigen , but on the other, they do make mistakes. In the case of allergies, this is sometimes an added problem for patients but is rarely life threatening. More seriously, there are other conditions, like coeliac disease, where cross-reactions initiate attacks on the body’s own components, causing severe symptoms.
Antibodies make mistakes because they recognise antigens by homing in on tiny chemical markers, not by looking at the antigen as a whole (see box on p. 15). Although this is a nuisance for allergy sufferers, it can be a bonus in fighting diseases. For example,
Antigens and allergens
An antigen is anything which elicits an antibody reaction. Each antibody is specific for a particular antigen.
When they tend to cause allergies (by provoking IgE antibodies rather than other kinds of antibody - these antigens are called allergens. Something such as grass pollen is both an antigen (because it elicits an antibody reaction) and an allergen (because it often elicits IgE antibodies in those who are allergy-prone).
when viruses (such as those that cause influenza) revamp their outer coat proteins to evade the immune system, the chances are that some antibodies will still recognise them because a few of the original chemical markers persist.
Understanding cross-reactions
Many cross-reactions are between related species, and this makes sense in biological terms. The tropomyosin story is a good example - not only is tropomyosin found in dust mite and shrimps, but it also occurs in other crustacean shellfish, such as crabs and lobsters, in molluscan shellfish such as clams and oysters, and in insects. If one goes back over 300 million years, all these animals were just a twinkle in the eye of some primeval invertebrate, the common ancestor of them all.
Tropomyosin is one of those triumphs of the evolutionary process - a protein that reached near-perfection hundreds of millions of years ago, in the long-vanished ancestral species, and remains so good at its job that it has only been tinkered with by natural selection since then, never radically altered. In other words, because it works so well, it has been ‘conserved’ by the various animal groups descended from the shared ancestor. Although there are some differences between the tropomyosins from different descendants, the similarities are considerable.
Relatedness counts here. Shrimps and prawns are pretty closely related, as anyone can see by looking at them. Their tropomyosins are extremely similar, as are many other allergens. You’re unlikely to be allergic to prawn but not shrimp. The more distant the relationship, the more differences accumulate in the antigens, so a cross-reaction between dust mite and shrimp is far less likely (the rabbi was unlucky).
Another conserved protein, parvalbumin, explains why people who are allergic to one type of fish are usually allergic to all kinds of fish (in spite of the fact that fish belong to several different families which are only distantly related). Those allergic to hen’s eggs will probably be allergic to the eggs of all birds, because the primary allergens (e.g, ovalbumin) are so similar.
These conserved proteins produce cross-reactions across huge gulfs, in terms of zoological and botanical relationships. Far more easily understood are the cross-reactions between close cousins, such as dust mite and storage mites, wheat and rye, pine pollen and pine nuts, or ragweed and sunflower (both members of the daisy family).
Relatedness can be useful in explaining cross-reactions, but often fails when it comes to predicting them. Some related species do not show as many cross-reactions as one might expect. Peanuts are legumes, and highly allergenic. One would expect some peanut-allergic individuals to be allergic to other members of the legume family, such as peas, beans, carob and soya. In fact, although some patients give positive skin-prick tests, very few show actual symptoms when they eat these foods. Where symptoms do occur, they tend to be mild.
Paradoxically, those who are allergic to peanuts very often develop an allergy to tree nuts, and this usually spans several different kinds of tree nuts – yet botanically all these are very distant relatives. No tree nut is a legume and while walnuts and pecans belong to one plant family, almonds belong to another, hazelnuts to another, cashews to a fourth, and Brazils to a fifth different plant family. Here relatedness seems irrelevant, and it is shared lifestyle (surviving as a nut-producing plant) that is crucial.
A nut is just an over-sized seed that has to survive being buried in the soil – either by the plant itself (in the case of peanuts) or by a nut-eating animal such as a squirrel. All nuts must resist rotting in the soil until the following spring, and therefore contain powerful bactericidal and fungicidal compounds. Some of these may have chemical similarities that cause cross-reactions.
These functional ‘lifestyle’ allergens of nuts may be even more widely shared, with many seeds having something similar: recent research shows potentially cross-reacting allergens in wheat, rye, hazelnuts, sesame and poppy. It is interesting that many of those developing new allergies to sesame or poppy are already allergic to wheat and nuts.
A few cross-reactions seem to defy any explanation, such as that between house-dust mite and kiwi fruit – this appears to be just a case of chemical coincidence. Other cross-reactions can appear equally bizarre but actually have a biological basis, notably that between latex (as used in medical gloves) and various fruits and vegetables, principally chestnut, banana, avocado and kiwi fruit. This cross-reaction is due to a shared enzyme called a chitinase that protects plants against insect pests. Latex, of course, comes from the sap of the rubber tree: the tree needs such insect-protection and its sap is richly laced with chitinase.
How antibodies work - and why they make errors
Antibodies are catapult-shaped, with two antigen binding sites at the ends of the two arms. The other end of the antibody molecule – the handle of the catapult – is free to bind to cell receptors.
When an antibody binds to its antigen there is a ‘chemical handshake’: a very specific recognition event involving one of the antigen binding sites and a particular small site on the antigen molecule called the epitope. The two lock together. Different antibodies may recognise different epitopes.
The antibody is recognising its antigen, but it is as if we recognised other people by homing in on one small part of them, choosing a different feature for each person, whatever is most distinctive about them – the quirky right eyebrow, the hook in the nose, or the mole on the cheek. The antibody does not ‘look at’ the whole antigen molecule, but simply recognises a characteristic cluster of chemical features at the epitope.
Cross-reactions can occur so readily because an antigen molecule only has to resemble another molecule in one or two small areas (the epitopes) for a mistake to occur.
antigen antibody molecule binding sites
cell receptor antigen molecule
epitope
surface of immune cell
(e.g. a mast cell)
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