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Conditions that respond to allergy treatment

Asthma – what we do and why we do it

David LJ Freed and John Mansfield

British Society for Ecological Medicine
c/o BSEM Administrator, New Medicine Group, PO Box 3AP, London W1A 3AP (0207 100 7090)

‘At this time when mortality rates from other chronic diseases are on the decline, clinical observations in recent years have demonstrated an increase in the mortality rate from asthma in several countries’
(Prof. U. Serafini, Rome 1992) [1]

And yet until the l950’s asthma was not thought to be a life-threatening condition,
as testified by:

Osler, 1892 ‘Death during the attack is unknown’ [2]
Oxford Textbook of Medicine, 1920 ‘Prognosis is excellent. The sensitive type probably never dies in an attack and the non-sensitive type rarely dies in an attack’ [3]
Coke, 1923 ‘The prognosis with regard to longevity is notoriously good’ [4]
Conybeare’s Textbook of Medicine, 1929 ‘It is doubtful whether death has ever been caused by uncomplicated asthma’ (i.e. asthma without emphysema) [5]

What on earth is going on here? Here we are in the 21st century, in the grip of a sustained worldwide epidemic of asthma deaths, and only a few decades ago our clinical ancestors were calmly saying that it never happened. Were they all blind? Were they fools? It seems hardly likely, since death from asthma suffocation is a peculiarly horrifying spectacle, and the medical giants of the past (keen clinical observers) were so impressed by the curious benignity of asthma that they all mentioned it.

Be that as it may, there is no doubt that within the last five decades we have witnessed a striking increase in asthma deaths, accompanied by a huge rise in asthma drug prescriptions and asthma hospitalisations [1, 6-16]. The phenomenon troubles every doctor who sees asthma, and attempted explanations have been many. The International Consensus Report on the Diagnosis and Management of Asthma, issued a few years ago by the National Institutes of Health [17], still reflects the views of most conventional chest physicians in laying the blame squarely on ‘underdiagnosis and inappropriate treatment’ (shorthand for not enough steroids). But this is hardly an adequate explanation for the strange harmlessness of the same condition a couple of generations ago, when diagnosis and treatment were primitive and steroids were used not at all.

If we accept that for some reason asthma is now a potentially fatal condition, even though it was not so in the recent past, then the physicians’ calls for earlier hospitalisation and more aggressive steroid treatment do appear reasonable. But we still have a duty to ask why asthma has become more dangerous and there are three disturbing factors which may provide answers: (i) air pollution has vastly increased over the last few decades; (ii) the drugs which are used to control asthma might be making the condition worse in the long term; and (iii) micronutrient deficiency is more prevalent.

The views that we are about to expound are our own (though broadly in tune with those of most members of the British Society for Ecological Medicine), but the data on which they are based are public property and verifiable by anyone with access to a library, who can check the citations at the end of this essay.

Recognised Risk Factors

There is no doubt that air pollution, both natural and man-made, is a major contributor to illness and death from asthma [18]. The classic artificial pollutant was the great 1952 winter fog that killed 4,000 Londoners [18]. Although carboniferous smogs have become less common in the UK due to air-cleaning laws, they have been largely replaced by diesel exhaust particles which act as an IgE adjuvant [19].

Among ‘natural’ pollutants are included the dust of soya beans, which causes a mini-epidemic at the port of Cartagena, Spain, on unloading days [20]. But probably the most famous natural pollutant is the housedust mite, Dermatophagoides pteronyssinus (and its minute faecal particles), and that is much more prevalent in modern homes because of greater warmth, insulation, and fitted carpets [21].

Apart from natural allergens such as dust mites and feathers, chemical pollutants are also becoming progressively more prevalent in modern houses. Energy-saving construction of houses has much to answer for; a house that keeps in heat also tends to keep in pollutants. Indoor chemical air pollution tends to be overlooked because of the emphasis on outdoor air pollution, but there are major reasons for believing that indoor air pollution is much more important (it is not diluted as is outdoor air pollution). Formaldehyde, used extensively in plasterboard and wallpapers, the burnt oxides of natural gas and oil, trichlorethylene and formaldehyde emanating from carpets, and the phenol given off by soft plastics, are all present in significant quantity especially in modern houses. They have been implicated separately and collectively in countless publications and the work was summed up in 1998 by Ashford and Miller in their book Chemical Exposures - Low Levels and High Stakes [22]. One in seven cases of adult asthma, according to one estimate, is attributable to household aerosol cleaners and ‘air fresheners’ [23]. Interestingly, nitrogen dioxide (and pertussigen, see below) both abrogate the normal tolerogenic effect of inhaled soluble antigen in mice [24].

Lastly, one must not forget that one can be allergic to micro-organisms, acquired naturally [25] or possibly in the form of vaccines [26], and the first route of exposure can certainly trigger asthma in susceptible persons.

As regards anti-asthma drugs, most concern has focused on the group of drugs called beta-agonists, starting with isoprenaline in the 1960’s and continuing with the new generation of ‘safe’, non-cardiotoxic analogues such as Ventolin and Serevent [7, 27-32]. Regular use of these drugs gives rise to a substantial rebound phenomenon when they are withdrawn [33], and increases the so-called ‘non specific’ reactivity of asthmatic airways, e.g. reactions to methacholine or histamine [27]. Tachyphylaxis also occurs, at least in vitro - that is, larger and larger doses are required to obtain the same degree of bronchodilation [27]. Furthermore, these drugs disrupt magnesium metabolism which in turn aggravates smooth-muscle lability (see below) [34]. In practice, at least one chest expert now tries to wean his patients off long term beta-agonists, explaining that they ‘keep your asthma active’ [35]. Interestingly, as long ago as the 12th century the Arab-Jewish physician Maimonides, in his Treatise on Asthma, advised against using strong herbal remedies for this condition [36].

Continuous beta-agonist bronchodilation causes long term deterioration of lung function [37]. Intermittent (on-demand) treatment is less dangerous in this respect, and we find that even nebulizer-dependent patients can often tolerate a ‘sabbatical’ break from treatment one day a week, with what we hope will be an improved long term prognosis.

After the upsurge in asthma deaths in the mid l960’s, which included well-publicised cases such as that of Brian Jones, the Rolling Stones musician, there was a general perception among the public that asthma inhalants were dangerous; drug consumption fell and mortality fell. By the mid 1970’s physicians had regained their confidence with the new generation of ‘safe’ bronchodilators and prescription rates started rising again, to be followed shortly by death rates [7]. This fall and subsequent rise in mortality does rather argue against the ‘increased pollution’ theory, since air pollution (at least the carboniferous variety) was rising pretty smoothly throughout those years [38].

Before leaving the topic of medication, it is interesting to note in passing that antihistamines impair the efficacy of allergen desensitisation, at least in mice [39].

Asthma is common. 11% of all children have wheezy episodes, which (if left alone) normally resolve by the age of ten [40]. The worry is that by calling these wheezy episodes ‘asthma’, and thus triggering the doctor’s prescribing reflex (furor therapeuticus), we might convert a benign transient wheeze nto a chronic condition that needs ever-increasing drug intake to keep it under control. To quote one recent Canadian view, ‘we should hesitate before recommending regular use of any beta-agonist’ [32], or to borrow the even more provocative words of one group of New Zealand asthmologists in 1992: ‘is the cure the cause?’ [11].

Micronutrient Deficiency

The arable soil of developed countries has become progressively depleted by modern farming practices. Conventional fertilizers replace nitrogen, phosphorus and sometimes sulphur, but not magnesium, selenium or a host of others, as food plants grow well without them and their macronutrient levels (protein, fat, carbohydrate) are unaffected.

Magnesium deficiency in particular has attracted increasing attention over the past few years. Magnesium is a known smooth-muscle relaxant and studies in acute asthma have shown that parenteral (IV) magnesium is of significant benefit given during an attack [42-43]. Experience has shown that increasing magnesium levels, primarily by supplementation (orally or by injection) lessens muscle spasm of all sorts but particularly bronchial muscle spasm. Inadequate magnesium leads to mast cell instability and also the inability of the bronchial musculature adequately to relax [41-45].

Another effect of magnesium deficiency has been demonstrated experimentally in rats. In a control group of rats antigen challenge increased histamine only modestly in urine, and not at all in the blood. However in rats with magnesium deficiency, urinary histamine and blood histamine levels were both greatly increased upon antigen challenge. The authors of this report concluded that there was a synergism of antigen challenge and magnesium deficiency on blood and urinary histamine levels. The results suggest that magnesium deficiency can aggravate type I allergic conditions, associated with abnormal histamine release after exposure to an IgE-stimulating antigen [46]. In patients with hay-fever and concurrent magnesium deficiency we have noticed that neutralisation therapy (see below) is frequently dramatically enhanced within hours by the injection of 2cc of magnesium sulphate given intra-muscularly.

Magnesium deficiency has undoubtedly increased in the population as a result of progressive magnesium depletion of the soil due to intensive farming. Magnesium loss also occurs during food processing, e.g. rice polishing. More recently other nutrient deficiencies (especially perinatally) have been implicated in allergy and asthma [47-50]. Conversely, vitamin A excess may aggravate asthma [51].


Many autopsies have been carried out on patients who have died of asthma. Two types of picture emerge. The most common is of widespread plugging of bronchi and bronchioles with thick mucus, often so thick and hard that it cannot be sucked up with a pipette but has to be cut with a knife. The mucus plug forms a perfect cast of the inner shape of the air tube, and is obviously the main cause of suffocation [1]. Embedded in the mucus are numerous inflammatory cells (neutrophils and eosinophils), together with clumps or even sheets of epithelial cells (the cells which normally line the inner surface). These patients have usually died in hospital after several days or weeks of increasingly aggressive treatment [52]. On the other hand there are those who die unexpectedly, in their homes or at work, and in these cases the airways are often empty on post-mortem, having relaxed after death from the tight and sudden bronchoconstriction that was the presumed cause of death. [52].

What Is Going On In Asthma ?

The wheezing of asthma is caused by narrowing of the bronchi and bronchioles. This is initially caused by tightening of bronchial smooth muscle and inflammation [53] and is reversible between attacks, although as the disease (and its treatments) become chronic, remodelling of the airways supervenes and that is much harder to reverse [54-55].

It is an axiom of biology that any body organ or mechanism, if apparently harmful, must also give rise to an equal or greater benefit – perhaps in a totally different context - so that there is a net survival advantage. The classic example is sickle-cell anaemia, a potentially fatal polymorphism which has nevertheless survived in malaria-endemic areas of the world because it confers partial resistance to the malaria parasite [56]. It is the duty therefore of every thoughtful biologist to ask, what is asthma for?

We offer here our own suggestions, and from now on we shall use the terms bronchospasm or wheeze to describe what we consider to be a physiological state, and asthma for its pathological sequel (when aggravated excessively by nutrient deficiency, medical treatment or other factors).

It has been standard biological teaching since the time of Celsus that inflammation is the body’s defence and repair mechanism for coping with ‘insults’ from the environment such as germs, harmful chemicals, extremes of heat and cold, radiation and physical traumata [57]. Inflammation in the tissues is characterised by the famous signs of heat, swelling, pain and redness, all of which reflect the increase in blood supply to the inflamed part, with dilation of blood vessels and migration of inflammatory cells from blood to interstitial fluid. Inflammation at mucous surfaces shares the first two of those characteristics and also has three of its own: (a) increased mucus secretion (containing some of the said inflammatory cells) (b) shedding (desquamation) of sheets of epithelium [53] and (c) involuntary expulsive efforts such as sneezing, coughing and diarrhoea [58]. Clearly, these features between them serve to trap particles and chemicals and expel them from the sensitive membranes, an enhanced form of the continuous shedding of surface cells that occurs normally in skin and gut.

Allergy, in our terminology, is an immunologic process that leads to inflammation. That means, by this definition, that allergy must be one of the body’s natural protective mechanisms albeit sometimes in exaggerated form. This line of thought reflects conventional biological thinking [57] (albeit rarely followed to its logical conclusion by clinicians) and insists that bronchoconstriction (wheeze) must itself be protective, in some way, against some insult. Mother Nature did not put smooth muscle into our bronchi just in order to make mischief, and that is why we have preached for the last three decades the need for clear terminology [58]; ‘allergy’ means different things to different people, and although we may be fully justified in acting to ameliorate the symptoms of poisoning, we should think long and hard before suppressing symptoms that are part of a body defence mechanism.

One can say with some confidence that narrowing or closure of the upper airways means that toxins and particles are impeded or prevented from reaching more distal reaches of the bronchial tree, thus preventing damage there [59], but we also suggest a therapeutic rôle, that is, that wheeze (before it turns into asthma and perhaps even then) helps to clear and repair existing lung damage. When the Highways Department decides to repair a stretch of motorway, it closes some of the carriageways and considerable congestion results while the repairs get done. In extreme cases the engineers may close the entire width of the motorway for a while, and traffic simply has to stop or use another route. The bronchi may be looked upon in the same light. For repairs to be carried out on an air tube, it may have to be narrowed or completely stopped for a while. Total airflow is of course restricted, although the chest has considerable spare capacity and gas exchange in the lungs is not seriously embarrassed until terminal stages. Furthemore, the bronchoconstriction in asthma is patchy; while one area closes, others remain open [60], and these can change over time.

Moreover, when the airways are narrowed another effect occurs, mostly un-noticed as all attention is focused on the distress of breathlessness and the effort required to breathe. Although the amount of air passing through that stretch of bronchus may be reduced, its velocity is increased and the flow becomes turbulent instead of laminar [58,61], giving rise to a ‘scouring’ action that would encourage the mucus (and any particles or chemicals trapped therein) to become detached from the inner wall of the bronchus and be forced up towards the throat. This ‘scouring’ imposes shear pressure on the mucus making it more liquid (a process known as shear-thinning or pseudoplasticity – similar to the phenomenon of thixotropy utilised in paint), thus more easily removed [58,61]. Overall mucociliary clearance of ultrafine particles is not reduced in obstructive lung disease [62] (although there is some controversy on this) and if reduced it rapidly returns to normal on recovery [63]. Thus in this view, the affected part of the lung is being cleansed by the bronchoconstriction and the mucus secretion. They are indeed serving a valuable purpose, albeit at the cost of reduced overall function while the work is being done – as in the case of the motorway. This, we propose, is precisely what normal transient wheeze achieves during common ‘wheezy bronchitis’, provided it remains untreated.

But this effect would be seriously compromised by any drug which prevented bronchoconstriction. It would be like calling an ambulance to an accident, then shooting the paramedics for making too much noise. Denied its physiological cleansing mechanism, the body would be expected to redouble its efforts to repair the damaged stretch of bronchus, with even more mucus secretion and yet tighter bronchoconstriction, leading to the typical picture of clinical asthma – and yet more drugs and perhaps ultimately suffocation. An even more worrying possibility is that the lungs might be totally prevented from reacting to a toxic particle or substance (such as a lectin; see below), which instead passes unhindered into the pulmonary vein, straight to the heart and thence the circulation.

Beta-agonists certainly would be expected to do this, and at first sight it would seem that we must support the belief of most chest physicians that glucocorticoids (‘steroids’) should be used more aggressively, since steroids suppress inflammation. But there are three main snags to the use of steroids: (i) steroids, even the inhaled variety, are just too dangerous [64-67]; (ii) not all mucus secretion is caused by inflammation; it can also be stimulated directly by certain plant toxins called lectins (the mucotractive effect) [68], and there are lectins aplenty in pollen grains and other allergenic particles [69]. Steroids do not in general prevent the effects of lectins, which have the potential to affect most body tissues [69].

And even (iii) if we could find the perfect drug, that entirely suppressed not only inflammation (both immune and toxic types) but also mucus-secretion (both inflammatory and mucotractive types), so that mucus-plugging and asthma fatalities were abolished (one does just wonder whether cromoglycate might not fall into this category, for those cases in which it works [70]), it would still leave the body open to pollen and mite toxins – not to mention viruses - which can exert effects on distant, non-pulmonary sites and might be even worse. We therefore derive scant comfort from the levelling-off in recent years (perhaps even fall) in asthma deaths in many European countries [71]. There is some suggestion that they may have been replaced by anaphylaxis deaths [72, see below], besides which neurodegenerative, autoimmune, neoplastic diseases and those associated with obesity are all inexorably rising. We may simply have jumped, propelled in part by our anti-asthma drugs, out of the frying-pan and into the fire.

Allergens and Toxins

We are not arguing that allergy is always good for us – it can certainly get out of hand in some circumstances and at times of emergency the patient’s long-term benefit may have to be deferred in favour of living long enough to achieve it. But all of the above considerations lead us to conclude that everyone needs the ability to wheeze. In essence bronchoconstriction, with or without superimposed inflammation, is a natural self-cleaning and repair mechanism for the bronchi and, as with all biological phenomena, some people do it more readily than others. In healthy people, wheeze or even mild asthma helps to maintain that health. But what is the chest protecting itself against? Germs, noxious gases, and airborne toxins are obviously ‘bad things’ that should be removed if possible from the body, but what about harmless allergens like pollen grains, mould spores, foods and Dermatophagoides droppings?

Sadly, allergenic particles are far from harmless. In vitro experiments with pollen grains and housedust mites showed a startling degree of toxicity [73]. A single pollen grain can lyse about 100 red blood cells by its soluble, low molecular-weight toxins (probably plant amino acids). Dermatophagoides is just as bad. Grass pollen toxins, extracted and purified from all antigens (and thus incapable of causing an immune response) caused tissue damage and inflammation when injected into healthy human skin (4/4 volunteers, two allergic and two not), and this inflammation was not suppressed by steroids [73].

Plant toxins are frequently small molecules, like the pollen toxins above. They are too small to be noticed by the immune system, although they can still poison the tissues. They sneak in, as it were, under the radar of the immune system. Fortunately for us, Nature usually packages them in large-ish particles (like pollen grains and mould spores, up to tens of microns in size), and these also contain large molecules which the immune system does recognise. While the particles are in contact with the mucous membrane they can cause considerable damage [74,75], stripping away surface cells, exposing nerve endings and thus contributing to the non-specific irritability that is the hallmark of asthmatic airways. But eventually the immune inflammation drives the whole particle and its soluble products out of the body (albeit at the cost of symptoms). We must therefore be very cautious about using drugs that prevent this natural defence mechanism.

Amazingly, foods and food additives can also be poisonous (albeit slowly). Most if not all of the vegetable kingdom possesses intrinsic natural poisons, some of them very toxic indeed (like the microdose of ricin on the tip of the poisoned umbrella that killed Gyorgi Markov - ricin is extracted from castor-oil seeds [76]). The only essential difference between, say, tomatoes on the one hand and deadly nightshade on the other is the dose and structure of the poisons (alkaloids) in them [76]. The science of food toxicology has been well-known to farmers and vets for a century or more [77], but is only now dimly reaching the consciousness of medics.

At first sight it is difficult to believe a role for foods in asthma. Airborne particles and chemicals are one thing, they hit the lung directly, but how can foods get involved? Actually the connection is more intimate than one would think. Foods are ‘filtered’ three times before they enter the bloodstream, firstly in the intestine, which suffers a major loss of epithelial cells daily in the process but should, in health, succeed in digesting all proteins and carbohydrates to a state of harmlessness. Next to the liver, where enzymes (the cytochrome P450 system and others) detoxify those poisons - drugs, chemicals, other xenobiotics - that have evaded digestion in the gut. And lastly, via the portal vein and the right side of the heart to the lungs, where any residual poisons and particles should be ingested by phagocytic cells, and where, if an extra excretion step is required, those cells can be passed into the air spaces of the lung for expulsion via the ‘mucociliary escalator’, along with inhaled toxins. The lung therefore is deeply involved in the final elimination of dietary poisons, as befits one of the major interfaces between body and environment, and the same considerations apply to foods as to inhaled poisons. We can eat toxins and get rid of them in the breath. It should be remembered that the lungs offer the only portal for elimination of fat-soluble toxins as those are absorbed direct from gut lumen to lymph and thence straight to the venous circulation, bypassing the gut and liver. Their intimate relationship with lymphocytes during their journey in the thoracic duct will make another story another time [78].

If we block the pulmonary excretion route for dietary allergens with medication, it would be reasonable to expect their effects to be felt elsewhere in the body. Fatal and near-fatal food-allergic reactions are associated with well-controlled asthma [72].

It is worth considering in passing the action of antibiotics. These are the only drugs in the pharmacopoeia that do not act on the body but on invading particles from outside . And they are the outstanding success story of modern medicine, a shining example of how study of aetiology (causes) can reap far greater rewards than study of pathogenesis (mechanisms). We could be applying that lesson to asthma, but instead, modern clinical immunologists (unlike their predecessors) turn their attention largely to suppressing the patient’s immunology rather than utilizing it in his defence.

The Unwelcome Conclusion

No doubt many factors have conspired in the last 50 years to turn asthma into a killer, but van Bever et al have suggested the shocking conclusion (with which we reluctantly concur) that doctors may have been one of the main culprits. Van Bever et al put the blame on three paediatric activities, namely (a) switching from aspirin to paracetamol, (b) exhibiting broad-spectrum antibiotics and (c) advising allergen avoidance in newborns [79]. To that we add now a fourth - the use of effective anti-asthma medications.

Any drug, be it beta-agonist or any other class, that effectively stops constriction and inflammation of the airways, thus depriving us of an essential defence, must render the patient more susceptible to the direct toxic effects of the particles, viruses and chemicals that the inflammation was trying to remove, and is therefore likely to increase mortality – and not necessarily from lung disease. This effect will be in direct proportion to the drug’s effectiveness at relieving symptoms. The physician’s approach (prescribing physick) - if effective - must inevitably cause deaths one way or the other, sooner or later, and the harmlessness of asthma up to the recent past is because the medicines used in those days were ineffective.

There is no doubt that genuine acute asthmatic emergencies do happen. We have witnessed them, as have all doctors and many parents, and in that situation we have no quarrel with drugs, even beta-agonists. But in the long term we simply have no evidence other than the sustained epidemic of asthma deaths, because no long term trials appear ever to have been done [80] in which treated asthmatics are randomised at first presentation either to active treatment or to lifelong (or at least decades-long) placebo. Although Medline lists over a million controlled drug trials in asthma, the BMJ’s Clinical Evidence [80] is able, as we go to press in 2008, to cite not one trial examining the critical question of long-term safety – a stark comment on the slender evidence base of much clinical therapeutics. Indeed, such long-term trials will probably never be done, because medical triallists cannot ethically bring themselves to randomise any asthmatic into a lifelong placebo group, and today’s ethics committees would surely refuse any such application even if the patients (and parents) were willing to comply. There simply is no population of untreated asthmatics for comparison (although Steiner schoolchildren might come close to that, and they indeed have less asthma than controls [81]), so epidemiology and conventional pharmacosurveillance procedures are likewise of little help. The long term management of asthma is one huge experiment, the results of which we are witnessing today but about which we cannot agree because it is uncontrolled. Only placebo-controlled, randomised, long-term trials can provide the evidence [82] and we have been unable to find one.

Doctors are hostile and uncomfortable with thoughts such as these. This unease is based on the fact that although we are doing our consciencious best, the patients are still dying and the policies that we follow are based on incomplete evidence, hypothesis, pious hope and persuasive advertising by drug companies.

What To Do Instead ?

1)You could try Fox’s approach [83] to a new case of wheeze/asthma in a child - reassure the parents, manipulate the chest to mobilise any fixation and ignore the rest of the problem. The patient may be terrified but he will probably not die, and indeed will probably recover in due course unless you treat him. Few physicians (or parents) could however feel comfortable with such a puritanical approach, and of course it will not work for an established asthmatic, in whom the process has by now gone too far.

2)You could try to remove the most likely offending substances. In practical terms this could begin before birth, with pregnant mothers avoiding the commonest food allergens (and chemicals), continuing avoidance during lactation and at the same time reducing the Dermatophagoides levels in the house by well-established house-cleaning methods [84-5]. Although laborious this regime might prevent some allergy in genetically-susceptible babies [86] – or might make it more likely, as argued above [79].

3)You could try to find out what is causing that individual patient’s asthma. This starts by taking a history orientated towards cause and effect. Patients who are sensitive to inhaled allergens often know it and have observed that dusty environments, damp mouldy places, animal danders, feathers and so forth provoke their asthma. Sometimes the asthma occurs seasonally and is hence related to summer pollens or moulds which are prevalent at certain times of the year. Patients with housedust, dust mite and mould allergies usually notice that, if they have been fortunate enough to holiday in hot dry places such as in the Mediterranean area, their asthma is dramatically improved. Accommodation in these areas usually excludes carpets and similar soft furnishings and there is hence far less dust mite in such buildings. The hot dry climate also mitigates moulds. These patients are usually prick-test positive to dust mites, moulds, animals and feathers as well as summer pollens.

Other asthmatic patients do not have these features in their history and may be negative to inhalant prick-tests. In the past such patients were often given the label intrinsic asthma (whatever that means). In our experience such patients are usually food intolerant and sorting out their specific intolerances usually leads to a successful resolution of their problems. A strategy that is sometimes used in clinics such as ours is to put a patient on a few-foods ‘oligo-antigenic’ diet (a dozen foods that rarely cause allergic reactions). In patients whose asthma is related to food the symptoms normally clear within about a week on this diet. Re-introducing foods into the diet sequentially provokes reactions which vary strongly from one patient to another, although cow’s milk and the various grains such as wheat and maize figure predominantly.

Dr Derek Wraith, who was a consultant chest physician at St. Thomas’ Hospital and at one stage President of the British Allergy Society, contributed a whole chapter on asthma to the book Food Allergy and Intolerance by Brostoff and Challacombe [87]. In one paper Wraith described a series of 265 patients with asthma found to be caused by food or food additives, confirming studies done by Rowe four decades earlier [88].

Although avoidance regimes such as frequent hoovering (and possibly anti-mite chemicals) are sometimes helpful, bedding and mattresses can be enclosed in mite-proof covers and carpets can be replaced by tiles, these procedures do not help if the patient spends substantial time in other locations. There is also really no satisfactory way of avoiding atmospheric moulds or summer pollens, short of emigration to a desert clime. Thus avoidance procedures have a limited value and for effective treatment we nearly always have to look to some form of desensitisation. Further information on two modern desensitisation methods (neutralisation and enzyme-potentiated desensitisation) is found elsewhere on this site and in reference [89], where several double-blind trials are cited.

It could be argued that desensitisation, if effective, is exposed to the same criticism that we have levelled at bronchodilators and steroids, namely that by suppressing the natural defence mechanism of bronchoconstriction they lay the body open to other effects of toxins. True, the huge decades-long trials needed to exclude that possibility have not been done, but it is unlikely to be true because desensitisation does nothing to the functions of the lung, it merely returns the body to its physiological state. Also it is specific, affecting only the body’s response to the allergens treated, not to viruses.

The Way We Manage Asthma

Some patients may respond to simple desensitisation to a cocktail of inhaled allergens and may need no further treatment. After a year or so they are normally completely desensitised (“cured”) and can stop treatment. Other patients may become symptom-free on the elimination diet. Some patients are complicated by the fact that they have both food and inhalant allergies and they need both approaches, sequentially or simultaneously. More complicated cases involve both inhalant and food sensitivities and nutritional deficiencies such as magnesium, vitamins B6, B12 or others, although these can often be detected by laboratory tests.

We don’t know all the answers but these methods get about 80% of our asthmatic patients better and independent of us and other doctors. Apart from diet, nutrition and desensitisation, other therapies can also be helpful, such as osteopathy to mobilise a rigid chest and psychotherapy to help with the emotional overlay and family strains, not to mention complementary methods which work (when and if they work) by unknown mechanisms.


The idea that generated this essay was originally planted in DLJF’s mind by a chance remark from Dr Gordon Archer some 40 years ago, who commented one night, during one of the rare leisure moments in Casualty at Withington Hospital, how the doctors of previous generations had not considered asthma dangerous. DLJF’s curiosity was piqued and, looking up the textbooks of the previous century, found it to be so. Thank you Gordon.

DLJF later became an allergist and later still an Ecological Physician, and began committing these heretical ideas to writing in 1992, in a private essay circulated to selected colleagues. At that stage JM joined in with so much additional material that it became a joint project and was published in What Doctors Don’t Tell You under the names of both authors. The article has now been revised in the light of new information published since then. Honor Anthony, Dick Benton, Sybil Birtwistle, Jonathan Brostoff, Chris Dawkins, Damien Downing, David Katz, Stewart Morison, Sarah Myhill and Richard Turner provided helpful comments, criticisms and encouragement.


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