Archive for the ‘Allergic Diseases’ Category

The simplest and most certain test for any sensitivity reaction is to expose the person concerned to the substance under suspicion and see what happens. This is known as a

challenge test. With true allergies, challenge tests are powerful tools, but they are also alarmingly close to reality. The risk of provoking a severe reaction requires a very

cautious approach.
By comparison, an indirect test – a roundabout way of seeing how the body responds, such as the skin-prick test (see p. 91) – has the advantage of rarely producing dangerous

reactions. The downside is that indirect tests can be misleading, precisely because they are not like the real-life situation. No indirect test is perfect – there are always

false positives and false negatives (see box on p. 91).
Challenge tests
If you undergo a challenge test with food or an airborne allergen, you will also be given dummy challenges with an innocuous substance which is indistinguishable from the item

being tested. Neither you, nor the tester who is scoring the reaction, should know which is which. This is called a double-blind trial because, to eliminate all possible bias,

both of you are in the dark. (The full name is a ‘double-blind placebo-controlled trial’ – the dummy challenge is also called a ‘placebo challenge’ or ‘control challenge’.)
The double-blind trial is a standard medical procedure and does not imply that the doctors think you are faking symptoms. Psychological forces are powerful things, and just

thinking that you might react to a test can be enough to produce a reaction – the process that generates the symptoms is largely unconscious.
Food challenge
A food challenge – eating the food that is under suspicion – is a key test for food intolerance (see p. 197). It is sometimes used for food allergy and other forms of food

sensitivity too, as a follow-up to skin tests. Some allergists use a food challenge only if the skin test is at odds with actual events reported by the patient. Other allergists

use food challenge more readily, to confirm skin-test results, and to assess the severity of the reaction.
Extreme caution must be exercised with immediate food allergy, because of the considerable risks involved. The test must be done under medical supervision with resuscitation

equipment to hand. A challenge test should never be done for true food allergy without some careful preliminary tests on the face and the lips (see box on p. 23). Even if these

tests produce no reaction, only tiny amounts of the food should be eaten to begin with.
Bronchial challenge
This type of test involves inhalation of an airborne allergen – such as pollen – suspected of causing asthma. Bronchial challenge carries the risk of provoking a severe asthma

attack, and few doctors use it unless there are compelling reasons to do so – such as demonstrating that someone’s asthma is due to an allergen encountered at work.
Skin-prick tests
This is an indirect method of detecting true allergic reactions. It is one of a family of skin tests that use a similar approach. The three different tests in this family are

known as: skin-prick tests or prick tests, puncture tests, and scratch tests.
For the skin-prick test – the technique used in Britain – a small drop of liquid containing an allergen, such as grass pollen, is placed on the arm. The doctor makes a small

prick in the skin, under the drop of liquid, allowing a minuscule amount of the allergen to get into the skin. A positive reaction is recorded if a red bump develops soon

afterwards. For accuracy, the bump must be compared to positive and negative controls (see below).
The puncture method is very similar to the skin-prick test but uses a slightly different technique for breaking the skin. The term prick-puncture test covers both techniques.
With the scratch method, the skin is scratched lightly, and the allergen solution is then applied over the scratch. This method gives less consistent results than prick-puncture

testing.
It is important to include a negative control in the test – a skin-prick test with plain salt water (saline). This should not produce much of a bump – if it does, the skin is

clearly over-reactive and the tests more difficult to assess. The doctor should also include a positive control – a skin-prick test with histamine, the substance that plays a

central role in allergic reactions. This should always produce a bump. If it does not, the skin is decidedly under-reactive, and the tests are invalid.
Taking antihistamines will make the skin under-reactive, and you should stop taking them before the testing, for a period ranging from a day to several weeks – it varies

depending on the particular antihistamine. Ask your doctor for specific instructions about stopping these and other drugs before testing.
Skin tends to be over-reactive to testing in people with dermatographism (see p. 52). Blood tests for specific IgE,
such as RASTs (see p. 92), are needed for anyone who has this condition. Eczema sufferers with a rash over large areas of the body may also require blood tests, if there is too

little clear skin for testing.
Skin-prick tests can produce both false positives and false negatives (see box below). Some allergic diseases will give a lot of false negatives and relatively few false

positives, while for others the reverse is true. The allergen itself influences the rates of misleading reactions: for example, tests for soya allergy are notoriously

unreliable, whereas those for peanut are far more accurate. The age of the person being tested also makes a difference. With all these influences at work, interpreting the test

responses is a real art, and the doctor’s experience counts for a lot.
All sorts of people offer skin-prick tests, including alternative practitioners. Get them done by a qualified doctor, preferably by an allergist, who will know how to make sense

of the reactions.
Note that the purpose of these tests, and of blood tests for specific IgE, is to identify the allergens that are bringing on your symptoms, not to predict how strongly you will

react to those allergens. The tests may give some Indication of the intensity of your reaction, but they cannot be regarded as a good guide to how you will respond to the

allergen in the future.
The safety record of skin-prick tests is very good. Occasionally a systemic reaction (anaphylaxis) occurs with these tests, but there are no records of any deaths. Nevertheless,

if you suffer from severe asthma or have experienced anaphylactic shock in the past, it is advisable for the doctor to have adrenaline and resuscitation equipment available.

Those with strong allergic reactions to latex may also react badly if they are tested with an allergen that cross-reacts with latex (e.g. cypress pollen), not just when tested

with latex itself. Taking beta-Mockers (see box on p. 150) increases the risk of a life-threatening reaction for anyone in these higher-risk categories.
False positives and false negatives
Apart from challenge tests, none of the tests used for allergy works with 100% accuracy. Most give both false positives and false negatives.
A false positive means that there is a positive test but no actual reaction when the allergen is encountered (e.g. eaten or inhaled). A false negative means that there is a

negative test result despite a genuine reaction (as shown by a challenge test, for example).
A test that gives relatively few false positives has good positive predictive value – in other words, if it suggests you are allergic to something, you probably are.
A test that gives relatively few false negatives has good negative predictive value. If it comes up negative, you are probably not allergic to that allergen.
Some tests for allergic reactions show good positive predictive value but poor negative predictive value, while for other tests the reverse is true.

Chemical Intolerance
`To start with, I just used to get this irritation in my throat when I was reading a magazine. Over the years it got much worse, and there was a dreadful burning feeling, not

just in my throat now, but also in my eyes and nose. Sometimes I could scarcely breathe. My doctor said it couldn’t be magazines and diagnosed asthma. Twenty years on, I can’t

look at a magazine, even for a few minutes, and other things affect me now too. If I go in a room with a photocopier running I start to choke and can’t breathe. Whenever I

describe this problem to anyone — apart from the doctor, that is — they almost always say they know someone else who has a similar problem. But the doctors still say that what

happens to me can’t happen.’
Mary has chemical intolerance, which is also known as chemical sensitivity, environmental Illness or idiopathic environmental intolerances. It is a condition that arouses more

passionate controversy than any other described in this book. Many believe that it simply does not exist, or rather that people who claim to have chemical intolerance are

actually victims of psychological problems, which express themselves as physical symptoms. Careful studies show that, while some people with supposed chemical intolerance do

fall into this category, others do not – they have no psychiatric problems, but they do appear to have valid symptoms when exposed to certain synthetic chemicals.
`People with MCS are desperate. They will go to great lengths and do almost anything to find a doctor, anyone, who believes them.’ So speaks one sufferer from MCS (Multiple

Chemical Sensitivity), the most extreme form of chemical intolerance. It is often severely disabling, with symptoms such as exceptional fatigue, nausea, headaches, poor memory

and concentration, dizziness. muscle aches, joint pain, chest pain and digestive problems. Those with MCS react to a very wide range of chemicals, and very often to foods and

food additives as well.
These severely affected patients are a small minority, however, and many more people are like Mary, with sensitivity to just one or two types of chemical exposure. Surveys in

the United States suggest that about 30% of the population are affected in this way. The authors of one such survey note that ‘the widespread idea that chemical sensitivity is a

condition of educated, urban housewives was not supported by our study. The region surveyed was rural… and individuals who reported chemical sensitivity were found in all age,

gender, income, race and employment groups.’
The chemical exposures that are identified as triggering symptoms include:
• perfumes
• pesticides
• cigarette smoke
• paint fumes
• petrol
• exhaust fumes
• cleaning products
• newspaper ink
• plastics, especially those with a strong smell
• glossy paper (e.g. In magazines).
Typical symptoms, in those with sensitivity to just one or two chemical products, are:
• a blocked or runny nose
• sore throat
• irritation of the eyes
• sinus pain and congestion
• headache
• breathlessness and wheezing
• nausea
• skin rashes
• extreme fatigue
• dizziness.
How does chemical intolerance begin?
For some of those with MCS, the problems began with a sudden over-exposure to a toxic chemical, such as a chemical spill, or pesticides from a crop-spraying plane. Others are

first affected by regular doses of pesticide at lower levels, such as spray drift from nearby fields or from a neighbour’s garden. It seems as if, for these people, their inborn

ability to detoxify both natural and manmade toxins is overwhelmed by an unusually heavy exposure, and never fully recovers. Although there have been no systematic studies of

this – it is difficult to imagine how they could be done –the wealth of well-documented cases is convincing. And studies of those exposed to high levels of pesticides in

accidents at work support the idea that this can cause lifelong sensitivity to very small doses of some synthetic chemicals. Sensitivity to alcohol and caffeine usually

increases enormously too.
In some cases, classical allergies also feature in the range of symptoms for those with MCS. If they had an allergic tendency before the accidental exposure to pesticides, this

is especially likely: after the accident, along with chemical intolerance, they have far more pronounced allergic reactions to common allergens.
The loss of tolerance to everyday chemicals may be related to some kind of damage to the enzymes in the liver that carry out the important task of detoxifying toxins that enter

the bloodstream. This detoxification system evolved to deal with natural toxins, such as those in plant foods, and those produced by bacteria living naturally in the gut. These

enzymes can also detoxify the widely used synthetic chemicals, when these are encountered in relatively small amounts, but the enzymes are overwhelmed by large doses.
Chronic Fatigue Syndrome (CFS)
This is a disease that probably has multiple causes rather than a single cause. The main symptom is fatigue that is not relieved by rest. Many people with CFS also have a

slightly raised temperature, problems with concentration and memory, headaches, sore throat and swollen lymph nodes (’swollen glands’). The lymph nodes are part of the immune

system, so this symptom suggests some disturbance of immune function. Other findings, related to immune cells in the blood, also support this idea. However, there are often

minor abnormalities in the brain as well, with some loss of the insulating material around the nerves (myelin).
For many patients, the disease develops in the wake of a viral infection, but for others the origin may be unclear. Whatever the origin of the disease, avoiding synthetic

chemicals is very helpful in many cases. Some sufferers also find an elimination diet helpful (see pp. 194-7). Doctors working in this area say that there is no sharp

demarcation between patients with Chronic
Fatigue Syndrome (CFS) and those with MCS.
Autism
In the search for a cause of autism, many possibilities are being investigated. The consensus now is that there is a genetic predisposition which, when combined with certain

trigger factors, leads to autism.
What are those trigger factors? Some researchers suggest that autistic children have poorly performing detoxification enzymes and are therefore sensitive to synthetic chemicals,

both in food and the environment. The suspicion is that these chemicals affect the developing nervous system.
Other researchers pinpoint food as the culprit. They believe that children who develop autism are affected by exorphins (see p. 76) produced from the proteins in wheat and/or

milk, and that these damage the child’s developing nervous system. There are claims that a dairy-free and gluten-free diet can help, but that it must be ultra-strict to work,

and may need to continue for at least six months before any improvement occurs. You must have your doctor’s approval for this.
Before starting them on such a diet, some doctors also give a course of anti-fungal drugs to those autistic children who have been treated repeatedly with antibiotics. This

combined treatment is reported to have very good effects for some children.
Treatment
Assuming that you really do have chemical intolerance rather than some deep-rooted psychological problem – and you have to be honest with yourself here, because otherwise you

will never get better – then careful avoidance of the offending synthetic chemicals is the only effective treatment. If you have eliminated everything that obviously affects you

and are not much improved, then try tackling common indoor pollutants (see pp. 128-30) as well.
Such measures are of value to some with chemical intolerance but may not be adequate for those most severely affected. If you need to take more radical steps, you may benefit

from the bedding, paints and other household items manufactured for those with chemical sensitivity. Once you reduce the level of synthetic chemicals in your everyday

environment, you may find that you can tolerate occasional exposures much more.
Some doctors recommend taking supplements of vitamins and minerals to speed your recovery. These (especially antioxidants – see p. 206) may be helpful for some people, but be

sure to get nutritional advice from someone with good medical qualifications, rather than a self-styled ‘nutrition therapist’.
Neutralisation therapy (see p. 211) seems to be effective for some people with chemical intolerance, but you will still need to avoid the offending substances. Hyperventilation

(see p. 236) can make chemical intolerance much worse.

Immune reactions to food
`When I finally found someone who could say what was wrong with me, it was such a relief. I can’t tell you how much ill-health and pain and misery I’d had up to that point. I’m immensely grateful to the doctor who sorted the problem out for me. My life has been transformed.’
Richard has eosinophilic gastroenteritis, one of the rarer immune reactions to food. Like all rare diseases, it can escape diagnosis for a long time. IgE (the allergy antibody – see box on p. 12) is sometimes involved in eosinophilic gastroenteritis, but it is not an essential part of the reaction. Those who, like Richard, do not make IgE antibodies to the problem food will not give positive skin-prick tests. For them, the possibility of food being responsible for their symptoms may well be overlooked*.
Another difficulty for patients such as Richard is that most of the non-IgE immune reactions to food affect babies and children exclusively. A few of them can also occur in adults, but this is very rare, so it’s not something that automatically springs to mind when the doctor is searching for a diagnosis.
Eosinophilic diseases
The key event in these diseases is the arrival of large numbers of immune cells called eosinophils (see p. 19) in the walls of the digestive system. If the eosinophils converge on the tube leading down to the stomach (the oesophagus) the disease is called eosinophilic oesophagitis, and the symptoms include reflux (regurgitation) of food, occasional vomiting, refusing food (in babies), stomach pain and disturbed sleep.
If the stomach is the focus for the eosinophils, this is eosinophilic gastritis, and there is vomiting, pain, poor appetite and therefore poor growth. There can also be obstruction of the stomach outlet which may, in a few babies, produce pyloric stenosis (the main symptom is projectile vomiting).
When eosinophils flock to the intestines as well as to the stomach, the disease is called eosinophilic gastroenteritis. In
terms of symptoms, the picture is not much different from the previous condition, but there can be diarrhoea as an additional symptom, and babies may be irritable and puffy in appearance.
These conditions are most common in babies, but sometimes they continue through childhood. Very occasionally they occur in adults too.
Heiner’s Syndrome
This disease affects babies only, and is very rare. It is a severe form of cow’s milk sensitivity leading to wheezing and haemosiderosis (bleeding into the lungs). The child usually seems sickly, growth is slow, and there may be recurrent bouts of pneumonia. A full diagnosis requires blood tests to check for anaemia, examination of sputum under the microscope, and a biopsy or lavage (see p. 92) from the lung. The only effective treatment is to remove cow’s milk from the diet completely. Needless to say, this must be done under full medical supervision.
Other reactions to food
The cause of these diseases is not fully understood, but the immune system is clearly involved.
Dietary protein entero-colitis syndrome
In babies, the symptoms begin with general irritability and vomiting between one and three hours after a feed. Unless the offending food – usually cow’s milk – is withdrawn promptly, there will be bloating, diarrhoea (usually containing blood), anaemia, and poor growth. Older children have similar symptoms, while adults suffer terrible nausea, plus stomach pains and vomiting.
Nickel in food
Nickel and other metals in food may cause immune reactions for those with sensitivity to such metals (see pp. 55-6). The symptoms are usually in the skin, but there can be a few digestive symptoms too.
Dietary protein enteropathy
The main symptom here is diarrhoea, usually very severe. Often babies vomit their feed as well. Most have little appetite, and if the offending food is not withdrawn they suffer from poor growth, anaemia and other signs of malnutrition. This is because damage to the lining of the gut prevents nutrients from being absorbed properly. Older children show similar symptoms.
Dietary protein proctitis
This is a far less severe problem. The babies with this disorder look healthy, but there is inflammation in the bowel and small amounts of blood are passed with the faeces.
Diagnosis
There are two aspects to diagnosis:
• what kind of disease is it?
• what food or foods are causing the reaction?
Your doctor will probably try to answer the first question by looking inside the digestive tract with special equipment (endoscopy) and by taking a small sample – a biopsy (see p. 92).
A blood sample may also be taken to look for raised levels of immune cells and antibodies. Skin-prick tests or RAST tests (see pp. 91-2) will be tried to rule out the possibility of true food allergy – and because IgE may play a small part in these other forms of food sensitivity (in the eosinophilic diseases, for example).
Often the tests yield no very clear answers, especially in babies, and an exact diagnosis is not possible. But failure to answer the first question does not mean that the second question should be ignored. Pinpointing the culprit food or foods is vital.
Identifying the food is easier the younger the child, simply because the range of foods eaten is so much smaller. Cow’s milk is the most common offender when the disease affects young children – particularly bottle-fed babies, since standard infant formula is made with cow’s milk. Your doctor will prescribe an alternative formula (see box on p. 66) for you to try. For older children and adults, an elimination diet will probably be required to identify the food concerned. Among young children, likely offenders include soya, egg, wheat, rice, chicken or fish. A simple elimination diet, similar to that used for atopic eczema (see p. 198) may be adequate. You must have full medical supervision for this.
In the case of eosinophilic reactions, skin-prick tests may help identify the foods concerned, but are usually of limited value, so an elimination diet is again necessary. Where adults are affected by eosinophilic diseases, sensitivity to several different foods is likely, so identifying the offending foods usually requires the most exacting form of elimination diet, using an elemental diet for the exclusion phase (see box on p. 196). The symptoms are very slow to disappear: it can take up to eight weeks of avoiding the foods before your ailing digestive tract recovers. Don’t give up too soon.
Treatment
Avoidance is the only way here. Special infant formula (see box on p. 66) is required for cow’s milk sensitivity in babies.
In the case of eosinophilic reactions, some doctors may use steroid tablets as an additional treatment, just for a few weeks, to get the inflammation under control. Some new studies show that the anti-leukotriene drugs (see p. 149) are very effective for eosinophilic gastroenteritis.
Controversial topics
According to some doctors, a reaction to food may, on rare occasions, produce vasculitis (inflammation of the blood vessels).
Vasculitis itself is a well-recognised condition. The blood vessels are damaged by inflammation, and become more leaky. Symptoms often begin with a general swelling (angioedema), and an outbreak of small red blotches deep in the skin — especially on the legs — where small amounts of blood have escaped. These blotches later turn purplish, then yellow, before fading. This type of rash is known as purpura. Sometimes there are larger emissions of blood, resulting in spontaneous bruising.
Many different conditions can cause vasculitis, but only a few doctors would agree that food sensitivity is one of them. The inflammation could be caused by circulating immune complexes containing food antigens bound to antibodies (see p. 13). There is evidence, in some patients, of a direct effect on the cells called platelets that cause blood to clot.
Equally controversial is the suggestion that food sensitivity can be the cause of trouble for some children with kidney disorders. Some research groups have found that a few children with certain kinds of kidney disease recover on an elemental diet (see box on p. 196). All those affected have a classical allergic disease such as asthma or atopic eczema as well, and they tend to be sensitive to several different foods, plus pollen or other airborne allergens. Circulating immune complexes might be involved here, but no one is sure.
Some cases of food-related rheumatoid arthritis and palindromic rheumatism (see p. 76) could be due to immune complexes involving food molecules becoming deposited in the joints, but it is not the mechanism in all, or even most, of those affected.

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

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

The days when doctors wanted their patients to obey orders and ask no questions are largely gone. Patients with allergies and other forms of sensitivity - or their parents -

have to play a key role in managing the disease. Most doctors now recognise this, and encourage their patients to learn about their illness, its diagnosis and treatment, and to

be partners in their own medical care.
Quite apart from this, there are aspects of allergy management where few doctors can afford the time to become experts. The nitty-gritty details of dust-mite avoidance or food

labelling practices are good examples. You can usefully supplement your doctor’s treatment here, by informing yourself.
But where should this process stop? That is a difficult question which doctors are increasingly forced to consider. One modern phenomenon, being discussed in many medical

journals at present, is the abundance of medical information on the Internet. Some doctors dread the arrival of patients who have logged on the night before their appointment

and are armed with a huge number of facts about their illness -some accurate, some utterly wrong and some highly debatable. But other doctors welcome the fact that patients are

actively interested in their health problems.
The reactions of doctors to ‘Internet patients’ highlight an issue that also runs right through this
book - that of medical orthodoxy. Who decides what is true and what is false in medicine, and how do they do it? Make no mistake - this is a deep and abiding problem which

afflicts not just scientific medicine, but science in general.
If a doctor, confronted with a web-page claiming that allergies are caused by space aliens intent on
destroying Western civilisation, snorts ‘Rubbish!’, he or she is not, strictly speaking, taking a scientific approach. In science, you should consider all the different

hypotheses.
In theory, science works by questioning everything and taking nothing on trust - but you can’t make much practical progress if you stick rigorously to that approach. Neither

scientists nor doctors start their careers by running experiments to establish the truth of everything they were ever taught. At some point in science, and in scientific

medicine, you have to assume that certain things are probably true, and proceed accordingly. If you make significant progress working on those assumptions, then the chances are

they were correct. But a good scientist always remembers that they are only assumptions.
Scientific medicine rests on a huge number of assumptions. Some of these are clearly accurate - for example, that eating wheat triggers coeliac disease -and it would be

time-wasting to argue about them. But this ‘fact’ about coeliac disease began as just a theory (see p. 70), and a highly debatable one. It has taken time for it to become

substantiated by more and more evidence.
Some medical assumptions become enshrined as facts rather too quickly. Fifty years ago, orthodox medicine accepted as a ‘fact’ that many asthmatic children had ‘intrinsic

asthma’, which was psychological in origin. Research since then has shown that there is almost always an allergy underlying childhood asthma. Many other examples could be given

of medical ‘facts’ that are overturned by subsequent research.
Doctors thirst for certainty, something that is quite understandable when they are faced with so much human need. A significant part of the healing power of medicine comes from

placebo effect (see p. 233), and that relies on patients having faith in the doctor. The traditional way for doctors to cultivate that faith was by assuming an air of absolute

certainty - about their diagnosis of the patient’s illness, about the treatment, and about medicine in general. This need for certainty has always hastened the transformation of

assumptions into facts.
The fatherly authoritarian attitude of old-fashioned doctors was, in large part, a reflection of how little they had in the way of useful treatments, and how much they relied on

placebo effect. Modern doctors have far more genuinely effective remedies to offer and can afford to take a different approach. Many now rely on a different kind of authority,

one based on intelligence, good information, flexibility, curiosity and openness. It’s a form of authority that allows a doctor to say ‘I could be wrong…’ or, ‘Let’s try this

and see what happens…’ without losing face.
Unfortunately, there is another powerful force at work in this complex situation, and that is quackery -the age-old business of selling phoney cures (see p. 209). Official

bodies within the medical community try to curb quackery by weighing the evidence about novel treatments and coming to decisions on their validity. This can be very useful. But

in deciding what is, and what is not, good scientific medicine, medical organizations always run the risk of mistaking their own unverified assumptions for facts.
Establishing criteria for good treatment is essential in medicine, but when this develops into dogmatism, that is decidedly unhealthy. Among the treatments that are being

dismissed as valueless today, there are
several that deserve a fairer hearing.
Some of these treatments have been shown to work by the most excellent of scientific methods. The use of elimination diets in Crohn’s disease is a good example - for some

patients, there is a huge and sustained improvement, suggesting that their disease was caused, at least in part, by food sensitivity. The tactic used by those who want to reject

this evidence is simply to ignore it. When scientific review papers (summaries of all the current knowledge and latest research) are written about Crohn’s disease, the research

on diet is usually not mentioned. Evidence that is routinely ignored in this way slips into oblivion because most doctors only have time to read the review papers, not the

original research reports.
Occasionally - and this is even more shameful -good scientific evidence that goes against the grain of current orthodoxy is actually misreported in review papers. This happened

with an impeccable scientific study showing the benefits of an elimination diet for some patients with rheumatoid arthritis. By missing out certain key facts, a review author

managed to give the impression that the results of this study supported the conventional view on the subject (that diet makes no difference to rheumatoid arthritis), whereas

they actually disputed the conventional view.
Unthinking rejection of new treatments often occurs with currently untreatable diseases such as autism and Chronic Fatigue Syndrome (CFS). Such medical problems always attract

experimental treatments, just as they always attract sheer quackery, and sorting out one from the other is not easy - it takes time, and a clear-headed approach, not knee-jerk

dismissal.

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

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

Various other things can irritate the skin and make atopic eczema flare up:
• cold weather
• dry air
• long car journeys
• sweating heavily; clothes or shoes that trap sweat may also cause problems
• dust mites, which can act as an irritant, even if not an allergen
• tobacco smoke
• solvents and other chemicals encountered at work
• skin contact with fruit (especially citrus), vegetables, and sometimes other foods. The spray generated by peeling potatoes can even produce eczema on the face.
Anything which increases blood flow through the skin makes the itching worse:
• heat, especially a hot bath or being too hot in bed
• anger or embarassment
• hot drinks of any kind
• coffee, tea and alcohol because of the drug-like substances they contain
• vinegar and spicy foods
• chocolate, soy sauce, yeast extract, orange juice, tomatoes and other foods that are rich in amines (see p. 200).
Various changes in the body can make the eczema worse:
• teething, in babies
• colds and other viral infections
• in women, certain phases of the menstrual cycle.
Many eczema sufferers are aware that their skin gets worse when they are upset, stressed or anxious Oust before examinations, for example). Like other allergic diseases, atopic eczema is not primarily psychological but, once it has begun, psychological factors can play quite a big part.
The good news…
…for children and teenagers, is that if you have eczema as a child, your chances of developing acne during your teens are greatly reduced.
Contact dermatitis too?
People with atopic eczema can develop contact dermatitis (see p. 54) in addition to their existing rash. There is always this risk with regularly applying creams to your skin, especially anything containing fragrance or lanolin. Antihistamine and antibiotic creams also carry this risk.
Even the ingredients in the creams prescribed for eczema – such as moisturisers and steroids – can sometimes provoke contact dermatitis. Creams are more likely to contain sensitising ingredients than ointments. Very occasionally, the sensitivity is to a preservative or emulsifier that is widely used in different ointments and creams, which means that switching brands yields no improvement. Steroid suspended in petrolatum (white paraffin jelly) is the least likely to cause reactions.
The rash produced by contact dermatitis looks no different from atopic eczema, so this sensitivity will be far from obvious. It will just seem as though the atopic eczema is not getting better.
Talk to your doctor if you think there may be a problem of this kind. He or she can check by using the suspect cream on one side of the body, and a different-but-equivalent product on the other side. Patch tests (see p. 92) may also help to identify contact sensitivity.
Diagnosis
There are five separate aspects to diagnosis:
1 Is this really atopic eczema? There are no clear-cut tests for atopic eczema. Instead the diagnosis is based on a ‘points system’ – how many of the typical features of atopic eczema are present? The doctor adds them up, and if there are enough, then it’s atopic eczema. Sometimes all the typical features are there and this is obviously the right diagnosis, but in other cases there may be room for doubt. The doctor should rule out the possibility of contact
dermatitis (see p. 54), especially if you have eczema only, or mainly, on the hands.
2 What avoidable irritants are making the skin worse?
3 Is the eczematous skin infected? The signs of infection are usually clear, but not always, especially with fungal infections. Steroid creams can sometimes mask the overt signs of infections: if atopic eczema is not responding to treatment this possibility should be investigated.
4 Are there any allergic reactions to those infections? Or to the normally harmless microbes that live naturally on the skin (see p. 17)? Skin-prick tests or blood tests can reveal such allergic reactions where fungi are concerned. Adults with persistent atopic, eczema which is getting worse rather than better are the most likely candidates.
5 Are there allergic reactions (or other sensitivity reactions) to food, or to allergens such as house-dust mite?
This fifth aspect of diagnosis is where controversy is rife. Many dermatologists feel that atopic eczema is treated quite adequately with moisturisers (emollients) and steroid creams. The search for allergic/sensitivity reactions – in other words, for basic causes – seems unnecessary for most patients, or more trouble than it is worth. Indeed, some dermatologists believe that looking for such sensitivity reactions is actually mistaken because they are not basic causes (see p. 42).
Other specialists disagree, and feel that allergic/sensitivity reactions are a basic causative factor in atopic eczema. They concede that there are many false positives, but in their opinion, there are enough true positives in the skin-prick test results to make it worth sorting them out from the false positives. Except for patients with very mild eczema, such doctors prefer to identify and eliminate the root causes, if possible.
Patch tests are now used by some of these doctors (see p. 69) – yet another contentious issue! The time-honoured use for patch tests is in contact dermatitis, and there is a lot of resistance to using them for atopic eczema. Traditionally, the immune reactions involved in atopic eczema and contact dermatitis are seen as entirely different – the former involving IgE and being a quick reaction (identified by skin-prick tests), the latter involving other players and
Sweaty sock dermatitis
More correctly known as ‘juvenile plantar dermatitis’, this rash on the feet affects an awful lot of atopic children. It is frequently misdiagnosed as athlete’s foot, and treated with anti-fungal drugs. The important clue can be found by looking between the toes: if there’s no rash there, then it is not athlete’s foot.
being much slower (identified by patch tests). New research into atopic eczema shows this view to be overly simple (see pp. 18-19) – and it provides a rational basis for using patch tests.
If, as a patient or a parent, you are keen to search for fundamental causes, remember that this should never displace treatments to quell infection or moisturise the skin and restore its protective structure. When these treatments are neglected the whole problem can get far worse, because of the vicious circles that sustain atopic eczema.
Treatment
Treatment for atopic eczema has five possible angles:
1 calming the inflammation
2 avoidance of scratching and rubbing
3 caring for the skin and restoring its normal structure
4 treating infections
5 avoiding allergens.
One or more of these aspects may be neglected, depending on what kind of specialist you are seeing.
Calming the inflammation
Steroid creams are the mainstay of atopic eczema treatment because they calm the inflammation in the skin. The creams do carry a risk of side effects, but are safe when used correctly (see p. 147). An over-fearful attitude to steroids creams can mean that the eczema never gets under control, and this can mean using more steroids in the long run. When treating an outbreak of atopic eczema with steroid cream, it is vital to continue applying the cream until the ‘hidden healing’ has occurred (see p. 146) – don’t stop as soon as the skin looks better.
Promising alternatives to steroid creams now exist: these are tacrolimus and pimecrolimus ointments (see p. 147). Unfortunately they are much more expensive, and your doctor will probably prescribe them only if there is some pressing reason.
Tar-based ointments have a much milder anti-inflammatory effect, and can be helpful for areas of thickened skin. They were once widely used for atopic eczema, but are used less now, in part because they stain fabrics and smell unpleasant. Sometimes they irritate the skin, too, and there are concerns about safety: they contain carcinogens, and significant amounts are absorbed into the bloodstream. However no evidence has been found that these cause cancer, despite intensive searching.
Antihistamine tablets are sometimes used and while they
may not help the eczema much, some evidence suggests that
they could reduce the risk of asthma developing later (see p. 249).
Powerful drugs such as cyclosporin are sometimes used in
severe cases of atopic eczema, to damp down the immune
response. They are taken by mouth, and can affect other parts of the body, not just the skin. Very careful monitoring is needed.
Sunlight is often beneficial, because it suppresses the inflammatory processes in the skin. However, not everyone improves with sun exposure – some get worse. Careful experimentation is the only way to find out: build up the length of sun exposure very gradually, starting with less than an hour a day.
Medical treatment with UV (ultraviolet) light can produce the same effect as sunshine and suppress inflammation. This treatment may be prescribed, but you should not try it for yourself with a sun-lamp. In PUVA treatment, a plant-derived substance called psoralen is given by mouth, or applied to the skin, to enhance the response to UV light.
Kicking the scratching habit
Scratching is a substantial part of the problem in long-standing atopic eczema. Experiments with healthy people and mechanical ’scratching machines’ show that perfectly normal skin will erupt into eczema if it is scratched intensively.
There is no steroid cream powerful enough to counteract the effects of scratching. But if scratching stops, then the skin can –with the help of medication – heal up.
Note that ’scratching’, in this case, includes rubbing the itch (directly or through clothes; using a hand, wrist, chin, leg, foot, or any other part of the body), touching or picking at the skin, rubbing against sheets, furniture or another person, or using a towel, flannel or hairbrush to rub the skin. All these activities can be habitual and quite unconscious, if atopic eczema has been present for more than a few months – you just don’t realise you’re doing it most of the time.
For many with atopic eczema, another problem creeps in –scratching without itching. This may be just habit, a response to boredom, stress or anxiety, or even part of the family dynamics, in which scratching has become a form of emotional expression. Scratching alone can set off itching, and a scratch-itch-scratch cycle ensues.
The first step in combating scratching (for an adult or older child) is simply to notice how often scratching occurs. Doctors at the Chelsea and Westminster Hospital in London issue their patients with little hand-held counting devices (tally-counters), and ask them to press the button on the device every time they scratch or rub. Over a period of days, patients discover – usually to their own amazement – just how often they do scratch. The point of the exercise is simply to become conscious of the scratching impulse, and to notice the situations which typically provoke scratching. You could use a small pocket-sized notebook and pencil to achieve the same end.
Once this awareness has been gained, then you are in a position to break the scratching habit. The methods involved –called ‘habit reversal’ – were first developed by a Swedish dermatologist, Peter Noren. It takes about 2-4 weeks for most people, but the change is long-lasting. Most eczema sufferers find that they recoup their time investment rapidly, once they are free from the chore of dealing with chronic eczema.
When you notice that you are about to start scratching, and before the urge to scratch overwhelms you, take control and do something deliberate with your hands – for example, clench your fists, while breathing deeply and slowly. Think cool non-itchy thoughts. The urge to scratch may pass. If it doesn’t, then you can allay the itch by pinching the itchy area gently, or pressing your fingernail into it, or lightly applying a little moisturiser.
In the bath or shower, don’t use flannels, and never rub or scrub the skin. Dry off by gently patting with a soft towel.
The aim is to get scratching episodes down to fewer than ten per day. In achieving this goal, relaxation exercises, stress management techniques, hypnotherapy or autogenic training (see p. 222) can also be very helpful, especially if you sometimes scratch in tense situations.
With small children, the parents have to do the noticing. Most are unaware just how much their child scratches or rubs the eczema – babies often rub against the side of the cot.
Once the awareness is there, a child over four can usually be taught the habit-reversal technique described above. With a younger child, the parents must distract the child when scratching is imminent, by talking or playing. If the child is scratching while asleep, parents should pick the child up and, very gently, hold the child’s hands away from the body. Situations and activities which commonly provoke scratching should be avoided, or planned for. Give the child something to hold while dressing and undressing, for example – keep the hands busy. But never say ‘Don’t scratch’ – it usually has the opposite effect in the long run.
For the first four days and nights, while you are trying to break the scratching habit, the child should never be alone, even for a minute – someone who is able to distract the child from scratching should always be there, and awake. Fortunately, children lose the habit far more quickly than adults.
Keep a child’s fingernails very short, and smooth them with an emery board too, so that if any scratching does occur the effects are minimised. (Soft cotton mittens, to be worn at night, are often recommended, but the cotton itself can be used to rub the skin – observe your child carefully! The same is true of all-over cotton suits.)
For this anti-scratching programme to be effective in healing the skin, there must be a determined effort with drug treatment at
Will it clear up?
Small children with eczema generally grow out of it by the age of two. Those who have eczema after this age tend to show a big improvement at puberty. Sometimes, however, the eczema can disappear at puberty, only to reappear later: so continue to be careful with your skin.
Atopic eczema is frequently the first sign of a tendency to allergies (see p. 22). Given this early warning sign, parents should take steps to avoid allergies developing, or at least reduce their severity (see pp. 244-9). One small piece of good cheer: atopic eczema and life-threatening food allergies are very rarely found together.
People with both asthma and atopic eczema frequently notice that when one improves the other seems to get worse. There is no explanation for this as yet.
Moisturisers - how to use them
Moisturisers (emollients) do two things: they increase the amount of water in the skin, and they lubricate the skin, making it less brittle.
A moisturiser is designed to leave an oily layer on the surface of the skin which stops the skin’s natural moisture from escaping. The most effective preparations, from this point of view, are ointments made from white paraffin, such as Vaseline, which form an uninterrupted waterproof layer: these are sometimes called occlusives. They contain no water, unlike creams. Although a cream forms a less formidable barrier to the escape of moisture from the skin, it does provide some moisture itself, which can soak into the skin.
The most important thing is to have something that you like using, so that you apply it regularly. There are lots of moisturisers available, so ask the doctor for different ones to try.
Applying moisturiser well is crucial:
• Apply moisturiser before your skin gets dry, as a preventive treatment.
• There’s no need to rub in your moisturiser (this can be a form of scratching). Just apply it very lightly.
• A thin layer is all that’s needed. A thick layer keeps in heat which aggravates the skin.
• Always apply within three minutes of a bath or shower.
• In addition, apply every 3-4 hours during the day. Carrying moisturiser around with you is helpful – get a small tube of moisturiser for this purpose.
• Ask the doctor to prescribe moisturiser in large quantities, to make sure you have enough. But beware of infecting big pots with Staphylococcus bacteria and then reinfecting your skin. Pump-action dispensers are safer.
Moisturiser can also be smeared onto bandages which are then wound around the affected areas at night to reduce the itch – or you can use ready-made ‘wet-wraps’ (ask your doctor about these). As long as the bandages/wraps are immovable, they will reduce nocturnal rubbing and scratching.
Avoid lotions, and any non-prescribed creams, as they could be irritating to the skin. Choose bath oils with care – some contain alcohol which is an irritant.
the same time. You should be using a steroid cream of sufficient strength, twice a day, and plenty of moisturising treatment.
By taking this ‘Combined Approach’, as Dr Christopher Bridgett and his colleages at the Chelsea and Westminster Hospital call it, you should be able to clear the eczema completely, even if you have had it for years and have tried innumerable different treatments. Once this has been achieved, you can maintain an eczema-free state by watching carefully for any outbreaks of itching, redness or roughness, and treating them immediately with a short course of steroid cream (see p. 146).
Skin care
Firstly, avoid all the irritants which you think may affect your skin. Give clothes an extra rinse cycle in the washing machine, to remove all detergent. or use a non-detergent system such as Eco-balls or Aquaballs. Wash all new clothes before wearing them, to remove chemicals such as formaldehyde. Wear soft cotton or silk next to the skin.
Where eczema affects the hands, special care is needed (see p. 57).
Water can be both good and bad for eczema. When you soak in a bath, water is absorbed by the skin cells, which helps correct the dryness of the skin. But when you get out of the bath, and the skin dries, the outermost layer shrinks and develops microscopic cracks, making it even less waterproof than it was before. The way around this is to apply a moisturiser immediately after a bath or shower –gently pat the skin until partially dry, and apply the moisturiser immediately to trap the water in the skin.
For anyone with a severe flare of eczema, current recommendations are:
• soak in lukewarm water for 20 minutes, twice a day
• pat dry
• quickly apply steroid cream to the eczematous areas, then moisturiser over the top, and to all other dry-skin areas
• make sure the moisturiser goes on within 3 minutes of emerging from the water.
This works well for some people, but not all. For a few eczema sufferers, the effect of taking natural oils out of the skin (which soaking does, to some extent) may outweigh the benefits of putting water in. Or they could be sensitive to something in the tap water – the chlorine, perhaps, or pollutants. It may not be obvious that this routine treatment is not helping. As Dr Michael Tettenborn, a British paediatrician with long experience of atopic eczema, observes: ‘By the time they’re referred to me, children are usually on the standard regimen of two-soaks-a-day. One of the first things I do, as an experiment, is tell the parents to just bathe them once a week and use a moisturiser and tissues to keep them clean the rest of the time. Some children do a lot better after that.

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.