Positive Health Online

Why should this be?

The person in the street and many well-meaning organisations like Greenpeace put it all down to increasing outdoor air pollution, particularly the nitric oxide emissions from petrol and diesel vehicles. But, this does not explain why the least polluted part of the United Kingdom, the island of Skye, has a higher incidence of childhood asthma, 17%, than Aberdeen or Cardiff which are both around 11%[2]. Leipzig, in the former East Germany, with absolutely horrific pollution had, just after the fall of the Berlin Wall, a lower asthma rate than Munich which is far less polluted[3]. Leading authorities in the medical world have been asked to report to the government on the influence of pollution in our major cities. At the most it is thought to be responsible for about 5% of asthma attacks. As the experience of the island of Skye illustrates, if we all went over to using electric cars, there would still be a huge problem with asthma.

What then is causing this problem

Clearly, the increased incidence of asthma has been so dramatic in the last forty years that genetic change can be discounted. Genes spread very slowly. A mutant gene could not possibly spread so rapidly as to cause this sort of increase within two generations.

There is good evidence in the medical literature and supported by day-to-day clinical practice, that there are six main factors combining to produce this increase. They are:

1.) A vast increase in indoor air pollution compounded by the thermal insulation of houses.
2.) Over-reliance on drug suppressive treatment for asthma.
3.) Monotonous, repetitive diets, relying heavily on grains such as wheat, sugars, milk products, soy and yeast, which in turn can lead to a high incidence of food sensitivity.
4.) Progressive nutrient deficiencies, especially of the mineral magnesium.
5.) Increasing gut dysbiosis related to high sugar consumption, high usage of antibiotics and the contraceptive pill.
6.) An increase in nitric oxides in outdoor air pollution.

1 – Indoor Air Pollution

Our immune system can be likened to a defensive army which protects us from a huge range of insults that can be thrown at us by our environment. These include bacteria, viruses, fungi, yeasts, toxins and allergens. The prime function of the immune system is to distinguish between invaders that may be harmful from those that are harmless. Thus the immune system should act effectively against microbes which may cause disease, but should not react against harmless items such as pollens, dust, dust mites and food molecules. This act of learning to distinguish and shrug off items that are harmless is called 'tolerance induction'. This process occurs when we first meet a new allergen as a baby. In these circumstances it has been shown that an antigen, if inhaled, automatically induces tolerance and prevents any production of the antibody Immunoglobulin-E. It works through the good offices of the T-suppressor cells, but unfortunately this system is not well established in newborn rats or mice. Hence, at this time in their lives they can be relatively easily sensitised by inhaled antigens. This may well explain why, for example, human beings are more likely to develop hayfever if they are born just before the hayfever season.

Of enormous importance is the fact that it has been shown that even in adult rats and mice, the inhalation of certain chemicals can interfere with their induction of tolerance. High on the list of these chemicals is nitrogen dioxide, which, of course, is not only present in car exhaust fumes, but is also spewed out from gas cookers, gas and oil boilers. These indoor air pollutants are normally discharged into hermetically sealed homes where they remain for some time. Since the oil crisis in the early 1970s there has been a great increase in the effective insulation of houses which, from a heat loss point of view, is excellent, but this also succeeds in vastly increasing the levels of chemicals and also, incidentally, dust mites, in the average home.

Thus, if an animal inhales a fair amount of nitrogen dioxide, it can irritate the nose and adjacent upper respiratory system. If this animal then inhales an antigen, like housedust mite, to which it has never previously been exposed, it will not become tolerant in the normal course of events.

Sulphur dioxide, which was such a major pollutant earlier this century has also been shown in experimental animals to prevent tolerance induction, but most sulphur dioxide was always encountered outside the house and was therefore subject to dispersal in the atmosphere. Ozone, for its part, has been shown not to interfere with tolerance induction. These studies were performed on animals and it is not certain whether the same effect occurs in human beings. However, scientists think that it is almost certain as it is such a fundamental biological mechanism. Thus,

a) the house dust mite is by far the most common single cause of asthma in the UK. In countries more than 600 miles nearer the Equator, dust mites are rare.

b) it thrives in humidity occurring in hermetically sealed double-glazed homes.

c) gas and oil utilities are frequently used in these same houses and produce nitrogen dioxide which is also retained.

d) in an American study published in The Lancet, cooking with a gas cooker generated concentrations of 200-400 parts per billion of nitrogen dioxide with transient peaks as high as 1,000 parts per billion. By contrast, it should be pointed out that outdoor levels of nitrogen dioxide of around 400 parts per billion are only encountered during very severe outdoor air pollution which will only occur occasionally, eg peak levels of 382 - 423 parts per billion were recorded during the severe pollution episode in London in December 1991. Thus the levels commonly occurring in the kitchen are only occasionally observed in outdoor air pollution. Of very distinct significance in this respect, was a study published in the American Journal of Epidemiology[4]. This was a case control study amongst children aged 3 or 4 years old diagnosed for the first time with asthma. In these children there was a striking association between the incidence of asthma and nitrogen dioxide exposure as measured with a personal badge over a period of 24 hours.

e) other chemicals such as formaldehyde, trichlorethelene, phenol, etc., are used increasingly in modern homes and reach high levels in those homes. These chemicals emanate from things such as carpets, chipboard, soft plastics, etc.

We can therefore now begin to see a scenario which fits with the known facts concerning the increased incidence of asthma. It would appear that the concurrent inhalation of indoor chemicals, pollutants and biological inhaled allergens, such as dust, dust mites, feathers, moulds and animal danders, in modern hermetically sealed homes, is very likely to be the main reason why most asthma starts in the first place.

This concept would mainly fit the development of what is known as 'extrinsic asthma'. That is asthmatic patients who have a history suggestive of dust, dust mite and mould sensitivity, backed up by positive prick tests.

'Intrinsic asthma' has a totally different aetiology and in my view is mostly linked with food intolerance and gut dysbiosis, which I will discuss later.

2 – Over-reliance on drug suppression

Mast cell stabilising drugs, such as Intal, are probably entirely harmless. The beta-agonist drugs, such as Salbutamol (Ventolin) have a wondrous immediate effect, but have been shown in countless studies to have deleterious effects in the long term(5,6,7,8). These studies all show increased bronchial reactivity in terms of decreased peak flow responses to challenge by inhaled allergens after a few weeks of the usage of these drugs. As a result of these studies the medical world is gradually moving towards the use of steroids in more patients, but of course, steroids, even in their inhaled form, have some well documented dangers. The crux of the concern many physicians have, is that approximately 11% of all children have very mild wheezy episodes, which are often resolved spontaneously by the time the child is 10 years old. By labelling these wheezy episodes, asthma, which is not incorrect, they trigger the well-intentioned physician to prescribe beta-agonist inhalers which will give instant and spectacular relief. However, this may cause a benign transient wheeze to convert into a chronic condition needing ever-increasing drugs to keep it under control.

3 – A monotonous repetitive diet

Food allergy or intolerance has, in my view, been scandalously ignored as a cause of asthma, and accounts for a high proportion of patients who have been labelled intrinsic. Dr Derek Wraith, who until he retired was consultant physician to the Chest Department at St. Thomas' Hospital in London, published research about 265 patients with asthma found to be caused by foods or food additives. The asthma in these patients was quite severe. 26% of them were on continuous or intermittent steroids and 44% were on regular bronchodilators. After avoiding incriminated foods, the numbers using steroids dropped to 3% and the number using regular bronchodilators dropped to 20%[9].

Food intolerance is poorly understood by most physicians. The foods that are involved are the common everyday foods, such as grains, milk, sugars, yeasts, soy, eggs and suchlike. Because patients ingest these foods on a continuous basis, the response to them is never obvious, due to a phenomenon called masking. This mechanism refers to the phenomenon by which doses of a food consumed regularly will ameliorate the effect of the initial consumption of that food, in the same way that an alcoholic will find relief from further doses of the alcoholic beverage to which he is addicted. When food intolerant patients are placed on an oligo-antigenic diet, avoiding all the common food intolerances, there is characteristically a withdrawal effect for the first four or five days, followed by a dramatic improvement within seven days. When foods are reintroduced, selectively, after the seventh day, responses can be observed to foods and this is described in great detail in the Wraith paper referred to earlier.

Clinical experience indicates that the foods that most patients become intolerant to are those which are consumed most regularly and it would seem that rotation of foods would be helpful in the long term avoidance of this problem.

4 – Nutrient deficiencies, especially magnesium

Magnesium is essential for the relaxation of smooth muscle such as is found in the bronchial tree. If this smooth musculature goes into spasm as a result of an allergic insult, it is more difficult for the bronchioles to relax if there is inadequate magnesium. Recent studies in asthmatic patients have shown that the administration of magnesium during an acute attack is effective[10]. A recent US government survey found that the average American consumes less than 40% of the recommended daily allowance of magnesium. Dr Mildred Seelig, the leading authority in the world on magnesium deficiency, has suggested that over 80% of the American population is notably magnesium deficient. Poor soils, intensive farming practices, acid rain, certain cooking practices and food processing all remove a large amount of magnesium from our food. Magnesium deficiency has also been shown in rats to have an effect on mast cell stability. Rats were exposed to an identical allergic challenge prior to and after their diets were reduced in magnesium. The rats in their magnesium deficient state showed increased urinary histamine and blood histamine levels when challenged with identical allergens, before and after the induced magnesium deficiency[11]. There is, in fact, extensive literature now implicating magnesium deficiency in the aetiology of asthma.

5 – Increasing gut dysbiosis

In 1987, Gumowski and Girard published a study in The Annals of Allergy entitled 'Chronic Asthma and Rhinitis due to Candida Albicans, Epidermophyton, and Trichophyton'[12]. In the summary of their paper they state that during the years 1982–1983 all cases of chronic asthma exhibiting a positive skin test to either Candida albicans, trichophyton or epidermophyton were selected for the study. 60 of these cases were of asthma and 75 were of rhinitis. All went through various nasal and bronchial provocation tests with the specific antigens identified. An immediate response was discovered in 91 cases, 40 of whom were asthmatic and 51 suffering from rhinitis. A RAST-candida albicans was done in 64 cases. Results were positive in 52 patients and in 46 of these there was a correlation between the RAST and the provocation test. Hypo-sensitization treatment was given to 92 patients. After 2 years of treatment a good to excellent response could be observed in 60% of the treated cases. There have been other similar studies[13]. Hypersensitivity to these yeast organisms has probably increased due to the increasing use of sugar, antibiotics and the contraceptive pill. It is possible that the aetiology of approximately 8–10% of patients with asthma may be linked with a hypersensitivity to these yeasts. Certainly the author has observed many cases where the use of long term anti-fungicides, such as Nystatin and Amphotericin by mouth, combined with low sugar and yeast diets has produced marked improvement in selected patients.

6 – Increase in nitric oxides in the outdoor air

The levels of nitric oxides have undoubtedly increased in the past 50 years, both from traffic pollution and pollution from gas and oil burning power stations. There is a possibility that because of the very small particulate size, that these chemicals may have a relatively worse effect than sulphur dioxide has had in the past. This should not, however, detract from the fact that much severe asthma is suffered by patients in environments with very low industrially pollution.

This paper represents a very short summary of a theme that is much more extensively developed in my book entitled The Asthma Epidemic. In that book I suggest that there should be much greater emphasis placed on determining the aetiology of asthma in individual patients and that this approach, which myself and many other physicians now use, is effective in reducing the severity and incidence of asthma without undue reliance on symptom suppressive drugs.

References

1. P G J Burney, S Chinn and R J Rona, 'Has the prevalence of asthma increased in children? Evidence from the national survey of health and growth', British Medical Journal 100 (1990): 1306-10
2. Jane Austin, 'Prevalence of asthma and wheeze in the Highlands of Scotland', Archives of Diseases in Childhood 71 (1994): 211-16.
3. 'Prevalence of asthma and atopy in two areas of West and East Germany', American Journ. Respir. Crit. Care. Med. 149 (1994): 358-64.
4. C. Infant-Rivarde, 'Childhood Asthma and Indoor Environmental Factors', American Journal of Epidemiology 137 (1993): 834-44.
5. B Pipworth, 'Bronchodilator subsensitivity to Salbutamol after twice-daily Salmeterol in asthmatic patients', Lancet 346 (1995): 201-6.
6. Cockcroft, 'Regular inhaled Salbutamol and airway responsiveness to allergen', Lancet 342 (1993): 833
7. New England Journal of Medicine, Feb. 20th, 1992.
8. Journal of Allergy & Clinical Immunology 76 (1985).
9. D. Wraith, in Brostoff & Challacombe (eds), Food Allergy & Intolerance (Philadelphia: Balliere Tindall, 1987).
10. E H Brunner et al. 'Effect of parenteral magnesium on pulmonary function, plasma C-amp, and histamine in bronchial asthma' Journal Asthma 22 (1985): 3; H Okayama et al. 'Bronchodilating effect of intravenous magnesium sulphate in bronchial asthma' Journal of the American Medical Association 257 (1987): 1076; E M Skobeloff et al, 'Intravenous magnesium sulphate for the treatment of acute asthma in the emergency department', Journal of the American Medical Association 282 (1989): 1210.
11. 'A synergism of antigen challenge and severe magnesium deficiency on blood and urinary histamine levels in rats', Journal of the American College of Nutrition 9.6 (1990): 616-22
12. P Cumowski, 'Chronic asthma and rhinitis due to candida albicans, epidermophyton and trichophyton, Annals of Allergy 59 (1987): 48-51.
13. I H Itkin & M Dennis, 'Bronchial hypersensitivity to extracts of candida albicans', Journal of Allergy 37 (1966): 187-95.