Posts Tagged ‘diet’

Avoiding Milk and Lactose
Fruit lassi
There are two quite distinct reasons for avoiding milk: either to avoid milk proteins or to avoid

lactose, the sugar found in milk. It is important not to confuse these two because the details of the

avoidance diet required are different. Only a few people need to avoid both milk proteins and lactose.
Diarrhoea and wind in response to drinking milk, but few other symptoms, usually indicates a reaction

to lactose — but a reaction to milk proteins could be an alternative explanation. If it is a reaction

to lactose, this may be due to either primary lactase deficiency or secondary lactase deficiency — your

doctor can order tests to make an exact diagnosis (see p. 79). Note that a bout of diarrhoea, however

caused, often produces a temporary lactose intolerance (secondary lactase deficiency).
Any symptoms other than (or in addition to) diarrhoea and wind strongly suggest a reaction to milk

proteins. This might be a true allergy, another type of immune reaction to milk (see pp. 72-3), or an

idiopathic intolerance reaction (see pp. 76-7). In theory, skin tests should identify true allergic

reactions to milk proteins. Unfortunately, skin tests are not infallible, and it is possible to have a

genuine allergy or other immune reaction to milk proteins, but give negative skin tests. This is

especially common with babies (see p. 65 and p. 69). There are no accurate tests that can confirm

intolerance reactions to milk proteins.
It is possible to have sensitivity to both milk proteins and lactose.
If tests do not give you a definitive answer, you may have to try both types of diet and see which one

works. Remember that lactose intolerance may be only temporary.
Avoiding milk proteins
If you have a sensitivity reaction to cow’s milk proteins, then you need to avoid:
•    milk and all milk-based drinks, including lactose-reduced milk (if you need to avoid lactose as

well, drops and tablets to reduce lactose — see Using lactase replacers, p. 183 — are safe and could be

used with a tolerated milk, e.g. goat’s milk)
•    cream, yoghurt, creme fraiche
•    all kinds of cheese, cottage cheese and cream cheese (some people may be able to tolerate

Norwegian brown cheese, called Gjetost, which is made with milk whey)
•    white sauce, bechamel sauce and other creamy sauces
•    custard, rice pudding and other milk-based puddings
•    almost all home-made cakes, biscuits, cookies, pancakes and pastry
•    some bread, rolls, waffles
•    almost all chocolate
•    casein, casemate, and lactalbumin in packaged foods (see p. 173); you may be able to tolerate

whey but experiment cautiously.
Unless your sensitivity is fairly mild, you will also need to avoid:
•    butter, except clarified butter (ghee)
•    most kinds of margarine (they generally contain milk derivatives, but
some are milk-free — health-food shops are a good source of these).
As long as you do not have a severe allergy to milk, you should be able to tolerate clarified butter.

Make this by melting butter over a low heat, pouring it into a glass jar, and leaving it to cool in the

refrigerator. The milk proteins will settle to the bottom, and be visible as whitish granules — only

eat the clear butter above this level.
Alternatively, put olive oil into a wide-necked container and place in the freezer. It will solidify,

and can be used as a spread in place of butter.
A few of those with cow’s-milk allergy can tolerate sheep’s milk, and possibly (but less commonly)

goat’s milk. However, most people must avoid these as well. (There are also rare individuals who are

allergic to goat’s and sheep’s milk but not to cow’s milk.) Ass’s milk, if you can get it, is tolerated

by most with cow’s-milk allergy. There are many substitutes for cow’s milk now available, such as soya

milk, almond milk, rice milk and hazelnut milk. Try a health-food shop for these. All can be used in

place of ordinary milk when cooking.
Margarine or clarified butter can be used in recipes that call for butter. Soya yoghurt and cream make

reasonable substitutes for ordinary yoghurt and cream.
Avoiding lactose
If you have lactose intolerance, you must avoid:
•    milk and all milk-based drinks, unless lactose-reduced
•    cream, creme fraiche
•    most kinds of yoghurt, especially mild yoghurt. A very strong, acidic yoghurt may contain

little lactose. The bacteria that make yoghurt turn lactose into lactic acid, so the more acidic it is,

the less lactose it contains.
•    cottage cheese and Norwegian brown cheese, or Gjetost. Other kinds of cheese are usually so low

in lactose that they are tolerated. Only those people with extreme lactose intolerance need to avoid

all cheeses.
•    white and bechamel sauce, custard, rice and other milk-based puddings
•    almost all home-made cakes, since milk is generally used for baking. Items cooked with butter

but not milk, such as biscuits, cookies and pastry, are usually tolerated, as is butter itself, and all

margarine.
•    lactose in medicines. Lactose powder is used in many tablets and capsules, just to bulk out the

drugs. The amount used can be sufficient to evoke symptoms in some people with lactase deficiency.

Certain asthma inhalers also contain lactose (see p. 162), and a small amount may be swallowed. The

lactose from inhalers will affect you only if you have severe lactase deficiency.
Soya-based products, and all other nut- or grain-based milk substitutes, are lactose-free. Sheep’s

milk, goat’s milk and other animal milks (including human breast milk) all contain lactose.
Using lactase replacers
Many people with lactose intolerance are able to eat a more varied diet by using lactase replacers.

These provide a temporary supply of the missing enzyme, lactase (see p. 79), which helps out by

digesting the lactose in milky foods. Lactase replacers must be taken at the same time as the milky

food, and are only effective for that one meal. The more lactose there is in the meal or snack, the

more of the lactase replacer you need – trial and error is the only way of working out how much you

need for a particular food. There are a number of different brands of lactase replacer now available,

and it is worth trying out several. Some people find that they are sensitive to an added ingredient in

some brands. Sources of lactase replacers include health-food shops and specialist suppliers – these

can be located through the Internet (see p. 255).
Savoury white sauce
Savoury white sauce is the base of many dishes. Here the flavour of the wine and stock goes well with

chicken, vegetables or fish.
PREPARATION TIME: 7-8 minutes MAKES: approx. 600ml (1 pint)
50g (13/4oz) milk-free baking margarine 50g (1314oz) plain flour
200ml (7fl oz) dry cider or dry white wine 400ml (14f1 oz) vegetable or chicken stock 1 bay leaf, salt

and pepper
Melt the margarine in a small saucepan and stir in the flour. Cook, stirring, over a low heat for
1 minute then stir in the cider or wine, followed by the stock. Add the bay leaf and simmer, stirring

occasionally, for 5 minutes until thickened. Season to taste.
Variations. add approx. 6 tbsp finely chopped herbs, e.g. parsley, chives, tarragon or chervil; or add

English or French mustard; or add lemon juice.
Sweet white sauce
PREPARATION TIME: 5 minutes MAKES: approx. 300ml (’/?pint)
2 tbsp cornflour
25g (1 oz) caster sugar
300ml (V2 pint) apple or white grape juice 4 tbsp soya cream
25g (1oz) milk-free margarine
In a saucepan, mix the cornflour and sugar with a little of the juice to give a smooth paste then

gradually stir in the rest of the juice and bring to a simmer over a low heat. Simmer for 1-2 minutes

until thickened, stirring all the time. Finally, add the soya cream and margarine.
Variations: melt in 1008 (3-/2oz) or more of milk-free chocolate; or add rum or brandy to taste; or add

4-6 pieces finely chopped stem ginger together with 1-2 tbsp of their syrup.
Pancakes
Soya milk has a slightly thicker consistency than cow’s milk and therefore more is used in this pancake

recipe than would be needed in a traditional one.
PREPARATION TIME: 25 minutes MAKES: approx. 16 small pancakes
150g (5V2oz) plain flour, sieved 2 large eggs
pinch salt
450ml (16f1 oz) soya milk
oil or milk-free margarine for frying To serve:
lemon juice and caster sugar or golden syrup
Combine the flour, eggs, salt and soya milk in a liquidiser until smooth. Alternatively place the

flour, eggs and salt in a bowl and slowly whisk in the soya milk to form a thin batter.
Heat approx.1 tsp oil or margarine in an 18cm (7in) non-stick frying pan and swirl until hot. Pour in

sufficient batter to just cover the base of the pan and cook until golden. Turn and cook on the other

side until golden.
Serve with lemon juice and caster sugar or with golden syrup.
Apple and frangipane tart
An alternative to a milk-based custard tart. The combination of apple and almond is delicious. Serve

freshly baked. It can also be eaten cold, but if possible, warm it a
little before serving.
PREPARATION TIME: 30 minutes COOKING TIME: 1-11/4 hours MAKES: 8 servings
Pastry:
175g (6oz) plain flour, sieved
1008 (3 V2oz) milk-free baking margarine, softened
25g (1 oz) caster sugar
Filling:
50g (13/4oz) milk-free sunflower margarine 1008 (3112oz) ground almonds
100g (3112oz) plus 1 tbsp caster sugar 2 egg yolks
2 tbsp dark rum, brandy or orange juice 2 large dessert apples
4 tbsp apricot jam
Work the flour, margarine and sugar together with 1 tbsp cold water to make a soft dough. Roll out and

use to line a deep 20cm (8in) fluted flan tin. Chill this while you prepare the filling.
Preheat the oven to 190′C/375′F/gas mark 5. Beat together the margarine, ground almonds, 100g (3Y2oz)

caster sugar, egg yolks and rum. Peel, core and roughly chop one apple and stir into the mixture.

Spread this in the pastry case. Core and thinly slice the remaining apple and arrange the slices on

top. Sprinkle with the remaining sugar and bake for 1-1′/’4 hours until risen and golden. Cool slightly

then brush the surface with the apricot jam (warm this gently in a saucepan first).
Coconut rice pudding with mango
This pudding is based on a Thai recipe. The rice pudding will become thicker the longer it cooks and

also as it cools. Make sure the mango is ripe.
COOKING TIME: 30-40 minutes MAKES: 6 servings
175g (6oz) pudding rice, rinsed 50-75g (131-2314oz) sugar
1 litre (13/4 pints) carton rice milk 400ml (14f1 oz) coconut milk To serve:
1 extra-large ripe mango, peeled and diced
toasted coconut shreds
Place the rice in a large saucepan with 50g (13/4oz) of the sugar and the rice milk and coconut milk.

Bring to a simmer, stirring. Simmer gently for 30-40 minutes, stirring occasionally, until the rice is

cooked and the milk absorbed. Add the extra sugar if wished. Serve warm or cold, topped with mango and

toasted coconut.
Baked strawberry creams with strawberry sauce
The riper the strawberries the better, to give intensity to both the creams and the sauce.
PREPARATION TIME: 30 minutes COOKING TIME: 20-25 minutes MAKES: 6
1008 (3112oz) caster sugar
4 tbsp Muscat wine
1 tsp lemon juice
350g (12oz) strawberries, hulled and sliced
4 large eggs, beaten Sauce:
225g (Boz) strawberries, hulled and chopped
2 tbsp icing sugar 2 tbsp Muscat wine To serve:
a few whole strawberries
Preheat the oven to 1 70′C/325′F/gas mark 3. Set six 1 50ml (Y4 pint) ramekins in a small roasting tin.

If you plan to unmould the creams, oil the ramekins lightly.
Place the sugar, wine, lemon juice and strawberries in a saucepan and heat gently to dissolve the

sugar. Bring to the boil and cook, uncovered, for 5 minutes. Cool slightly then puree in a liquidiser

and whisk into the beaten eggs. Pass through a sieve then pour into the ramekin dishes.
Pour hot water from a kettle around the ramekins and cook in the centre of the oven for 20-25 minutes

until lightly set.
Remove the dishes from the tin and allow to cool. Chill, if wished.
Combine all the sauce ingredients and liquidise until smooth. Pass through a fine sieve.
Serve the creams in the ramekins with a little sauce poured on top and decorated with a whole

strawberry, or carefully unmould, pour a little sauce over, then decorate with a whole strawberry.
Variation: oil the ramekins. Dissolve 100g (31/2oz) caster sugar in 4 tbsp water in a small saucepan

over gentle heat, then cook to a rich caramel without stirring. Pour a little caramel into each oiled

ramekin then continue as above. Pour the wine for the sauce into the pan used to make the caramel and

warm gently to dissolve any leftover caramel, then continue with the sauce as above.
Frozen vanilla dessert
This is a cross between a sorbet and an ice cream.
PREPARATION TIME: 30 minutes, plus freezing MAKES: 4-6 servings
1 vanilla pod, split
150g (51/2oz) caster sugar 500g carton soya yoghurt
Place the vanilla pod and sugar in a saucepan with 300ml (1/2 pint) water. Dissolve over gentle heat

then bring to a simmer and simmer for 20 minutes. Leave to cool then remove the pod, scraping all the

seeds from it and returning them to the syrup. Beat in the soya yoghurt and freeze.
You will get the best texture by using an ice-cream machine. Alternatively, freeze in a plastic

container then remove from the freezer and beat the mixture well until smooth (you can do this in a

food processor). Return to the freezer. Repeat this process once or twice.
Baked strawberry cream with strawberry sauce
Variations: add 100g (31/2oz) melted plain chocolate; or add 2 tbsp instant espresso coffee dissolved

in 2 tbsp hot water. Alternatively, dissolve 100g (3/2oz) caster sugar over a gentle heat in a small

saucepan until it turns to a rich caramel; then add 100g (31/2oz) unblanched almonds and stir with a

metal spoon until they start to pop. Transfer to an oiled tray and leave to set. Crush roughly and add

to the basic mixture.
Fruit lassi
This refreshing Indian drink can also be made with frozen fruit, in which case don’t use iced water –

cold will do.
PREPARATION TIME: 10 minutes
MAKES: approx. 1.35 litres (21/4 pints)
500g carton soya yoghurt
50-75g (1314-231aoz) sugar
225g (8oz) berries such as raspberries, strawberries, blackberries or blueberries or the equivalent

weight of chopped fruit such as mango, peach or papaya
600ml (1 pint) iced water
Place all the ingredients in a liquidiser and blend until smooth.
Frozen vanilla desert
Banana and strawberry shake
A special treat for a child who cannot have milk.
PREPARATION TIME: 5 minutes MAKES: 600ml (I pint)
2 large, very ripe bananas
150g (5112oz) strawberries
1112 tbsp olive oil
a little nutmeg or other spice, if liked 200ml (7fl oz) water
Peel the bananas and roughly chop the fruit. Combine all the ingredients in a blender until very

smooth. Serve immediately, or cover tightly and store in the refrigerator.
Variations: use a nectarine or a skinned peach instead of strawberries; use coconut milk (available in

tins) instead of olive oil, and the flesh of a small mango, or half a large mango, instead of

strawberries.

`When I first arrived in Charlottesville in 1982, the senior allergist said “I’ve got to warn you that here in Virginia we have patients who have very severe fungal infection of their feet, and they also have urticaria. If you treat their feet, their urticaria gets better.”‘ Professor Tom Platts-Mills of the University of Virginia in Charlottesville is recalling how his innovative studies of fungal infections and allergy began. That surprising observation about athlete’s foot (a fungal infection) and urticaria (nettle rash) was made by his predecessor, Professor John Guerrant,
‘I followed his advice,’ Platts-Mills continues, ‘and found he was right. Then I started noticing asthmatics in our allergy clinic who also had fungal infections of their feet. They were mostly men with severe adult-onset asthma. We gave them skin-prick tests with the fungus Trichophyton and these were positive – showing they had an allergic reaction to it. So we tried treating them with anti-fungal drugs and the asthma got much better.’
This discovery is not an isolated instance. Research over the last decade or so has revealed that allergic reactions to long-standing infections (chronic infection is the medical term) are far more common than anyone expected. Infections by fungi are frequent offenders.
An infection becomes chronic because, although the immune system tries to rout the infectious agent, it never succeeds. Making IgE may be part of that futile defensive effort. Once the immune system starts making IgE against the allergens produced by the infectious microbe, new symptoms may begin, or existing allergic symptoms may get much worse. The link between the infection and the allergy is far from obvious, however. Both the allergens and the IgE can be carried in the
Fungal infections
‘Fungus’ means everything from an edible mushroom or a huge bracket fungus to the specks of mould on stale bread or a shower curtain. Fungal infections are caused, not by mushroom-like fungi, but by inconspicuous mould-like forms, or by yeasts (which are single-celled fungi).
Once they are flourishing, some fungal infections may be seen as whitish or creamy-coloured patches. But at an earlier stage, the fungi are so small that they cannot be seen without a microscope. They spread as invisibly as bacteria or viruses.
Some infectious fungi can exist in two different forms – a mycelial form (long thin strands, as in a mould) or a yeast form (single cells).
bloodstream, so the symptoms may be somewhere else in the body, far away from the site of infection.
If the symptoms of the infection itself are relatively mild, they may not receive medical attention. Infection-plus-allergy often explains severe long-term allergic problems for which no cause could previously be found. This is the kind of case that gets labelled as ‘intrinsic’ or ‘endogenous’, because all the allergy tests have proved negative. Most patients in this category have had years of simply being treated with steroids (often at high doses) to suppress the symptoms.
Sometimes the infection-plus-allergy is part of a larger picture, with other allergens or irritants also contributing to the symptoms, but with no stunning improvements when they are avoided because the allergic stimulus from the infection remains.
The links between allergy and fungal infections – all those that have been discovered so far – are described below. In such cases, anti-fungal drugs, taken by mouth, usually in capsule form, could be of value. However, they must be taken for an adequate length of time, normally several months.
Bear in mind that, with the possible exception of chronic sinusitis, an allergic reaction to fungal infection is a relatively uncommon cause of symptoms. It is important that, with the help of your doctor, you start with the more likely suspects such as airborne or contact allergens. These are described in detail, for each allergic disease, in the relevant sections of Chapter 2.
Asthma
the common causes and usual treatment of asthma.
Trichophyton – the fungus that causes athlete’s foot – can provoke allergic reactions that contribute to asthma, as already described. This fungus may also infect other parts of the body. Trichophyton diseases have names that begin with tinea (athlete’s foot, for example, is tinea pedis). Other terms you may come across are intertrigo (an itchy rash which develops in skin folds) and onychomycosis (also called `ringworm of the nails’ or tinea unguinum). The research on the link with asthma was published in a respected medical journal, The Lancet, but has been widely ignored, so if you think you have this problem, you may have to be quite persistent with your doctor. Very thorough treatment with anti-fungal drugs (swallowed in capsule form) is required.
Chronic urticaria
many possible causes of chronic urticaria.
Trichophyton infections in any part of the body (see above) can provoke allergies, producing chronic urticarla. A great variety of other infections, including fungal, viral and chronic bacterial
infections, can be the root of the problem in chronic urticaria . However, this may not be an allergic reaction. It could be a direct effect of the infection, provoking the immune system in such a way that it triggers mast cells by itself, without IgE.
Chronic sinusitis
 the causes and treatment of chronic sinusitis.
Long-standing (chronic) sinusitis may be due to a fungal infection with a subsequent allergy. This is now called allergic fungal sinusitis. Some doctors believe that a sensitivity reaction to fungal infection (not necessarily an allergic reaction) could account for 96% of chronic sinusitis. However this is widely disputed .
Atopic eczema (atopic dermatitis)
the causes and treatment of atopic eczema.
The Trichophyton fungus can infect eczematous skin, though this is far less common than infection by Staphylococcus aureus (see below). Among patients infected by it, there can be an allergic reaction to Trichophyton which then makes the eczema worse.
There can also be an IgE reaction to a yeast, Pityrosporum ovale (also called Malassezia ovalis), in atopic eczema. This yeast is a commensal – i.e. a natural, and normally harmless, inhabitant of healthy skin. The inflammation of eczema makes the immune system far more tetchy so that it reacts allergically to this yeast, an innocent bystander which it normally disregards.
Candida  can also provoke an allergic reaction in eczematous skin. This is a more complex story, because while Candida is a commensal in the gut, it does not normally live on the skin. However, it may flourish in the disturbed skin of eczema patients.
Those with atopic eczema may also develop an allergic reaction to toxins from Staphylococcus aureus, a bacterium that often infects skin which is inflamed by eczema and damaged by scratching. Antibiotics are needed to treat the infection .
Seborrheic dermatitis
Not so long ago, this disease – which causes a red, scaly rash on the forehead, nose and cheeks, and sometimes on the chest –was labelled ’cause unknown’. Now most doctors believe that the yeast Pityrosporum ovale could well have a role in causing it. This yeast is part of the normal skin flora (see above), but it is found in greater numbers on the skin of seborrheic dermatitis patients. As well as overgrowth of the yeast, there is an immune reaction against it, usually involving the antibody known as IgG, rather than Fungi in the lungs
One form of infection-plus-allergy has been well recognised for many years - allergic bronchopulmonary aspergillosis, often shortened to aspergillosis.
The problem starts with the fungus Aspergillus fumigates, a ubiquitous mould that is found in special abundance in damp straw, compost heaps, bird cages and any decomposing material. Its spores are everywhere, and most immune systems quickly defeat them, but in some people, especially those with asthma, the spores begin to grow in the lungs. The fungus is found in the lung mucus, but does not actually invade the lungs. However, an allergic reation then occurs to the fungus.
This disease often goes together with asthma, or can be mistaken for asthma. There are three clues that point to aspergillosis:
• rubbery plugs of phlegm, either golden-
brown or green in colour
• fever whenever the asthma is severe
• worsening symptoms despite treatment.
Allergic bronchopulmonary aspergillosis is treated with steroids to control the allergic reaction, and physiotherapy to clear the mucus from the lungs.
Anti-fungal drugs have not proved very effective in the past. There are some newer anti-fungal drugs that may well be more useful, such as itraconazole and terbinafine. These are not widely used for aspergillosis at present, except in patients who also have cystic fibrosis or an immune deficiency. Because there has been no large-scale trial of these drugs, they are not usually given to people who simply have aspergillosis. However, they are sometimes prescribed for people who are unable to take steroids, or are not responding to steroid treatment. Anti-fungal drugs may become more widely used in the next few years, so it is worth discussing the possibility of this treatment with your doctor.
the allergy antibody IgE. Only about 12% of people who suffer from seborrheic dermatitis make IgE against the yeast.
One problem with seborrheic dermatitis is that, while it may improve with anti-fungal treatment, it usually comes back when the treatment stops. Doctors have therefore been looking for ways of keeping seborrheic dermatitis at bay after a successful course of anti-fungal treatment. One method that seems to work is to use a good anti-dandruff shampoo, in place of soap, to wash your skin once a week.
A medical earthquake
The recent discoveries about infection-plus-allergy have not posed any serious challenge to conventional thinking about allergy, because a disease of just this kind - aspergillosis (see box at left) - was already well known. A far more fundamental shake-up of traditional ideas about allergy and sensitivity has been necessitated by new research into atopic eczema. It is little short of an earthquake in the basic concepts of allergy and sensitivity.
To understand the extent of this earthquake, you need to know about the time-honoured system for classifying hypersensitivity reactions, which recognises four distinct types:
• Type I hypersensitivity — the IgE-mediated allergies  such as hayfever.
• Type II hypersensitivity - irrelevant to allergy, these antibody reactions mainly occur after transplant surgery, if the transplanted organ is rejected.
• Type III hypersensitivity - caused by a massive overload of antibodies and antigen in the blood. It is a feature of certain infections and autoimmune diseases, and can also occur in allergic reactions, though this is rare (13).
• Type IV hypersensitivity - the odd man out, because antibodies are not involved, or are not of central importance. Immune cells that can launch a direct attack are the movers and shakers here. These attacking-cells are sensitised for a particular antigen, such as dust mite or lanolin. Type IV hypersensitivity is a very slow reaction. Generally speaking, 48 hours pass, after an encounter with the offending substance, before the symptoms appear. The most common form of Type IV hypersensitivity is contact dermatitis (54).
Mystery has always surrounded atopic eczema. Although it crops up in the same atopic families that suffer from hayfever and asthma, and high levels of IgE in the bloodstream are typical of the disease, the actual role played by allergies in causing the symptoms is far from obvious.
The results of skin-prick tests - the standard test for an IgEmediated reaction - are puzzling. Patients tend to give a lot of positive results, many of which don’t mean much - the substances concerned do not provoke actual symptoms. On the other hand, skin-prick tests are often negative for substances that clearly do cause symptoms in challenge tests. Many children who regularly get eczema when they drink cow’s milk, for example, give a negative skin-prick test to milk. This conundrum has puzzled allergists for decades.
New discoveries about eczema do not entirely solve the puzzle, but they do go some way towards an answer, by revealing an immune response that cuts across the traditional categories. The most surprising fact is that even where skin-prick tests are positive and milk-specific IgE is involved in milk-induced eczema, this is not necessarily a standard IgE-mediated allergy.
While IgE antibodies may be involved, they are not necessarily teamed up with mast cells, their usual partners in crime (see box on p. 12). Instead, the IgE molecules are attached to special skin cells called Langerhans cells and dendritic cells. These have the role of picking up the antigen and showing or ‘presenting’ it to attacking-cells in the skin (a task called antigen presentation which is the ‘go’ signal that starts off all immune reactions).
The involvement of these attacking-cells, which are sensitised for a particular antigen, was a big surprise when first discovered. It makes this resemble a Type IV hypersensitivity reaction rather than a Type I.
IgE is not essential here, it seems — some patients do not have IgE for the substance that triggers their atopic eczema — but when Langerhans cells and dendritic cells are associated with IgE they do become far more zealous. This excitement is communicated to the attacking-cells, which mount a more powerful attack.
It looks as if what really matters in atopic eczema is the presence of antigen-specific attacking-cells in the skin, plus the heightened activity of the Langerhans cells and dendritic cells. If the individual has IgE for the antigen, it can play a part, but it is not essential.
In other words, this reaction cuts across two different categories of immune response — Type I and Type IV. (However, the kind of antigens that provoke the reaction are typical of IgEmediated allergy, rather than the kind of antigens that provoke contact dermatitis.) This has been exploited in a new and more sensitive set of diagnostic tests for food-induced atopic eczema (69).
Why atopic eczema is a feature of atopic families is the crucial question that remains unanswered. One factor may be that high levels of IgE in the bloodstream (not IgE for a particular allergen, but total IgE) make the whole immune system more excitable and prone to over-react. The next few years will no doubt solve this part of the puzzle too.
Peace-keepers or aggressors?
`It is bad enough having a child on an ultra-strict diet — Tim can’t have even a trace of cow’s milk or else he becomes violently ill. What makes it worse is when people — teachers, for example —ask what’s wrong. I take a deep breath and say “eosinophilic oesophagitis” then watch their eyes roll in disbelief.’
Tim’s disease is caused by a particular type of immune cell called an eosinophil. In the right circumstances, eosinophils can be valuable — like IgE and mast cells, they are geared to destroying parasitic worms . They produce some very toxic substances to kill these invaders, and it is the toxins that cause serious symptoms for Tim and others like him.
Any disease with ‘eosinophilic’ in the name involves vast numbers of eosinophils converging on some unfortunate part of the body. The stimulus that attracts them often remains unknown but once there, the toxins they generate cause inflammation (140) of a particularly violent kind.
It is only in recent years that doctors have begun to distinguish between patients such as Tim and children with classical food allergy, and to understand the cause of Tim’s symptoms. Several different forms of eosinophilic food sensitivity are now recognised (72). The exact relationship with IgE-mediated allergy remains a puzzle, because some sufferers make IgE to the culprit food but others do not.
That is not all — the eosinophil is finally coming out of the shadows and being recognised as an important agent in classical allergic diseases as well.
The fact that eosinophils appeared during the aftermath of an allergic reaction had long been known, but their role was misunderstood. What confused researchers was that eosinophils can break down histamine, the substance that kick-starts allergic symptoms. This ability gave eosinophils the appearance of peacekeeping troops, coming in at the close of battle to restore order. In fact, eosinophils are major aggressors — they do a whole lot of other things besides breaking down histamine, most of them pro-inflammatory. They can release toxins, just as they do in eosinophilic diseases, and they attract other inflammatory cells into the area. In short, eosinophils play a big part in keeping allergic reactions going once the initial burst of activity is over. This `Late Phase Reaction’ is enormously important .

 

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