Looking back over my life, I am struck by how important chance has been. Chance creates opportunities — and my life has been abundant with opportunities. I have had the rare experience of changing careers several times. I have been associated with the birth of several new organisations and seen them become successful.1

My decision to study medicine was considerably influenced by my father, Kenneth Hetzel, a consultant physician at the Royal Adelaide Hospital, who became Dean of the Faculty of Medicine at the University of Adelaide (1953–1959). A greatly respected clinical teacher with a passionate interest in medical research, he was an inspiration to me.1

I graduated from the University of Adelaide at the end of 1944. Early in my course, I had enlisted in the Royal Australian Air Force, but after being diagnosed with pulmonary tuberculosis in 1945, I was unable to undertake military service. Many of my contemporaries did not return from war service. This left me with a strong desire to make the world a better place!

As a student, through membership of the Student Christian Movement, I adopted a Christian commitment. This led me to a holistic medical perspective that I have consolidated with fairly extensive reading in philosophy and theology, with particular reference to the interaction between science and religion.1

My holistic perspective led to an interest in endocrinology, including “stress”. I became aware of the ideas of Hans Selye, who had first recognised the importance of the role of the adrenal cortex in the body’s response to stressful stimuli. This followed the earlier work of Walter Cannon, who established the role of adrenalin. Selye proposed the concept of “diseases of adaptation”, including essential hypertension as the result of “adrenal exhaustion”.

I conducted an investigation of the adrenal cortex in hypertensive patients using a bioassay in mice for glucocorticoids (cortisol), which was a considerable challenge. The studies revealed normal adrenal function except in Cushing syndrome.2 There was considerable interest in stress at the time, and I had many requests for reprints! My finding was later confirmed by others.

In 1951, I received a Fulbright Research Scholarship and proceeded to the New York Hospital Cornell Medical Center to work as a Research Fellow in Medicine under Professor Harold Wolff. He was leading a systematic study of physiological changes in a variety of organs and systems during different emotional states associated with stressful life experiences.

I was assigned to study the endocrine (adrenal, thyroid) and metabolic systems. I believe I was the first to report an increase in cortisone secretion in humans associated with emotional states such as apprehension and exhilaration.3 These changes were accompanied by an increase in metabolic rate and other changes similar to those observed in physical trauma.4

After a period of training in clinical endocrinology at St Thomas’ Hospital in London, I returned to Australia in 1956 to become a Michell Research Scholar in the newly established Department of Medicine at the University of Adelaide under Professor H N Robson, the Foundation Professor of Medicine. In 1959, I was appointed Head of the Department of Medicine at the newly opened Queen Elizabeth Hospital (QEH) at Woodville, first as Reader and then, in 1964, as Michell Professor of Medicine.

My point of view in practice, teaching and research was a holistic one embracing the whole person — body, mind and spirit. My clinical teaching also took account of the social environment in relation to the occurrence and management of disease. It involved the health care team and included the hospital chaplain.

My clinical teaching paid special attention to the personal and social aspects of a patient’s illness. I emphasised to my students that there is both a “scientific diagnosis” of the mechanism of disease and a “personal diagnosis” of the personal and social situation of the patient, both diagnoses being equally important.

My research team at the QEH included graduate students and was particularly focused on the pathogenesis of Graves disease (hyperthyroidism), which was shown to be an autoimmune disease.5

My interest in thyroid disorders led to my involvement (from 1964 to 1972) in studies of severe iodine deficiency in the Papua New Guinea (PNG) highlands in relation to goitre and brain damage (cretinism).

Confronting the challenge of trying to improve public health in a developing country had a permanent impact on me. I was a member of the Foundation Council of the new University of Papua New Guinea (1965–1972) and assisted in the establishment of a university medical school from the previous Papuan Medical College, following the model in Fiji.1

My interest in public health arose from a number of factors. Firstly, although trained in internal medicine and endocrinology, I had a strong interest in psychosocial aspects of health and disease. This interest became explicit during my 3 years as a Research Fellow in New York studying the relationship between psychosocial stress and physical illness.1

Secondly, my experience in PNG stimulated my interest in the health services of developing countries, particularly when I first clearly recognised the importance of the organisation of health services. I was impressed with the very effective organisation of services in PNG, including the provision of services at village level through the Aid Post Orderly and the organisation at district and regional level, with the result that PNG had a major public health program embracing the whole country. The Director was Roy Scragg, from Adelaide, who provided visionary leadership over 12 years.

Finally, Australian Frontier (1963–1972), established by the Australian Council of Churches, provided me with experience of a social mechanism for helping communities develop their own ways of dealing with social problems through promoting human values. Special health problems explored by Australian Frontier included the needs of migrants and Indigenous people, as well as elderly, young, disadvantaged, poor and disabled people — a good introduction to social medicine!

In 1967, these experiences together led me to apply for and then be appointed to the Foundation Chair of Social and Preventive Medicine in the new medical school at Monash University, Melbourne.

In teaching with a small, dedicated staff, we adopted the “ecological model” of health, which included human biology, environment, lifestyle and health services.1 This involved the discipline of epidemiology. I was particularly interested in bridging the gap between research and action.

At Monash University, between 1968 and 1976, we conducted various epidemiological studies related to the rapidly expanding metropolis of Melbourne. We began with studies of suicidal behaviour and the management of traffic casualties. These were followed by studies of the mental health of students, the health and health behaviour of Indigenous people, the reproductive behaviour of Greek migrant women, and more general studies of women’s health.1

All of these projects required epidemiological data. Studies were carried out by a series of research fellows who completed higher degrees with the assistance of Tony Ryan, a Senior Lecturer who had recently had postgraduate training in epidemiology at the Harvard School of Public Health.

These studies led at the time to innovations in the provision of community services — such as the Lifeline Service in Melbourne; an Aboriginal Health Service managed by Indigenous people in Alice Springs; interpreter services for Greek and other migrants in Melbourne hospitals; and improved services at the Alfred Hospital emergency department for traffic casualties and victims of self-poisoning.

In addition, we developed a Community Health Centre in Prahran, following an earlier health survey that showed the need for both health and social services to be available at one site.6 This was a very hot political potato at the time (1973–1974), in the face of opposition from most of the local general practitioners and an Australian Medical Association resolution condemning me for the initiative! After an uncertain beginning, the centre became well established in meeting the needs of the people of Prahran.

I became interested in the challenge of bridging the gap between epidemiological findings and their public health application, with particular reference to road safety campaigns. The first major success in this area was in 1971, when legislation was introduced to make the wearing of seatbelts compulsory.

I developed my “wheel” model for the social learning process in relation to seatbelt legislation and then proceeded to apply it to the development of random breath testing (RBT) legislation (Box 1). The process begins with collecting and analysing epidemiological data, then disseminating them in suitable form through the media. This leads to wide public discussion. When a consensus emerges, a plan is designed to tackle the problem that has been defined by the data and the discussion. Political agreement is required before the necessary legislation can be passed. After the legislation has been introduced, the program is implemented and evaluated. Evaluation requires collection of new data, which then provide the basis for the next cycle. I used this model in relation to a series of public health issues.1

1 My “wheel” model, showing the social process involved in public health advancement in relation to blood alcohol levels and random breath testing legislation

Much later, I was able to review subsequent data on alcohol consumption, which indicated that up to 1975 there had been a steady increase in national consumption to the level of 10 L per person per year. By 1997, this figure had dropped to 7.6 L. The fall began in 1983, which was after the adoption of RBT in Victoria (1979), South Australia (1981) and New South Wales (1982). There had therefore been a change in drinking behaviour after the introduction of RBT, and this change has persisted. Such a change in Australian drinking habits would not previously have been thought possible!

The invitation to give the 1971 Boyer Lectures for the Australian Broadcasting Commission was a big shock! I chose the topic “Life and health in Australia”, which was based on the teaching and research work of the young Monash University department (Box 2).7 The lectures were later expanded into a book, Health and Australian society,8 first published in 1974, with two subsequent editions in 1976 and 1980. The first book of its kind, it was used as a student text for teachers, nurses, social workers, physiotherapists and medical students. I was pleased to discover it was also read by politicians!

2 “Life and health in Australia”, my presentation for the 1971 ABC Boyer Lectures

The Boyer Lectures and the book, together with other press coverage of our work, introduced public health and epidemiology to the public in the form of major modern Australian epidemics such as traffic crashes, suicidal behaviour, coronary heart disease and cancer of the lung. In the 1970s, this was new information to the public and caught media attention.

Public perceptions of epidemiology have expanded greatly since then, so that the media are now well aware of the discipline in relation to heart disease, cancer, the effects of Agent Orange, infectious diseases and many other problems. This greater public awareness has been very important for public health.

The redirection of the Animal Nutrition Division of the Commonwealth Scientific and Industrial Research Organisation (CSIRO) to become the Division of Human Nutrition gave me a remarkable opportunity — unprecedented for a medical graduate — when I was appointed Chief and took up my position in 1976. In my plan, I proposed a study of the relationship between diet and “diseases of affluence” (particularly coronary heart disease and cancer) using a multidisciplinary approach involving epidemiology, behavioural science, nutrition, physiology and biochemistry. A staff of 80 enabled me to develop this approach.

A book called The LS factor — lifestyle and health, written by Senior Epidemiologist Tony McMichael and myself, described research at the Division over a 10-year period (1976–1985). It covered areas such as diet; diet and cardiovascular disease; diet and cancer; alcohol and tobacco consumption; stress; and the development of preventive services.9 Our book has even been translated into Chinese!

Our work in New Guinea, carried out in collaboration with the PNG Public Health Department, raised my awareness of the problem of iodine deficiency. This problem eventually took over my life after I formally retired from the CSIRO at the end of 1985.

Combating iodine deficiency has been for me a great personal adventure in international health. It all began in 1963, when I was asked by the Editor of the Medical Journal of Australia to review an article by Terry McCullagh on the use of injections of iodised oil (Lipiodol) in PNG.10 This was new technology proposed to help control the severe goitre problem (Box 3) in remote villages in the highlands where iodised salt (the usual remedy for the problem) could not be easily introduced. An initial controlled trial carried out by McCullagh, at the request of the Director of Public Health, John Gunther, showed that one injection of iodised oil would prevent goitre for up to 3 years.10 However, in 1963, it was not known whether iodine deficiency was present in PNG.

3 Severely iodine-deficient mother and child, Papua New Guinea

The mother has a large goitre and the child is also affected. Cretinism in a child can be prevented by correcting iodine deficiency before the onset of pregnancy.1

In due course, our laboratory studies in collaboration with the PNG Public Health Department revealed that there was severe iodine deficiency and that it could be corrected for up to 5 years by a single dose of Lipiodol.11

Apart from the very large and frequent goitres seen in the villagers, there were many severely brain-damaged people who were also deaf-mute and often had a squint and a spastic weakness of the limbs (Box 4). This condition (“cretinism”) was being reported at the time in similar remote mountainous regions of South America, India and China, and had been observed earlier in Europe.12

There was considerable dispute as to whether or not the condition was related to iodine deficiency. It had apparently spontaneously disappeared in various parts of central and southern Europe without any known correction of the iodine deficiency.

After we had successfully demonstrated the long duration of the effect of a single iodine injection, I realised that with iodised oil we had the means to carry out a controlled trial (which would not have been possible with iodised salt) to see whether correcting severe iodine deficiency would prevent cretinism.

After approval by the PNG Research Advisory Committee, the trial was set up in the Western Highlands north of Mount Hagen. In collaboration with the PNG Public Health Department, we began the trial at the time of the first census in 1966. Families were alternately given injections of iodised oil or saline. Over the next 3 years, follow-up assessments of brain damage in young infants were carried out without knowledge of which injections the mother had received (ie, double-blinded). Particular attention was paid to the motor milestones, such as age of sitting up and walking. Any evidence of deafness reported by the mother was confirmed by a simple tuning-fork test.

This critical phase was undertaken double-blind with great skill and dedication by Peter Pharoah, an experienced PNG medical officer who was seconded to this work by the Public Health Department at my request. After more than 3 years of careful and laborious work, involving Pharoah in extensive climbing to reach the mountain villages, the code was broken. There was no doubt that mental retardation (evident in 26 cases in the control group) had been prevented by injection of iodised oil before pregnancy. In six of the seven retarded infants born to mothers treated with iodised oil, the mothers were already obviously pregnant when injected, and there was doubt about the birth date of the seventh infant.

4 A young Papua New Guinean cretin with squint, ataxia and mental deficiency

After completion of the study, injections of iodised oil were given to 120 000 people in the highlands, and an iodised salt program was introduced.

The report of this work was published in the Lancet13 and was duly accepted as definitive.14 The spontaneous decline in iodine deficiency in Europe has since been attributed to diversification of the diet, associated with economic and social development, and the use of iodine supplements.12

The finding clearly demonstrated, for the first time, that the cretinism observed was the result of fetal iodine deficiency in the first half of pregnancy. The trial also showed the effectiveness of prevention by correction of the deficiency before pregnancy. Unfortunately, although this form of cretinism is preventable, it is not reversible.12

During the 1970s, it became apparent to me that there was a great gap between our knowledge of the effects of iodine deficiency on brain development and its application in the developing world. More evidence was needed.

One of the factors leading me to take the position at the CSIRO was the possibility of developing an animal model to confirm the effect of iodine deficiency on fetal brain development. This was duly done (for the first time) both in the sheep and the marmoset monkey over the period 1976–1985 by an excellent CSIRO team with past experience of trace element deficiencies in sheep.15

These animal studies indicated the significant effects of iodine deficiency on growth and development. The effects on the brain were part of a spectrum of effects including abortion and stillbirths as well as goitre, brain damage and growth retardation of the fetus.

Clearly, a new concept beyond that of “iodine deficiency and goitre” was needed to better reflect the increase in knowledge that had occurred over the preceding 25 years, particularly in relation to brain development. After much pondering and two stimulating visits to China, and with the sympathetic encouragement of colleagues, I proposed the epidemiological concept of “iodine deficiency disorders” (IDDs) to denote all the effects of iodine deficiency on the growth (and especially brain development) of a population that could be totally prevented by correcting the iodine deficiency (Box 5).16 This concept was rapidly adopted internationally — the term was even used in China without translation! My Chinese colleague pointed out that Confucius would have approved of the term, as it referred to the primary cause and would therefore lead to appropriate measures for control!

The announcement by the World Health Organization of the global eradication of smallpox in 1980 encouraged me to raise the possibility of eradicating IDDs with available technology using iodised salt or iodised oil.16

In China (1981–1984) and Indonesia (1976–1981) I had seen the massive nature of the problem of iodine deficiency. The WHO subsequently estimated that there were two billion people at risk in 130 countries and recognised iodine deficiency as the most common preventable cause of brain damage.17

Preventive measures suitable for mass application (use of iodised salt or iodised oil) and simple methods of epidemiological monitoring and surveillance (salt iodine and urine iodine measurements) were available. However, there was great delay in applying existing knowledge on IDDs to preventive programs in areas of need — to the detriment of the many millions in developing countries who were suffering irreversible brain damage due to iodine deficiency.

In a report to the United Nations (UN) Nutrition Subcommittee, I stressed my concern about the gap between knowledge and application. To help bridge the gap, I proposed that an expert consultative group of scientists and other public health professionals be established to help develop national IDD control programs in collaboration with the WHO and UNICEF.1

The decision to establish the International Council for Control of Iodine Deficiency Disorders (ICCIDD) was made in Delhi, India, in March 1985, when I put the proposal to a group of 10 consultants and advisers who were attending a WHO/UNICEF workshop on the control of IDDs in South-East Asia. This was followed by an inaugural meeting, supported by WHO and UNICEF, in Kathmandu, Nepal, in 1986 (Box 6).18 I became Executive Director, and later Chairman, of the ICCIDD.

The ICCIDD now consists of a multidisciplinary international expert network of 700 endocrinologists, epidemiologists, nutritionists, public health administrators, technologists, communicators, economists and others from 100 countries, with a majority from developing countries, who are committed to helping national governments and international agencies develop national programs to eliminate IDDs as a public health problem.19

Since 1986, the ICCIDD has held a series of regional meetings with the WHO and UNICEF to foster the development of national control programs. The meetings have been attended by ministry of health representatives from countries in the region.

I adapted my social process wheel model (Box 1) to the IDD elimination program.19 Particular importance was given to political will, which had been lacking in the past but had now been mobilised through the UN system, particularly the World Summit for Children, held in 1990. The outcome of the Summit was a declaration signed by 71 heads of state and eventually by 88 other governments. The declaration accepted a series of goals for the better health and education of children throughout the world, including the virtual elimination of IDDs by the year 2000.

A report to the 1999 World Health Assembly (WHA) indicated that, of the 130 countries that had a significant IDD public health problem, two-thirds had introduced universal salt iodisation programs. Between 1990 and 1998, the number of countries with salt iodisation programs had increased from 46 to 93.17

However, there is a need to ensure the sustainability of this achievement. This depends on epidemiological surveillance with urine iodine measurements to confirm the absence of iodine deficiency. Sustainable elimination of IDDs is only possible if surveillance continues — recurrence can readily occur, and has indeed occurred.17,19,20 In 2001, the ICCIDD adopted a mandate for the future dedicated to the elimination of iodine deficiency as a cause of brain damage (Box 7).20

At the 2005 WHA, Canada and Australia proposed a resolution requiring countries to report to the WHA on the monitoring of their iodine deficiency elimination programs in 2007 and every 3 years thereafter. The resolution was adopted and provides the necessary political support for future sustainability of the programs.

I believe the non-government organisation model is relevant to many other international health problems. A multidisciplinary group of concerned scientists and public health professionals can come together to define a problem and then develop a program designed to solve the problem in collaboration with UN agencies.12,19,20

It has been a great experience to assist in the development of a UN program to eliminate iodine deficiency — the most common preventable cause of brain damage. The program was made possible by targeted research that established the relationship between iodine deficiency and brain damage — research that included epidemiological study in the field in PNG and later studies in animal models. Rapid development of the elimination program was made possible by the effectiveness of introducing iodised salt as a population measure and the application of a simple laboratory method to determine urine iodine levels as a marker for iodine deficiency and to correct any deficiency in populations. A dedicated group of multidisciplinary professionals in the ICCIDD provided the scientific leadership in collaboration with national governments, the WHO and UNICEF, assisted especially by aid programs of Australia, Canada and the World Bank.

I have been very fortunate, for more than 50 years, in the people I have been associated with — my family, friends and colleagues have always been a support and inspiration to me.

6 Inauguration of the International Council for Control of Iodine Deficiency Disorders (ICCIDD), Kathmandu, Nepal, 1986

L – R: Basil Hetzel, Executive Director (Australia), John Dunn, Secretary (USA), and John Stanbury, Chairman (USA). Inset: the logo adopted by the ICCIDD emphasises the importance of the effects of iodine deficiency on the brain.