Professor Ann Woolcock was born in Reynella, South Australia in 1937. She graduated in medicine from the University of Adelaide and pursued postgraduate studies in respiratory medicine at the University of Sydney. Her MD thesis, awarded in 1967, was on the mechanical behaviour of the lungs in asthma.
From 1966 to 1968 she worked at McGill University in Canada then returned to the University of Sydney to continue her work on asthma. Her research in asthma and epidemiology showed that asthma was caused by allergens but that there is a genetic component. In 1989, she wrote, with others, the world's first national guidelines for asthma management, the Australian Asthma Management Plan.
In 1984 Professor Woolcock was appointed to a personal chair of Respiratory Medicine. She founded the Institute of Respiratory Medicine, based at the Royal Price Alfred Hospital in Sydney, and opened in 1985. The Institute was renamed the Woolcock Institute of Medical Research in her memory in August 2002.
Interviewed by Professor Jonathan Stone in 2000.
Your life has been a great journey. Tell us about the beginnings – your family and Reynella.
Reynella is about 20 kilometres south of the Adelaide GPO. It used to be a country town where wine was grown, but is now part of suburbia. I went to Reynella Primary School and then to Walford House Church of England Girls Grammar School, in Adelaide. My family had lived in various parts of South Australia before settling in Reynella, where they had the general store.
Did your parents encourage you to go to university?
Yes. It was not quite clear what I would do, but it was accepted and they were very supportive. They didn't have very much money, so sending me and my two brothers and sister to private schools was quite a hardship for them. Following that, my sister and I went to Women's College – St Anne's – in Adelaide. My brothers, for various reasons, didn't go to the university but chose to do other things.
And you did medicine.
Yes. I started off in science, as it had been assumed I would, because at school I was much better at science than arts subjects. I was a really bad speller and I didn't write very good essays, and I used to come bottom in English – except in the Leaving Certificate, where I got a distinction, much to the consternation of my English teacher. But I could do science so I enrolled in that. After one year of science I wanted to do physiology and maths, but that combination was not offered in year 2. I investigated transferring to medicine, partly because I was having a really, really good time as an undergraduate (especially away from home) and I thought that six years of medicine would be much better than three years of science. I hadn't matriculated for medicine, however, because I did not have a foreign language – I was very bad at French, not only at English – and during the holidays after my first year at uni I had to swot up and sit for a supplementary in French. So I matriculated in medicine, and went into second year of that.
Did you find Adelaide University a quiet place, or a bit radical?
I was on the SRC and on the Union, and a member of at least six clubs, including the Dramatic Society. The university was much engaged with the town, and we used to have a huge amount of fun compared with students today, I think. We used to have Prank Day and Procession Day, and did things that would tease the Vice-Chancellor, like putting nude statues up flagpoles. Such things were daring and very funny, we thought then. It was a good place, small enough for us all to know each other – 120 people (13 girls) in medicine.
You graduated at a very high position in your year, and fairly soon came to Sydney. What brought you here?
After doing my first year as an intern at the Royal Adelaide Hospital I decided to leave, even though Mr Lendon said, 'They'll never have you back again, you know, if you leave.' I went to Broken Hill for my second year out: one of my friends was going, I had known the place as a small child because my grandfather had been working there, and the job in the Broken Hill and District Hospital seemed like a good one for me to learn how to do everything. Certainly I learnt how to do everything very quickly, from autopsies to cardioversions to diagnosis, through to deliveries of babies.
I had the best of both worlds there. I had fun with the miners – I could see them as outpatients and then go and see them at weekends – and the medical fraternity was part of the Establishment, so when any important ABC visitor came we were always invited to the concerts and things. I had a really great year in Broken Hill but I could not spend my life there. Yet, about halfway through that time, I decided not to go back to Adelaide. I wanted to do research, largely at the suggestion of Sol Posen, an older person with whom I became very good friends when he tutored me and some others during our final year of medicine in Adelaide. He was very interested in research and convinced me that it was good to ask questions.
So from Broken Hill I wrote to the professors of medicine at Melbourne, Sydney and Brisbane and said, 'Do you have any jobs doing medical research?' The only person who replied was Ruthven Blackburn, from Sydney, who made a list of the jobs going in research: one at Royal North Shore Hospital, one in pathology at the University of Sydney and one at the Page Chest Pavillion, at Royal Prince Alfred Hospital. I came down and had an interview for those three jobs. I could have probably chosen any of them, because in those days there were more jobs than there were people, but I chose the one in the Page Chest Pavillion – which I had seen advertised and thought was for a more senior person, because I didn't have any qualification except two years out. It was to set up a lung function laboratory in the Page Chest Pavillion. Until that time all the lung function tests had been done in the Blackburn Building, the patients having to be wheeled across from the Page and then back again.
Up and down the hill.
Yes. I was given a room in Page, started to buy some equipment and gradually set up a lab there.
In 1963, during my first year in Page, John Reid (the Professor of Respiratory Medicine, who had employed me) said that John Colebatch and Denis Halmagy, who had been using a lab in the Blackburn Building, were leaving. There was a room and equipment, and I should set up to do some research experiments in asthma because the Asthma Foundation was just being set up. So I started to do some research on asthma at the same time as I was setting up the lab in the Page Chest Pavillion. The next year I transferred to an Asthma Foundation scholarship, and then I did three years for an MD thesis.
John Reid would then have been close to the peak of his career. Were you able to interact with his forward thinking?
To some extent, although I was always regarded as 'the little girl from Broken Hill'. He already had several very bright people working with him as scholars, most of whom had first class honours from Sydney, but he was always very good to me. And then I was very good to him, gradually helping him with junior people as I got more senior, and helping him run the lab.
I suspect that doing that MD shaped much of the rest of your work.
Yes, but it was only an accident that I did the mechanical behaviour of the lungs in asthma: I had Asthma's grant, and the equipment available was for studying the mechanics of the lung. John Reid was a gas exchange person, not a mechanics person, so bit by bit I had to teach myself how to use that very old equipment – four transducers, four transistors, and very old polygraph recorders.
What finding of your thesis do you remember most kindly?
Well, I used to wheel patients who were still having very severe asthma attacks, complete with their oxygen and everything, over to the Blackburn Building – my hair stands on end now – and measure their lung volumes. I showed that during acute severe asthma the lungs overinflate a lot and then come down again. Although chest X-rays are taken at total lung capacity and you can see the lungs big and getting smaller, it hadn't been realised how much bigger they actually get. Then I measured the elastic recoil of the lungs, showing that although the elastic recoil in chronic asthmatics stayed higher than usual, it could change too. The way in which that happens has still not really been explained. If you bring the lung up and hold it, it is a bit plastic, so you can actually stretch the whole thing and it will stay up there, but then gradually you can bring it back again. We are now going back to do some studies to see how much of that is irreversible.
Another interesting finding came about because my husband had started the Department of Nuclear Medicine – the first; there were no nuclear medicine bits in any other department of medicine. The professor there allowed us to do perfusion, mainly, but also perfusion ventilation scans (some of the first that were ever done). We did those during an acute asthma attack and showed that the perfusion was really very abnormal and got better as the patient got better from these acute attacks.
With so much under way, you went to McGill. What was that period like?
That was a terrific period of exactly two years (I arrived on 1 September '66 and left on 1 September '68) during which I published seven pretty important papers, mostly on dog work. I hadn't done any dog work here, and so that taught me how to do different things. I was looking at the large and the small airways, the mechanical behaviour of the lungs, and collateral ventilation and things like that in the lungs.
I understand you developed a test of the resistance in the airways.
That's right. The test, called 'frequency dependence of compliance', is not done much now, because it requires the patient to swallow a balloon through the nose. It's uncomfortable and there are probably other ways of doing it, but at that time it was the standard sort of test and it made everybody think about how to measure the small airways. That is the hardest part of the lung to get to and we still don't know how to do it very well. You can get to the alveoli through the pleura, and you can get to the large airways via a bronchoscope, but in between is difficult.
Such productivity and novelty in your work would probably have allowed you to stay over there, but you came back.
I had plenty of offers to stay in the lab at McGill or to go to other places in North America, because by that stage I knew a fair amount about the mechanics of the lungs and I had been fairly productive. But for a whole lot of reasons I decided to come back to Australia. Put it this way: it was better to be a big fish in a little pond than one of the many fish in a big pond.
When you returned to Sydney, the damaging effects of cigarette smoking were slowly beginning to be realised. You made major, influential epidemiological contributions in this country. Can you tell us a little bit about them?
This all started because my husband was interested in the epidemiology of liver disease in New Guinea, and I asked if I could come as a pair of hands when he was doing epidemiological studies. He said, 'Yes, but don't worry about the liver. It's not your subject. Why don't you think about why virtually everybody coughs?' In New Guinea, coughing is said to be part of aging. I started to learn some epidemiology and we found there was no asthma in Papua New Guinea but a lot of chronic obstructive pulmonary disease (COPD). It was quite severe and people died of it early. When we started to define this disease, we found some very interesting things: the COPD can arise in non-smokers, it may be more prevalent in women than men, and it is not just in people living in smoky houses. (It was present also in people living on the coast, where it is hot.) We did many studies and published a lot on this disease, and that is still the definitive work because studying asthma became more fashionable. People are only now starting to go back to measure COPD in developing countries.
Then, on one of our trips to New Guinea, we heard somebody giving a sermon at the Baptist mission at Baiyer River (and it sounded a pretty good sermon to me). The speaker was Stephen Leeder, who with his wife was there for a year. We started talking to him, asking what he was going to do, and so when he came back to Sydney he did a PhD with us on a project that we had started to do, to see if smoking in primary and secondary schoolchildren did in fact affect lung function.
That was a huge study funded by the Tobacco Foundation – it was all right to have Tobacco Foundation money in those days – from 1973 through '75. As research assistant to collect all the data we appointed Jenny Peat, an honours BSc from the United Kingdom who had just come out here with her husband, Derek Peat. (He ran the continuing education for a long time.) We set up with the Department of Electrical Engineering in 1972 to try to get this computerised, and you should have seen the funny computers we had. Having done that study for his PhD thesis, Stephen also published the results: there were effects on the lung function of children, very early, from smoking.
Perhaps your longest-term interest has been asthma. It is a challenging enigma of a disease, with all sorts of genetic and environmental factors. Clearly, one that has been important in your work is allergens, particularly those related to insects. How did that story unfold?
Working with my husband in New Guinea had taught me a lot about epidemiology, a useful tool to find out what things were changing and what the risk factors were. Then we started thinking about the epidemiology of asthma, setting up some epidemiological studies really properly to get a test of airway hyperresponsiveness which we could do in schools. We used a questionnaire and we had the skin prick tests to look at allergens, and airway hyperresponsiveness tests. We set up a protocol but we had lots of stops and starts in getting the methods right. By 1982 we had funding and things were ready. With Jenny Peat, we did studies in Wagga Wagga and a suburb of Newcastle, Belmont.
At about the same time, Wes Green was over in the Department of Medicine measuring house dust mites. Then Euan Tovey came to work with us too – he had done a doctorate with Brian Baldo at North Shore before working overseas with Tom Platts-Mills, the leading house dust mite person in the world, and had returned to North Shore. He was the person who discovered that the major allergen in house dust mite is in their faeces, and he has been interested in that ever since.
Do antibodies to that turn up in asthma patients?
Yes. So when we were doing these epidemiological studies, not only did we measure what was in the children but we went to their houses and vacuumed their beds, or got them to bring dust from their vacuum cleaners, so we could know how much house dust mite they were exposed to. Throughout the 1980s a big controversy raged about whether asthma caused allergy or allergy caused asthma, or whether they were two phenomena in the community that happened to be related. It was clear to me by 1990 that allergy is the hugest risk factor. If you do a logistic analysis on all this epidemiological data from children, there is no escaping that the major risk factor and therefore cause of asthma is being allergic. It is allergens.
I gave a talk at the 1990 meetings of the American Thoracic Society in which I dared to say that I thought asthma was caused by allergens. This was at a pulmonary meeting, not an allergy meeting, and pulmonologists are pretty conservative people. The audience gasped, that I would dare to say something so dramatic. But now, 10 years later, everyone accepts that most of asthma is driven by allergy, even though we don't understand the relationship.
What is the current buzz in allergens?
The problem is that up to 50 per cent of the population and 40 per cent of children are allergic, but only 10 per cent have asthma as we know it. Not all allergic people have asthma, and that is still not explained. There seem to have to be two abnormalities: being allergic and having some other abnormality that turns the airways on to being hyperresponsive.
It seems that to become allergic you have to have a gene (which runs in families) to make a specific IgE when you inhale an allergen. But that gene seems to be present in about half of the population – and it does not seem to be related to race. All races can become allergic, although there is some suggestion that Chinese might be more allergic. The ability to actually get asthma is much smaller, and it is infinitesimal to zero in some populations. For example, children of Australian Aborigines living in the desert in Central Australia virtually have no asthma. In Papua New Guinea village life, they have no asthma. In an Eastern Suburbs home in Sydney, however, you find that up to 30 per cent of the children have wheezed at some time, and probably 11 or 12 per cent of them actually have asthma.
The reason for the huge difference seems to be environmental. The Aborigines are less allergic as children but the parents have the same degree of allergy, of skin test positivity, as Caucasians. So it is as if they acquire the atopy later. And acquiring it later in life does not seem to have as big an effect as getting it as a child. So we know that if you could delay the onset of atopy it would be important.
Whether atopy is actually increasing in the world is not known, because no-one besides us has done serial measurements on the same population cohorts. In Australia it does not seem to be increasing much; it seems that what is happening is that more of the allergic people are getting asthma now. But some of the factors – not just genetic but environmental – associated with being atopic are becoming clearer. There's some interesting data. For example, in large families, the fourth and fifth siblings are very rarely atopic or allergic. If you send your child to child-care, they are less likely to get allergies than if they stay at home.
Some data from New Zealand shows that the more antibiotics given, the more likely children are to be atopic. And the fewer the antibiotics, the less likely they are to be atopic. That suggests that if you get infections, particularly bacterial infections, early in life, you are a bit protected from becoming atopic. More recently, the Italians found that recruits going into the army who were positive – had antibodies – to Hep A and to E. coli and other bacterial gut pathogens were less likely to be atopic. So something to do with eating a little bit of dirt or being exposed to bacterial infections seems to protect you from being atopic.
We still don't know what makes only some people who are allergic get asthma, but those things seem to be related to exposure and to diet. It's a bit complicated. If it was easy, someone would have solved it.
Asthma being such a widespread, enigmatic disease, any number of hopeful 'cures' must have to be dealt with.
Every week the media report another 'breakthrough for asthma'. We just plough on. I still get an enormous number of people ringing up because Mrs Somebody said such-and-such, or somebody in the press heard this and is it true, or there has been a breakthrough because somebody has got some new cure. You have to take it all and say, 'Well, we'll wait and see when everybody else has repeated the work.'
Will the Russian breathing control method succeed, or is it going to die?
I think it is going to die scientifically, but not commercially. A lot of asthmatics are sick of doctors and sick of their steroids – they want something to do, don't mind paying the money, are part of a group feel-good – and so the breathing control people are offering a sort of service. It is possible that the way you breathe has an important influence in how severe asthma is. But they have the idea that CO2 is a bronchodilator, and if you hold your breath the CO2 goes up, dilates your airways and 'cures' your asthma. That doesn't make any sense. Although CO2 is a bit of a bronchodilator in animals, if you give people with asthma CO2 to breathe, put their CO2 up a bit, they do not bronchodilate very much.
There are many new theories about how the smooth muscle is controlled by ordinary tidal breathing, so the Harvard School of Public Health is working on the ordinary tidal breathing of rabbits, changing the rate and the frequency and their depth of tidal volume during stimulation to make their airways constrict, like an asthma attack. Actually, just our tidal breathing as we sit here now is enough to stretch the smooth muscle and the airways. If we stop doing that, the smooth muscle undergoes less and less hysteresis and gets stiffer and stiffer unless it is kept going by some means. It can go into a state of latch bridge – the actins inside the myosin – where the thing is contricted to its minimum size and all the bridges are acting so slowly it is stuck. To open it and pull it back to its original length takes a lot of force, a lot of stretching and probably a lot of beta agonists. So there is a doubt about the rate and depth of breathing in someone who has already got asthma – this is not going to bring on the disease, but someone with the disease – keeping all the muscle in a nice fluid state.
For the individual asthma patient – forgetting about the community – death and morbidity rates have fallen. What have been the great breakthroughs?
During my career, the death rates went up in the early 1960s, down in the '70s, up in the '80s and down again in the '90s. This seems to be related to treatment and treatment ideas. Treatment now is excellent: the drugs available are really good, so virtually every asthmatic can be controlled if they get the right doctor who knows how to do it. The problem is that it takes time and effort.
Is the right treatment multifactorial – reducing the allergen exposure and so on?
Yes, but that's one of the things we really still don't know. If you take children and put them in the alps, or if you put people in hospital away from their allergens, they get better, irrespective of everything else. We know that allergen avoidance works.
In the real world, people are exposed to a lot of allergen all the time, and reducing it in a house and keeping it out (particularly in Sydney) is very difficult. It's in your clothes and everywhere. We do make an attempt to ventilate houses, to have covers and so on, to reduce it as much as possible, but the most important thing is the right treatment – which has to be begun early until control of the asthma is achieved, and then kept going. That means people taking inhaled corticosteroids if they have persistent asthma.
Most people are happy to do that these days, but when their symptoms go away they stop their treatment. Just stopping the symptoms doesn't get the whole thing under control. So it's a big effort to educate people about what we are aiming for. Asthma is such a variable disease that it's hard: it doesn't really matter what some people take, they're still going to live to 90 without much impairment, whereas other people are really going to have their life shortened or a lot of morbidity unless they undertake the treatment. They have to be found and time spent with them, just as in diabetes.
Let's look at how you forged your career. After university in Adelaide, clinical experience in Adelaide and Broken Hill, research in Sydney leading to your MD, and two years in Canada, you found yourself in Sydney again, working hard – and visiting Papua New Guinea for epidemiological research. How did you manage?
At the end of 1968 I was just married and I didn't really have a job. I did have the third year of a travelling scholarship from the Asthma Foundation, so I had money for a year. I came back to John Reid's laboratory and set up some things I wanted to continue from overseas, particularly with excised lungs. After that I didn't really have any money. I got the Basser Fellowship from the College of Physicians for a while, but it didn't seem to worry me that I still didn't have a job. I did research but to earn money I went out and did clinical work at Concord Repatriation General Hospital, North Shore and the Prince Alfred. So I travelled a lot around Sydney, learning a great deal. But during those years, '69 through '73, I had two children and I had to pass my Fellowship exams, which I hadn't done before I went away. And I gave talks at meetings and things.
Not having a fixed job, I didn't have much teaching. Mainly I was looking after my two children but I became the Clinical Supervisor at Concord, looking after the students in the clinical school, which was fun and did involve a fair bit of teaching. I had quite a number of PhD students. And so my head was down, basically – I wasn't too worried about anything else except doing research.
They must have been extraordinary years.
Yes. But I should say that by 1969 I was 31, I had an MB BS MD FRACP (it was actually MRACP in those days), I had 30 publications, and I was married, with a child. No-one can do that at 31 any more. I had been able to go to university at 16, graduate, and then spend the year I was 22 as an intern. I could do three years here for my MD, then spend six months seeing the world and two years away, come back and sit for my membership, and nobody cared that I hadn't done all the set tasks that people have to do now.
They make you queue longer these days.
In 1971, John Reid killed himself. That was very tragic, because his was a great mind. He was way, way ahead of his time in the experiments he did. He did ventilation perfusion and the distribution of ventilation with xenon, with Kemp Fowler, a long time before anyone else, and he made a rat model of five per cent hypersensitivity to pneumonitis before anyone else had even thought about it.
It was hard to replace such a bright man. Australia couldn't really afford the salaries, et cetera, to replace him with a professor who was overseas, such as John West. Eventually, in 1973, the job was advertised as a senior lecturer, and I applied and got it. That was my first full-time job. I just stayed there and then I became associate professor and later a professor. And that was that.
Was there a 'glass ceiling' in those years?
No, I don't think there was. I just came up through the ranks and I don't think I was ever discriminated against because I was a woman. Perhaps I was unlucky, in that although John Turtle and I were the short list of two for my husband's job when he retired and it was a complete toss-up between us on our CVs, John Turtle got it and I didn't. You could sympathise with the university for not giving the job to the retiring person's spouse. That's a marriage ceiling, not a glass ceiling. I didn't appeal against it, because John Turtle is a great guy and he has done a lot, and he's been good at that Chair. And they gave me a Personal Chair in respiratory medicine at a time when they had only one other, in physics.
The man you married had a great career of his own – he was the great builder of his department. What was his intellectual influence on you?
Very early on, when we were first married, he said that if you wanted to be an academic you could be and you should be. He pushed me, saying that I should never say no until I had reached enough maturity and established myself that I could say no. So I said yes to everything. He helped me a lot. If I wasn't home for dinner or the children needed help, he was very supportive. There was never a problem. And he has been very helpful in giving me advice about how to proceed next – because I tell you, it's getting harder, not easier. He is unbelievably supportive of me.
In addition to your own children, your postgraduate students (I have a list of well over 20) could be called your academic children. They include our current Dean, Stephen Leeder, and Iven Young and Norbert Berend.
Iven has been the head of the unit at Prince Alfred since I stopped in 1993 – after nearly 20 years, from 1974, a long time. Norbert Berend is the general manager of North Shore Hospital at the moment. He went there from the respiratory unit.
So yours has been a major influence. This must have been an extraordinary group and you must have a lot of bright memories of them.
We had a lot of good times: they shared a lot of data and worked very well together, and that's good. But in the days when those graduate students were coming through, there was more time. We could actually have morning and afternoon tea, and discuss politics – we could even go camping on weekends. Students these days don't get to do such things nearly as much.
You still have some postgraduate students, though.
Oh yes – a few too many. They're all very good. Some are women whom I persuaded to do their PhDs (part-time) because they needed to have had them years ago.
The thesis of one of your students was on ethnic variations in lung function. How did that come about?
That came about because we were very interested in why the lung function and the vital capacity, which we usually measure against age and height, was different in New Guinea. It was even different in the highlanders from the lowlanders. I got interested in the shape of the chest wall as a determinant of lung function. There are very big ethnic differences, but we have now come to the conclusion that lean body mass gives a very good correlation with vital capacity, and it seems to be totally related to growth hormone. The amount of growth hormone that is produced will result in a lean body mass and a size of lung which is exactly appropriate for your activity. So if you have a big lean body mass you're going to have big lungs. You can get a big lean body mass by living in the mountains, where you have to climb up and down, or becoming a swimmer or a rower, particularly in an Olympic team.
Such people look like highlanders, as it were?
That's exactly right, whereas some ethnic groups – particularly Indians, for some reason – who aren't necessarily very athletic have different shaped chests, and smaller lungs for their height. They fall off this curve of lean body mass versus vital capacity.
Have the groups who have lived such long periods at high levels evolved with a genetic difference, or is it really a response to where they live?
I don't know. The only way you could find that would be to study children of the highlanders who had only ever lived on the coast. There's a great deal of variation and you're looking for tiny differences. Vital capacity is reproducible to two or three per cent, so you have to do a large number of people.
A major part of your career has been at the Institute for Respiratory Medicine. You have been its director since the mid-1980s. How was it founded?
Well, in about 1980 my husband said to me, 'Money is going to get difficult in the university and in the hospital. If you want continuity of funding for your different groups doing all these things, you need an independent source.' And so we set up the institute. He was very helpful: he went to Sir James Vernon and Mr Keith Steel, who at that stage were the heads of AMP and of CSR, and although they did not actually help raise much money they helped me establish a constitution, get incorporated, get a correct board and get all the nuts and bolts in place so we were totally independent. And we got MOUs with the university and the hospital so that we are in the hospital, from which we get our accommodation and certain things, and from the university we get salaries, like mine. We try to marry the two, to get the best of both worlds while being independent of either. So I can appoint a secretary and not worry about what the university's salaries are, but I put all my National Health and Medical Research Council grants through the university, so the university gets the kudos. We are like a department in the university, trying to pioneer a new kind of institute – practical and very clinical – separate from others like the Howard Florey or the Centenary.
Do you see a lot of patients?
Yes. We have clinics over in the medical centre, and many of the patients we see there we use for experiments or for clinical trials. We're very much into nurturing young clinicians who show an interest in research. That is very hard in this environment, and getting harder.
Is the Institute for Respiratory Medicine returning to epidemiology?
No, we've been doing it all the time. We have now about eight groups within the institute, from epidemiology through. We have an asthma group that does clinical trials and an asthma group that studies physiology mechanisms, an allergen group and an epi group (which studies mainly asthma but also, as a tool, does epidemiology of sleep disorders, COPD and TB). Then we have a cells group, which is quite small, and the molecular biology group which works a bit with Judy Black and with Immunology. We don't set that up separately: I'm very much for building networks and having people work together rather than reinvent the wheel. Then we have a sleep group, a paediatric group and a cystic fibrosis group, mainly over in the hospital. And – I've just been doing the finances – we have an 'other' group of all sorts of people who want to bring money in and find it's more sensible to work in the institute, where we've got a bit of space, than in a hospital or in the university. But it's a bit complex.
Sometimes the most creative things are not perfectly plain.
That's what's good about it. If we can get all the groups together, we have a meeting every Friday morning and everyone can say, 'This is what I am going to do. What do you think?' People from other things can come in and say, 'Look, from an epi point of view you should do this,' or 'This is the questionnaire you should use,' or 'Why don't you get some blood and send it to So-and-So.'
I understand that late last year the institute became part of a new cooperative research centre. Where is that going to take you?
A long way, I hope. It is a CRC for Asthma, one of four new CRCs given last year. It is between the University of Western Australia, Phil Thompson; Monash University, Robin O'Hehir; Sydney University, mainly at the Children's Hospital; ourselves; and the Garvan Institute. With 13 projects, over seven years, our aim is to reduce the burden of asthma – working mainly from what we know about asthma right now but a bit more on developing new techniques, new methods of diagnosis, new methods of drug delivery. We want to get better diagnostic tools for the GP. It is going to take us into the community more, and towards networking with other people. It has just started, and there is a huge amount of work to do to set it up.
You mentioned nurturing young clinicians who are interested also in research. Having lived with the hospital, the university and the institute for some decades now, how do you assess the future of that relationship? Does it need working through?
Oh, it needs a lot of attention. The NH&MRC has just got some clinical fellowships to allow people, if they want to, to have a career like mine – doing clinical work and relating to patients, and doing clinical research plus basic research. Basically, 90 per cent of people differentiate themselves very quickly into pure clinicians who get their satisfaction (what I call their 'lollies') out of seeing Mrs Smith one to one, asking Mrs Smith her problems and getting her better. There's another group who get their lollies out of research: they really want to say, 'Well, how did this virus get in? Let's see if we can measure the virus,' and are quite interested in lots of viruses.
Very few medical graduates, perhaps only 10 per cent, are really quite good at and want to do the clinical bit – it's a pleasure to help Mrs Smith – while also asking some questions. It's very demanding, because clinical work and research each take a lot of time, and to do both well is quite hard. There is no mechanism for it. Even if you can get that balance, the university wants you to teach and administer on top of doing your clinic and research, and it's not possible any more. And if you get into the hospital, although some of them aren't too bad, mostly they're expecting you to do clinical work. A staff specialist job is very busy and you're just eaten up by the time – you need great strength to go home and then write up papers, or do experiments. We need a system that nurtures the interface between clinic and research.
The NH&MRC and the Wills committee addressed this to some extent, but we need it to be brought to everybody's attention more and more. Basic scientists and clinicians have their problems – not enough money and all that – but they can go off and do their basic things. But unless you have the interface, you don't have good teaching, you don't have good progress, you don't have good things coming back to the patients about what they should do. This is very evident in the United States, where there is a huge gap in respiratory medicine between the clinicians and the basic researchers. Australia has done well in preserving people like myself and the people I am trying to train. People like John Reid, and before him Landy, really cared about this interface and nurtured the young ones who could do it, and that's what I want to keep doing.
How do you advise your postgraduate students now? Do you say, 'Come and enjoy these three years, but then life is going to be hard'?
They're all very different. Mostly I say, 'Come and try it. See how you like it.' And sometimes you get a surprise – you think someone is not going to like it but it fits them like a glove; you think other people are just turned out for it, but they don't like it. I've had people who have lasted only a week in the lab: they say they can't stand it and you find them back in the wards all the time, because wards is where they want. You have to acknowledge that and change the direction of what they do. And some people just get the training for a piece of paper so they can get a better job. You have to take the good with the bad. If I get one in four who is a real-life clinical academic, then I'm doing really well. That's what I am trying for.
When you look forward to what you are going to do with the institute and the centre, what are your hopes for new steps that will decrease morbidity and mortality?
We have to make very simple protocols that people can understand. We are going towards giving people electronic diary cards, which people seem to love and which work very well: they record data about their symptoms in the last 24 hours and how much bronchodilator they have taken, and then they blow into this machine which records a month's worth of data and downloads it. They can see for themselves what has happened to them over the last month, and adjust their therapy. If you give people a peak flow meter and ask them to record the reading on a piece of paper, some obsessional people do it but some people don't do it at all, and others do it in a higgledy-piggledy way. If you can get rid of the paper and pencil and just have one piece of apparatus which they only have to press Yes/No on as an answer and blow into, it seems to work extremely well.
The drugs are getting much, much simpler. It used to be that you could take your choice of 10 drugs but doctors didn't know quite which one to give: 'Try this,' and 'Try that.' I think that guidelines will be there for the 'gold standard' of treatment and what you should expect if you use two kinds of drugs – you probably only need two kinds. It will become simplified: if you can't get control with other drugs, you'd better go back and use these two classes of drugs.
Is the strong genetic component going to offer a way through?
I wish it would. People know that allergies run in families, and which families have what. You can soon find that out with skin testing. There is clearly a genetic component to the other abnormality, the hyperresponsiveness or whatever it is that makes the airways narrow too much. On the island of Tristan da Cunha, everybody is related to one of the four men who established families there. Two of those men had bad asthma. A huge number of people on the island have airway hyperresponsiveness, but only some of those have the symptoms of asthma. It's clearly something that is inherited, but what that is we don't really know. It could be many, many things, such as the structure of the muscle or something to do with it – one of the enzymes such as MLCK isoforms or even isoforms of the muscle itself. Nobody knows what it is, but it does appear that apart from being genetic it is inducible by environmental factors as well. So our next NH&MRC grant is to look at this in a population to see if some people have this inherent abnormality before they have symptoms and before they have airway hyperresponsiveness. We are still gathering an understanding.
What are your hopes for the institute's future?
That's a big problem. We incorporated in 1982 and actually opened in '85; in 2000 we've got a lot of people working for it. I would like to see it expand, to network with the other departments of respiratory medicine in the University of Sydney. We are already talking to Norbert Berend, and to Jonathan Wheatley at Westmead, about being much more involved. It's hard to do it physically, but you can do a lot by email, you can have meetings every little while, you can share research fellows, research assistants, patients, and we are doing that.
I would like to see us as the pioneer institute, not only bridging the gap between the university and the hospital, and being independent and giving people freedom, but also running the whole gamut in respiratory disease from basic science – cellular science, basic physiology – through clinical science, epidemiology through public health, and on into commercialisation.
Whether this survives is going to be up to the next generation, and up to having enough funding for that next level of people who are wanting to be not senior lecturers in the university or full-time staff specialists full time but on the interface. What is next is finding money for them so there are enough of them, a critical mass.
© 2017 Australian Academy of Science