Many authorities in medicine admit that most of the drug therapies for asthma are making the problem worse.
One of the biggest medical failures of recent years is treatment for asthma. Despite greater diagnostic skills, better identification of causes of the disease and ever whizzier drug cocktails to treat it, doctors and asthma associations are stymied by the fact that the epidemic incidence of asthma and asthma related deaths are continuing to go up. Indeed, many authorities in medicine admit the cure is infinitely worse than the disease and that the drugs developed to alleviate symptoms of asthma are mainly behind the sharp rise in deaths.
Things have reached such crisis proportions that last April a UK task force on asthma was set up by the National Asthma Campaign to investigate why deaths are going up and how safe or appropriate the drugs are for relief of the problem. A similar study is also being conducted with participating medical centres from New Zealand, Germany, Britain and America. Here is the latest about the dangers of conventional treatments and a variety of alternatives for controlling your symptoms without drugs.
As with most allergies, cases of asthma are sharply on the rise. In a recent study of children in Aberdeen, cases diagnosed as asthma had more than doubled over a similar survey in the same area conducted 25 years ago. (The researchers said that part of the increase may be due to changes in diagnostic labelling that is, more wheezing identified as asthma and heightened awareness by GPs of respiratory symptoms.) But other enquiries suggest the real percentage increase may be higher; the UK asthma taskforce disclosed that treatment for asthma has doubled in the past 10 years. During that time, hospital admissions have trebled for all victims and risen fivefold among young children. In Britain alone, the number of deaths rose to 2000 in 1988 and has only fallen slightly since. This compares to a death rate of virtually zero before the 1950s.
Allergist Dr David Freed quotes a 1929 medical textbook (J J Conybears’ A Textbook of Medicine, published by Livingstone in Edinburgh) as saying, “It is doubtful whether death has ever been caused by uncomplicated asthma [ie, asthma without emphysema].” The rise of asthma corresponds to an epidemic of all forms of atopic (hypersensitivity) disease, including hay fever and eczema.
Why is this happening in such epidemic proportions? No one doubts that the hypersensitivity causing the muscles of the little bronchioles to constrict (and the tubes to become inflamed and filled with mucus) has to do with allergies. The conventional view maintains that the main culprits are grass pollen or the house dust mite Dermatophagodies pteronyssinus. This little creature is much more prevalent in homes today because of fitted carpets, heat and insulation, according to Sporik et al, writing in the New England Journal of Medicine in 1990. It is also believed to be genetic. One third of patients have a relative who has suffered from asthma, according to Dr Ruth Lever in A Guide to Common Illness (Penguin 1990).
In people prone to asthma, the low ozone levels of urban environments can make things worse, according to a Canadian study in the Lancet (27 July 1991). A recent study from France also showed that bronchospasm can be triggered by commercial polyurethane foam for insulating homes. But house dust mites seem to be a very small part of the story (see box, p 3 for other prevalent causes).
The root of the allergy could be a slight malfunction in the immune system, having to do with essential fatty acids (EFAs). American immunologist and WDDTY panel member Leo Galland, who has performed a good deal of groundbreaking work in this field, cites several studies in Superimmunity for Kids (Bloomsbury £9.99) showing that children with asthma have difficulty converting EFAs into prostaglandins which regulate the function of the immune system. Prostaglandins are controlled by enzymes; a vital one in converting omega-6 EFAs into an intermediate stage from which they go on to become prostaglandins is D-6-D, or what Galland calls the Delta Force. Galland has found that in children and adults with allergic asthma (as well as eczema and hay fever) the Delta Force is much less active than normal. “As a result,” he writes, “prostaglandin production is short circuited.”
Drug treatment for asthma is given largely on a suck it and see (or more properly, an inhale it and see) basis, ending up with the patient taking a medicine chest of potentially lethal drugs. Recently the British Thoracic Society published new guidelines for following a “step” approach, only graduating on to the next step in terms of potency of drugs if the step before hasn’t helped. It also advises that when control is established with one step, to consider moving down to the step below.
Step one begins with short acting inhaled beta2-agonists for patients who experience symptoms infrequently or with only mild exercise induced asthma. These adrenoreceptor stimulants cause the nervous system to act on adrenaline receptors throughout the body. But unless the drugs are highly selective, aiming only to stimulate “beta2” receptors (which relax bronchial muscles and reduce the chemicals causing inflammation) they can cause the heart to race and force it to produce larger quantities of blood, thus raising the blood pressure. In the past, doctors made use of non selective adrenoreceptor stimulants like adrenaline or isoprenaline, which work on the heart muscles. But other than for life and death emergencies, it’s now agreed that drugs like adrenaline shouldn’t be used since they can induce a heart attack.
The selective beta2-agonists of drugs are sold in the UK as salbutamol, or albuterol in the States (with brand names Ventolin ,Ventodisks or Salbulin), fenoterol (Berotec) and terbutaline (Bricanyl).
If inhaled beta2-agonists don’t do the job or you find you’re using them more than three times a week, the doctor moves up to step two, which includes anti inflammatories. Children are usually started on a six to eight week trials of sodium cromoglycate (Intal) three or four times a day. This drug, called a mast cell stabilizer, works by preventing the mast cells lining the bronchial tubes from releasing chemicals causing the bronchial muscles to contract. It is effective in preventing an attack from starting, but cannot treat an attack once it has begun.
A similar but more potent drug is deocromil (Tilade).
Most adults (and children who haven’t been helped by the sodium cromoglycate trial) are placed on inhaled steroids, which are supposed to reduce the daily dose and hence the general risks of corticosteroids. These drugs include beclomethasone (Becotide) and budesonide (Pulmicort). This anti inflammatory drug is used concurrently with a beta2-agonist inhaled up to four times a day.
Step three employs the same steroids but a more powerful inhaler. Dry powder inhalers have cartridges which blast the powder when you breath in, and utilize more drug than the usual pressurized aerosol cartridges. Another possibility is the use of a spacer, which offers a “space” between the inhaler and the mouth to allow more time for the propellant chemical to evaporate before the drug reaches you. There are also nebulizers which produce a spray, slowly releasing the drug into the bronchial tubes.
If this still doesn’t control your asthma or you have persistent symptoms at night despite all the other inhaled therapies, the BTS suggests that you move on to step four, increasing the daily dose of inhaled steroids and using an additional bronchodilator such as theophylline or aminophylline on top of the other medication. Theophylline belongs to a drug category called the xanthines, which includes caffeine. Theophylline works by relaxing the bronchial muscles and also breaking down a chemical that controls the muscles in the bronchial tubes. Another possibility is to take oral beta2-agonists, which release more drug into the body, or a non selective adrenoreceptor stimulant like ipratropium bromide, which affects your heart as well as your bronchial muscles.
If all else fails, you are put on a course of oral steroids, in addition to the other drugs in step four. You might even be given a trial of cyclosporin, originally developed to prevent the body’s rejection of organ transplants and now medicine’s drug of the month, investigated for everything from psoriasis to arthritis.
Beta2-agonists have been associated with an increased risk of death or near death. According to the Adverse Drug Reaction Bulletin (June 1992), which devoted an entire issue to asthma, the marked rise in asthma deaths during the 1960s in many countries “coincided with the introduction of high strength isoprenaline inhalers”. When the inhalers were withdrawn, mortality fell to previous levels. But the problems haven’t just been due to non selective beta2-agonists. In many countries, a renewed rise in asthma deaths occurred in the 1980s, particularly in New Zealand, which one study showed was linked to the popularity of fenoterol, but also theopylline and oral steroids.
Another study of beta2-agonists conducted by a variety of medical schools in America and Canada, including Montreal General Hospital and Yale University (New England Journal of Medicine, 20 February 1992) showed that the use of beta-agonists administered by a metered dose inhaler, specifically albuterol (salbutamol) and fenoterol, was associated with an increased risk of death or near death.
Several other studies have shown that regular inhalation of beta2-agonists cause “hyperresponsiveness” that is, excessive constriction of the bronchi (Journal of Allergy and Clinical Immunology 1985: 76).
The June issue of the Adverse Drug Reaction Bulletin postulated that beta2-agonists could be behind the increase in deaths by causing fatal abnormal heartbeats, spreading whatever the allergen is to more remote airways and thus increasing inflammation, or causing the bronchial muscles to constrict to a fatal degree.
Regular use of these drugs also causes the disease to worsen. Yet another study published in the Lancet in 1990 (336:1391:6) showed that patients receiving fenoterol regularly (that is four times a day) with additional inhalations as necessary had worse outcomes after six months than those given inhaled drugs only as needed. Regular use of certain beta2-agonists also causes a greater decline in lung function than does “on demand” use (The British Medical Journal, 7 December 1991). And some patients have been shown to have symptoms improve once doses of inhaled beta2-agonists are reduced.
The new long lasting and high potency beta2-agonists like salmeterol (Serevent), soon to be available for children, which control asthma symptoms for 12 hours at a puff, could exacerbate the problem.
Steroids used for asthma control pose many more risks than previously thought. Many doctors are turning to steroids as a first port of call after all the recent bad press for beta2-agonists. But recent studies have shown that inhaled steroids (which were supposed not to pose the usual risks that swallowed ones do) are not as harmless as medicine previously supposed. The consensus up until now has been that beclomethasone dipropionate (BDP) of 400-800 ug daily is appropriate for the 3-5 year old age group. However, a group of paediatric consultants from various hospitals in Britain wrote to the Lancet (14 December 1991) to point out various studies showing that this dose of BDP was the equivalent of 20-40 mg of prenisoline in causing suppression of the adrenal and pituitary glands. This dosage also produced significant growth retardation in a group of children studied.
Inhaled steroids have also caused symptoms characteristic of Cushing’s syndrome: obesity, moon face, thinning skin and stretch marks, as well as bruising.
Another unforeseen risk is that many otherwise benign infections become life threatening in children on drugs like steroids, which suppress the immune system. America’s Food and Drug Administration has asked manufacturers of all steroids to add the following warning on all drug packs: “Children who are on immunosuppressant drugs are more susceptible to infections than healthy children. Chickenpox and measles, for example, can have a more serious or even fatal course in children on immunosuppressant corticosteroids. ” Besides the disease itself, the risks of vaccination multiply (particularly with one employing a live virus) if a child’s immune system has been suppressed.
As for adults, some studies have shown that even low doses of inhaled beclomethasone (400 ug) per day) reduce bone formation (The Lancet 6 July 1991). Deaths from lack of adrenal gland function have occurred when patients have switched from oral to inhaled steroids without overlapping the drugs. There is also the problem of recurrent thrush of the mouth.
Because some of the drug escapes into the blood stream, even when inhaled, people on high doses run the usual risks of steroids. These include over activity of the adrenal glands, which produces Cushing’s disease, a fat abdomen, buffalo hump in the back of the neck, high blood pressure and muscle weakness.
Steroids can also cause muscle wasting, hyperglycaemia, water retention, skin atrophy, bruising and stretch marks, insomnia, serious mood changes, symptoms of schizophrenia or manic depression, possibly cataracts or glaucoma, menstrual problems, impotence, loss of libido or even allergic shock. More dangerously, prolonged use of steroids causes the pituitary gland to stop producing ACTH, a hormone which regulates the adrenal glands, needed by the body during stress.
All this in a drug which can only suppress inflammation, not cure it, by constantly masking what is undoubtedly a healthy allergic response.