Until the 1950s asthma was not thought to be a life threatening condition. Thus the Oxford Medicine in 1920 said: “Prognosis is excellent. The sensitive type probably never dies in an attack and the non sensitive type rarely dies in an attack”.
There is no doubt that within the last three decades we have witnessed a striking increase in asthma deaths. The International Consensus Report on the Diagnosis and Management of Asthma, issued recently by the National Institutes of Health, 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 weren’t used.Most concern about asthma drugs has focussed on the group called beta-agonists. After the upsurge in asthma deaths in the mid 1960s, there was a general perception among the public that asthma inhalents were dangerous; drug consumption fell and mortality fell. By the mid 1970s 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 (Recent Advances in Respiratory Medicine Vol 4, 1986, 1-11).
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 the airways leading to the lungs 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. Embedded in the mucus are numerous inflammatory cells (neutrophils and eosinophils), together with clumps or even sheets of epithelial cells (cells which normally line the inner surface). These patients have usually died in hospital after several days or weeks of increasingly aggressive treatment (J Allergy Clin Immunology 1987, 80: 415-6). 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 broncho-constriction that was the presumed cause of death (J Allergy Clin Immunology 1987, 80: 415-6).
The wheezing of asthma is caused by narrowing of the bronchi and bronchioles. This is caused by inflammation. 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 trauma.
Allergy, in immunologist’s terminology, is an immunologic process that leads to inflammation. In other words allergy is one of the body’s natural protective mechanisms. Asthma itself must be protective in some way against some insult.
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 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. Although the amount of air passing through that stretch of bronchus may be reduced, its velocity and turbulence are increased (The Lancet 1989, ii: 836-7), 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 effect would be seriously compromised by any drug which permitted the secretion of mucus but prevented it from being carried away (by preventing, the bronchoconstriction that sets up the scouring).
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 steroids should be used more aggressively, since steroids suppress inflammation. But there are four main snags to the use of steroids: (1) steroids, even the inhaled variety, are just too dangerous (Br Medical Journal 1990, 300: 1548-51); (2) they don’t always work (Clin Exp Allergy 1992, 22: 315-7) as for instance when the inflammation is caused not by an immune reaction but by direct toxicity and (3) not all mucus secretion is caused by inflammation. It can also be stimulated directly by certain plant toxins called lectins (The Lancet 1978, i: 585-6), abundant in pollen grains and other allergenic particles (J Nutr Med 1991, 2: 45-64).
Steroids also wouldn’t be expected to stop mucus secretion but merely prevent the mucus from being coughed up. The mucus would stay in the airway, getting drier and stickier.
And even if we could find the perfect drug, that entirely suppressed not only inflammation but also mucus secretion so that mucus plugging and asthma fatalities were abolished, it would still in theory leave the body open to pollen and mite toxins, which would probably exert effects on distant, non pulmonary sites and might be even worse.
Asthma, like other forms of inflammation, is actually a natural self cleaning and repair mechanism for the bronchi.
Experiments with pollen grains and housedust mites showed a startling degree of toxicity (Allergy 1983, 38: 477-486) causing inflammation. But eventually the immune inflammation drives the whole particle and soluble products out of the body (though at the cost of causing symptoms). We must therefore be very cautious about using drugs that prevent this natural defence mechanism.
It is the doctors who have turned asthma into a killer. Any drug, that effectively reverses constriction and inflammation of the airways, renders the patient more susceptible to the direct toxic effects of the particles and chemicals that the inflammation was trying to remove, and therefore is likely to increase mortality.