Owens v Repatriation Commission

ALBERT JAMES OWENS v. REPATRIATION COMMISSION
No. G1000 of 1993
FED No. 827/94
Number of pages - 15
Administrative Law
(1994) 35 ALD 278

COURT

IN THE FEDERAL COURT OF AUSTRALIA
NEW SOUTH WALES DISTRICT REGISTRY
GENERAL DIVISION
LOCKHART J

CATCHWORDS

Administrative Law - Veterans Entitlements - whether adenocarcinoma of the colon was a war-caused disease - whether the Tribunal erred in law in its reasons for decision - whether Tribunal erred in its interpretation of "reasonable hypothesis" within s.120.

Administrative Appeals Tribunal Act 1975, s.44
Veterans' Entitlements Act 1986, s.120

HEARING

SYDNEY, 19 August 1994
#DATE 3:11:1994
#ADD 17:3:1995

Counsel for the Applicant: Mr M B Smith

Solicitors for the Applicant: Legal Aid Commission of New

South Wales

Counsel for the Respondent: Mr D Ryan

Solicitors for the Respondent: Australian Government Solicitor

ORDER

1. The application be dismissed.
2. The applicant pay the respondent's costs of the application.
NOTE: Settlement and entry of orders is dealt with in Order 36 of the
Federal Court Rules.

JUDGE1

LOCKHART J This is an appeal, on a question of law, pursuant to s. 44(1) of the Administrative Appeals Tribunal Act 1975 (the AAT Act) from a decision of the Administrative Appeals Tribunal, Veterans' Appeals Division (the Tribunal).

The Tribunal (constituted by Deputy President B J McMahon, Dr J D Campbell and Vice Admiral D W Leach) affirmed a decision of the Repatriation Commission (the Commission) dated 3 June 1988 which refused a claim made by the applicant, Albert James Owens, for pension on the grounds that certain medical conditions were not war-caused diseases. One of the conditions was adenocarcinoma of the colon (bowel cancer). Before the Tribunal, the claim in relation to the other conditions was either withdrawn by the applicant or conceded by the Commission. Thus, the only question left for determination by the Tribunal was whether adenocarcinoma of the applicant's colon was a war-caused disease. The Tribunal concluded that it was satisfied beyond reasonable doubt that there was no sufficient ground for determining that the applicant's adenocarcinoma of the colon was war-caused. The Tribunal then affirmed the decision of the Commission in so far as it related to that disease.
When the hearing of this matter commenced before this Court on 19 August 1994, counsel for the Commission said that the Commission wished to argue that the Tribunal had no jurisdiction in the matter. I gave leave to the Commission to file and serve a notice of motion to strike out the appeal from the Tribunal's decision as incompetent or to have leave to cross-appeal from the Tribunal's decision. I allocated a date for the hearing of that aspect of the matter (21 September 1994). As counsel, solicitors and the parties were in Court on 19 August ready to deal with the appeal on the merits (that is, the appeal from the Tribunal's decision affirming the Commission's decision with respect to the adenocarcinoma), I took the course of hearing the evidence and argument on that question in the interests of saving time and costs. Both parties concurred in that course. On the conclusion of argument I adjourned the further hearing of the matter to 21 September 1994 and gave directions to the parties for the filing of affidavits in relation to the motion on jurisdiction. On 21 September, when the motion was called on for hearing, counsel for the Commission told the Court that the Commission no longer sought to raise the jurisdiction question and asked for the motion to be dismissed. The Court then dismissed the motion with costs.
The question for decision by this Court is whether the Tribunal erred in law in its reasons for decision.
I turn to the facts. The applicant was born on 15 May 1919. On 27 March 1941 he enlisted in the Australian Armed Forces and served with them until 27 November 1945. At his induction medical examination on 11 March 1941 no specific medical problems were reported in relation to his gastrointestinal tract. Between January and April 1945 he was admitted to hospital several times where amoebic dysentery was diagnosed. After these repeated episodes of amoebic dysentery, the applicant was left suffering from neurogenic diarrhoea which meant a constantly loose bowel.
Amoebic dysentery is an infection by a parasite - the amoebic parasite - and this usually occurs in the bowel and almost always in the large bowel. There is not a great deal of amoebic infection in Australia, but it is an endemic condition in certain parts of the world such as Africa and other tropical countries. The most common site where infection occurs is in the right half of the colon. Amoebic dysentery can give rise to a number of complications within the bowel.
On his medical examination at or about the time of his discharge from the Armed Forces (27 November 1945) a note was made of the applicant's continuing problems with neurogenic diarrhoea. The examining officer noted that the applicant was passing motions four or five times a day and, if excited, his bowels became very loose. There was no other precipitating factor noted in relation to his diarrhoea. A physical examination failed to reveal any specific abdominal abnormality. As a result of the medical history which he gave the medical officer, a decision was made that there was a 5% level of incapacity related to sequelae from his amoebic dysentery. This disability was accepted as war-caused.
In his evidence to the Tribunal the applicant said that he was told to have his bowel condition checked every twelve months after his discharge from the army. This was done, but no report of abnormality was detected apart from the continuing general non-specific diarrhoea. The applicant said that this strain and stress caused his bowel to be overactive and on many occasions he was forced to pass motions up to eight times a day.
An operation was carried out on 28 November 1986 to remove cancer that had been detected in his bowel. The applicant said that since the operation his diarrhoea had become chronic and that he still had six or more motions daily.
There was no relevant medical history concerning the applicant's gastrointestinal tract (apart from the annual examinations) until 25 November 1986 when he was first seen by Dr Hennessy, a gastroenterologist. A history of lower abdominal pain and excessive wind for approximately two months was given. A barium enema examination performed some two years earlier had revealed evidence of diverticular disease. He was treated with medication for diverticulitis during the late 1970s. That condition has not been accepted as a war-caused disease under the Veterans' Entitlements Act 1986 (the VE Act). On the basis of recent symptoms the applicant's local medical officer, Dr Drew, performed three blood stool examinations which were positive. The applicant was referred to Dr Hennessy who undertook a colonoscopy on 27 November 1986. This revealed evidence of a large spastic sigmoid colon considered to be related to diverticular disease, and the presence of a large ulcerating polypoid carcinoma in the proximal ascending colon just above the caecum. Biopsies were performed which confirmed malignancy.
The applicant was subsequently seen by Dr Tom Hugh, a general surgeon, who performed a right hemicolectomy on 28 November 1986. In a subsequent letter to the applicant's local medical officer, sent on 17 May 1991, Dr Hugh said that the carcinoma had arisen in a villous adenoma and that therefore the applicant should have regular colonoscopy as such tumours tend to be multiple. This finding was confirmed in other reports in evidence before the Tribunal.
A "follow up" colonoscopy was carried out by Dr Hennessy. This revealed evidence of continuing spasticity of the sigmoid colon, but it was considered that this was related to diverticular disease. Dr Hennessy commented that there was no other evidence of polyps or other pathology in the large bowel.
In its reasons (par. 11) the Tribunal said:

"It is generally accepted that there are 3 factors for which there is scientific evidence of a likely causal connection with cancer of the colon. The first of these is an hereditary predisposition. This is agreed upon by both Professor Kune and Dr Levi (to whom reference will later be made). A genetic predisposition to this condition is not necessarily associated with a family history but represents an inherent potential for an individual to develop the condition later in life. The second generally agreed cause is a certain dietary pattern, often referred to as western style, involving a relatively high fat and low fibre diet. The third factor is the consumption of alcohol, particularly, but not exclusively, beer. The applicant did not rely upon any of these generally accepted elements of the etiology of his condition. He relied upon a suggested connection with amoebic dysentery, or in the alternative with an irritable bowel syndrome."

Amoebic dysentery and irritable bowel syndrome are two of the applicant's disabilities which it is accepted were war-caused. The question to which much of the medical and other evidence in the case went in the proceeding before the Tribunal was whether a relevant nexus can be established between either of those conditions and the applicant's bowel cancer.
The medical witnesses who gave evidence before the Tribunal were Professor Kune and Dr Levi.
Professor Kune is Emeritus Professor of surgery at the University of Melbourne and a consultant surgeon at the Royal Melbourne Hospital. He has been actively involved for 30 years in cancer related work including the diagnosis and treatment of various cancers, particularly cancer of the bowel. He has also been involved in cancer epidemiology, which is a study of the causes and thereby of the possible prevention of the common causes of cancer including bowel cancer. Since 1978 he has been the principal investigator of the Melbourne colo-rectal study, which is a population-based study of the causes of bowel cancer. He has published widely in his field. He gave evidence on behalf of the applicant.
Professor Kune's first report of 14 August 1992 said that there was no evidence that previous amoebic dysentery was related to cancer of the colon. He later withdrew that opinion. Professor Kune said in this report that there is a possibility that the applicant's symptoms of frequent bowel motions commencing during war service and continuing thereafter were due to mild chronic ulcerative colitis and that this condition predisposed him to the subsequent development of colon cancer. Ulcerative colitis is a most important predisposing factor in the causation of large bowel cancer and there is a good deal of scientific evidence to indicate that at least one of the causal factors in its development is an emotional disturbance. He said there is only a small amount of evidence that frequent loose bowel motions or diarrhoea are associated with carcinoma of the colon. He said that on the current evidence it is unlikely that frequent loose bowel actions as a non-specific symptom are a contributory cause of colon cancer. He said on p. 5 of his report:

"It has also been suggested that the irritable bowel syndrome can be a predisposing factor in the subsequent development of large bowel cancer. This suggestion makes sense biologically, that is, it is consistent with the concept that someone who suffers from the irritable bowel syndrome for many years with frequent loose bowel motions, may develop structural changes in the lining of the large bowel, leading to hyperplasia of the lining cells, then to dysplasia and neoplastic change, that is, leading to the development of an actual bowel cancer. The difficulty with this suggestion is that up to the present time there have been no systematic studies to either confirm or deny this suggestion. There is thus some evidence that chronic non- specific diarrhoea is more common in bowel cancer cases than in controls. There is also a biologically plausible suggestion that the irritable colon syndrome/diverticular disease may be one of the predisposing factors in the development of large bowel cancer. Regrettably, a systematic examination of these associations has so far not been made. It is therefore biologically plausible that such an association is a factor in the development of colon cancer."

In his second report of 9 November 1992, Professor Kune affirmed this opinion and again confirmed that no scientific literature regarding the relationship of either condition (amoebic dysentery or irritable bowel syndrome) to bowel cancer had come to hand. He reported:-

"Since my report of 14 August 1992, no further data has come to hand in the scientific literature regarding the relationship between amoebic dysentery and carcinoma of the colon, diarrhoea/dysentery and carcinoma of the colon, irritable colon syndrome/diverticular disease and carcinoma of the colon, so that my opinion of 14 August 1992 remains unchanged. It is biologically plausible, as I stated in my previous report, that irritable colon syndrome/diverticular disease may be one of the predisposing factors in the development of large bowel cancer. However, there has not been a systematic examination of these associations up to the present time. It is therefore biologically possible and plausible that such an association is a factor in the development of colon cancer, but there are just no data available, either to confirm or to deny this suggestion."

Professor Kune's next report is dated 22 February 1993. By then he had become aware of a paper by Mr A A Abioye of the Department of Pathology, University College Hospital, Ibadan, Nigeria published in the African Journal of Medicine and Medical Science in 1976. Professor Kune said in this report that he had made a:

"detailed literature search regarding the evidence of an association between amoebic dysentery and cancer of the large bowel ... This subject was most recently reviewed by Abioye in 1976 who reviewed the literature and noted case reports which have shown an association between amoebic infection of the bowel and large bowel cancer."

Professor Kune went on to say in this report:

"The difficulty is that a systematic study and comparison either in a cohort study or in a case control study relating the association between amoebic infection and colorectal cancer, so far has not been made. Also, there is no indication of any latent period. In the case of Mr Owens, the latent period between his amoebic dysentery and diagnosis of colon cancer was some 40 years. Thus, it makes sense biologically that previous amoebic infection of the large bowel could predispose that person to the subsequent development of colon cancer and there is also some association in case histories reviewed by Abioye and quoted above. Regrettably, a systematic examination of this association has not been done so far. This is a possibility which cannot be excluded in the case of Mr Owens and may be the basis of a reasonable hypothesis, although it needs to be stated that the evidence for this is not strong."

Shortly before the hearing before the Tribunal, the Professor became aware of another paper published by Dr E Camacho of the Faculty of Medicine, University of Guadalajara, Mexico, published in 1971 in the Journal "Diseases of Colon and Rectum". The professor described the Camacho study as:

"a scientific study conducted in Mexico first drew attention to the possibility that amoebic infection of the caecum may be a pre-cancerous lesion in the subsequent development of cancer of the caecum ..."

He said of the Camacho study:

"This study showed a very high incidence of adenocarcinoma in the caecum of 18% in those with a previous amoebic infection. Conversely, another group of patients with cancer of the caecum studied by these scientists, showed previous amoebic infection in 20% It has also been noted in communities where amoebic infection is endemic, such as Nigeria, that the distribution of large bowel cancer in terms of frequency of occurrence of various sites along the large bowel, is similar between amoebic lesions and cancer, whereas in communities in which amoebic infection is not endemic, the distribution of the frequency of cancer at various sites along the colorectum is very different."

Copies of both papers were tendered in evidence before the Tribunal. Reference was made to a third Paper by A O Williams and others in 1967, but no copy of this was available before the Tribunal.
The Tribunal said of Professor Kune's evidence that, on the basis of these two papers, he was not prepared to say that there was a definite causal or contributory connection between the two conditions (amoebic dysentery and cancer of the colon). He said that neither of the two authors mentioned were definite in their conclusions. All that both had done was to "float" the possibility of an idea which has since not been followed up, either by the authors or by another other published researcher.
Professor Kune was prepared to say that if there was a connection, then he could suggest a possible mechanism of how amoebiasis may be related to colorectal cancer. These mechanisms would include structural changes produced by the amoebic infection in the lining of the bowel and a lower level of immunity being associated with amoebic infection and perhaps also further lowering of immunity when the infection actually occurs.
The Tribunal said that the tentative observations expressed in the papers, to which reference has just been made, were of little assistance for various reasons, but primarily because in the Tribunal's view they did not assert a positive connection between amoebic dysentery and carcinoma of the colon. Each of the two papers purported only to raise ideas for further consideration. The Tribunal said that the authors and Professor Kune did no more than suggest a possibility of a connection which might be worth exploring further.
The Tribunal then said in par. 22 of its reasons:

"The reference to the latency period is an important observation. Even in the Camacho paper, the patients studied had an ongoing serious inflammation of the bowel. There is no evidence before us that Mr Owens developed his carcinoma until some 40 years after the dysentery episodes from which he had previously suffered. This alone would negative the application of the possibility referred to by the authors."

The Tribunal went on to say:

"The other possible hypothesis related to the applicant's irritable bowel syndrome. Professor Kune could not point to any literature in support of such an hypothesis. He explained that he reached his conclusion by reference to other types of cancer in which hyperactivity sometimes resulted in a carcinogic effect. It seemed logical to him that excessive bowel movements and diarrhoea could lead to excessive multiplication of lining cells, which could lead to the likelihood that 'something could go wrong'. Excessive activity could lead to the production of abnormal cells, some of which could possibly be malignant. On the basis of what was suggested in Mr Abioye's article in relation to amoebic dysentery, he also postulated, in relation to irritable bowel syndrome, that increased activity could lead to a change in the level of immunity with the possibility that 'something may go wrong in multiplication of cells'. He agreed that there have been absolutely no studies made of the possible connection, although he said that there had been discussion on the subject in circles in which he moved. He agreed that what he postulated was the possibility of a connection that was worth exploring, based on clinical evidence in relation to other carcinomas." (par. 23)

"As he put it - if there was a relationship, then his hypothesis of the mechanics would be that there would be excessive production of mucous and fluid (hypoplasia) which would increase the possibility of abnormal cell changes. He said that this is how he imagines the association might develop and that the longer the increased activity went on, the greater the chance of association. He thought that the possible connection was plausible and that it was worth further consideration. He said he would not say that there is certainly no relationship, but he could go no further than saying that it was a possible relationship which one might entertain. He affirmed his previous use of the term 'biologically plausible'." (par. 24)

The Tribunal then turned to the evidence of Dr Levi who gave evidence on behalf of the Commission. Dr Levi is Head of the Department of Clinical Oncology at the Royal North Shore Hospital, Sydney and is an eminent clinician and researcher in this field. The Tribunal said that Dr Levi confirmed that there is no experimental, epidemiological, or clinical evidence to support a past history of amoebic dysentery predisposing to development of carcinoma of the colon. A similar conclusion could be drawn in relation to the irritable colon, although this condition could be associated with the development of diverticulosis and diverticulitis which might have occurred in Mr Owens' case.
The Tribunal said of Dr Levi's evidence (par. 26):

"He made the telling point that the evidence of the operating surgeon, identifying a villous adenoma, would be conclusive of the cause of the applicant's cancer. This condition indicated to him that the cancer was of genetic origin - that is to say that a known inherent tendency to malignancy was demonstrated by the discovery of this adenoma. In his view, the particular cause of Mr Owens' cancer had been identified and to suggest any other possible cause would be to espouse a theory contrary to known facts. The villous adenoma in his opinion was the most normal and accepted way of explaining the cause of Mr Owens' cancer."

The Tribunal said (par. 27) that the procedures that it should adopt in considering a case of this kind were set out by the High Court in Byrnes v Repatriation Commission (1993) 177 CLR 564 at 571 in the following passage:
"The position may be summarized as follows

(1) First, sub-s.(3) of s.120 is applied: do all or some of the facts raised by the material before the Commission give rise to a reasonable hypothesis connecting the veteran's injury with war service? The hypothesis will not be reasonable if it is contrary to known scientific facts or is obviously fanciful or untenable. If the hypothesis is not reasonable, the claim fails. Proof of facts is not in issue at this point.

(2) If a reasonable hypothesis is established, sub-s. (1) of s. 120 is applied. The claim will succeed unless:

(a) one or more of the facts necessary to support the hypothesis are disproved beyond reasonable doubt; or

(b) the truth of another fact in the material, which is inconsistent with the hypothesis, is proved beyond reasonable doubt, thus disproving beyond reasonable doubt the hypothesis."

The Tribunal said (par. 28) that the reference in Byrnes to a hypothesis which was fanciful or untenable was a reference to the phrase used in East v Repatriation Commission (1987) 74 ALR 518 at 533, also reported at (1987) 16 FCR 517 at 532 which was cited with approval by the High Court in Bushell v Repatriation Commission (1992) 175 CLR 408 at 414. In East their Honours considered that a hypothesis could not be reasonable, inter alia, if it is:

"'obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous'."

The Tribunal concluded (par. 29) that both of the alternative hypotheses put before them were too tenuous. The Tribunal referred (par. 30) to an earlier decision of the Tribunal in Re Chandler and Repatriation Commission, Decision No 8738, 26 May 1992 where (at par. 92) it was stated (to use the language of the Tribunal in the present case in par. 30):

"that this Tribunal must decide how far along the scale of possibility the hypothesis lies and whether it is to be categorised as too tenuous to be a reasonable hypothesis or as pointing sufficiently to the causal relationship so that it is a reasonable hypothesis. This Tribunal is to be satisfied beyond reasonable doubt that there is no sufficient ground for determining that the disease was war-caused only if, after considering the whole of the material before us, it is of the opinion that it does not raise a reasonable hypothesis connecting the disease with the circumstances of the applicant's war service. It is not a question whether a reasonable hypothesis has been raised."

In a critical passage in its reasons (par. 31) the Tribunal said this:-

"A mere possibility, however biologically plausible, falls short of a proposition possessing some degree of acceptability or credibility, if it does not point to, and not merely leave open, the conclusion contended for. It is true that a hypothesis does not require proof. It can not be said, however that a mere suggestion for research is itself an hypothesis raised by the facts. Neither the tentative papers cited in relation to the amoebic dysentery connection nor the biologically plausible speculation of Professor Kune amount to more than this. In the present case, in any event such a suggestion, even if it amounted to an hypothesis, would be negatived because the facts indicate a clear and recognisable cause for the disease without resort to any suggestion or hypothesis. The fact of the demonstration of the villous adenoma has not been taken into account by the applicant in formulating his alternative hypotheses. They are therefore not based on the raised facts. The mere fact that Professor Kune is eminent in the relevant field of knowledge (and there is no question that he is) is not sufficient to support an hypothesis in these circumstances. We accept that conflict with other medical opinion is not sufficient to reject an hypothesis as unreasonable. That is not all that we have before us however."

In conclusion the Tribunal said (par. 32):

"We are satisfied beyond reasonable doubt that there is no sufficient ground for determining that the applicant's bowel cancer was war-caused, because we are of the opinion that the circumstances and submissions put before us do not raise a reasonable hypothesis in the alternative connecting his disease with the circumstances of his war-service. This is because neither suggestion that has been made can be called an hypothesis and secondly because, in any event, both suggestions are contrary to the known and established cause of the condition."

The Tribunal then affirmed the decision of the Commission in so far as it relates to adenocarcinoma of the colon.
Counsel for the applicant argued that the Tribunal's conclusion in par. 32 shows that it rejected the applicant's claim by applying the direction in s. 120(3) of the Veterans' Entitlements Act 1986 (Cth), and that it never reached the stage of applying the s. 120(1) standard of disproof beyond reasonable doubt.
Counsel argued that the Tribunal erred when giving two reasons why the hypotheses explained by Professor Kune did not satisfy s. 120(3), namely:

(i) neither of the suggested connections could "be called an hypothesis"; and "in any event"

(ii) both were "contrary to the known and established cause of the condition".

Counsel submitted that the Tribunal's reasons were contrary to the interpretation of "reasonable hypothesis" provided by the High Court in Bushell at 414-5 and 428; Byrnes at 571; and by the Federal Court in Repatriation Commission v Webb (1987) 76 ALR 131 at 135, and Repatriation Commission v Whetton (1991) 31 FCR 513 at 515-6, 519-20.
Counsel for the applicant then challenged the second reason of the Tribunal for applying s. 120(3). It was submitted that this second reason was the Tribunal's conclusion, that the hypothesis "would be negatived because the facts indicate a clear and recognizable cause for the disease without resort to any suggestion or hypothesis". It was argued that this conclusion of fact rejects the opinion of Professor Kune by preferring the evidence of Dr Levi as showing "conclusively" that the tumour was solely of genetic origin.
It was argued by counsel for the applicant that the use by the Tribunal of Dr Levi's evidence was contrary to the directions of the High Court in Bushell, as explained in Byrnes, since the Tribunal "determined the cause of the cancer as a fact to an unstated standard of satisfaction but possibly on the balance of probabilities" and "accepted as definitive of the cause of the cancer the evidence of the Commission's medical practitioners" at a stage where "the existence of conflicting medical opinions is insufficient to categorize a hypothesis as unreasonable". It was submitted that the Tribunal should not have treated Dr Levi's opinions and the material on which he relied as part of the relevant "raised facts"; but should have treated the case as one where "the applicant relied on part only of the material and left an assessment of the weight of the other material to be performed on the standard of disproof beyond reasonable doubt under s. 120(1)". Counsel argued that the material did not indisputably reveal an unanswerable flaw in the hypotheses of Professor Kune favouring the applicant, but raised conflicting hypotheses as to the causation of his cancer.
Counsel for the Commission argued that the Tribunal found correctly that the alternative hypotheses put forward on behalf of the applicant were too tenuous. The question whether or not an hypothesis is reasonable is a question of fact for the Tribunal to decide. Provided the Tribunal made no error of law, so as to attract review by the Court under s. 44 of the AAT Act, it was for it to decide whether or not the facts raised by the material before it gave rise to a reasonable hypothesis.
Central to the case is s. 120 of the VE Act which so far as relevant provides as follows:

"120(1) Where a claim under Part II for a pension in respect of the incapacity from injury or disease of a veteran, or of the death of a veteran, relates to the operational service rendered by the veteran, the Commission shall determine that the injury was a war-caused injury, that the disease was a war-caused disease or that the death of the veteran was war-caused, as the case may be, unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.

...

(3) In applying subsection (1) or (2) in respect of the incapacity of a person from injury or disease, or in respect of the death of a person, related to service rendered by the person, the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining:

(a) that the injury was a war-caused injury or a defence-caused injury;

(b) that the disease was a war-caused disease or a defence-caused disease; or

(c) that the death was war-caused or defence-caused; as the case may be, if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person.

...

(5) Nothing in the provisions of this section, or in any other provision of this Act, shall entitle the Commission to presume that:

(a) an injury suffered by a person is a war-caused injury or a defence-caused injury;

(b) a disease contracted by a person is a war-caused disease or a defence-caused disease;

(c) the death of a person is war-caused or defence-caused; or

(d) the claimant or applicant is entitled to be granted a pension, allowance or other benefit under this Act.

(6) Nothing in the provisions of this section, or in any other provision of this Act, shall be taken to impose on:

(a) a claimant or applicant for a pension or increased pension, or for an allowance or other benefit, under this Act; or

(b) the Commonwealth, the Department or any other person in relation to such a claim or application;

any onus of proving any matter that is, or might be, relevant to the determination of the claim or application.

..."

The argument of counsel for the applicant that the Tribunal applied subsection (3) of s. 120, but never considered subsection (1) can be shortly disposed of. The Tribunal decided that the material before it did not raise a reasonable hypothesis connecting the operational service of the applicant with his incapacity, so that there was nothing upon which it could find that the incapacity was war-caused within the meaning of s. 120(1). If the material had raised such a hypothesis, the operation of subsection (3) would have been spent and the matter would have fallen for determination in accordance with subsection (1). The Tribunal did not reach that point because of its finding that the material did not raise a reasonable hypothesis connecting the operational service with the incapacity. Hence, the claim had to fail before the Tribunal.
I have read carefully Professor Kune's oral evidence and his reports and the two articles (one by Abioye and the other by Camacho). Much of what the Professor said in his reports was referred to by the Tribunal and is set out earlier. The Tribunal also referred to certain of his oral evidence; but it is necessary that I recite some of it in order to place the whole of his evidence in perspective. He referred in his oral evidence to the statement in his first report (i.e. the report of 14 August 1992):

"There is no evidence that previous amoebic dysentery is related to cancer of the colon."

He said it was after that report that he made a more thorough examination of the literature and material and discovered other information and hence, did not stand by that statement. He said that none of the three articles which he had read were the result of a "well controlled study" and this was a pity because it would give a much better understanding of one of the possible causes of bowel cancer; he said this in the context of amoebic dysentery and its possible relation to bowel cancer. He agreed with Deputy President McMahon that when he used the word "hypothesis" he meant "a possibility of a connection that is worth exploring".

Counsel for the applicant put a question to the Professor in these terms:

"My final question, doctor, is in this case that we have got the history of the two conditions and 40 years after the diagnosis of amoebic dysentery and after an extended history of irritable bowel syndrome the development of this cancer of the ascending colon. The applicant draws a connection between the history of these symptoms and the development at the much later date of the cancer itself. In your view, is that connection or that proposed connection absurd, fanciful or untenable? - I don't think it is absurd or fanciful or untenable, no. Could it be described as plausible or worthy of further consideration? - Yes, I believe it is plausible and I believe it is worthy of further consideration. As a scientist my difficulty is that regrettably on neither count, neither on amoebic infection nor on the irritable colon diverticular disease aspect, those two separate things, has there been a careful controlled epidemiological study made and that is my difficulty as a scientist. I believe that both of these are worthy of further consideration and further research, certainly from our community's point of view, further research into the association between irritable colon syndrome and diverticular disease and bowel cancer is certainly worthy of further study."

Professor Kune said of the two papers by Abioye and Camacho (and perhaps the third paper) that:

"They are of interest because they raise a possibility. As a person, you know, devoted to trying to find out why people get cancer it certainly interested me and then putting it all together I think it's of interest that we certainly either need to do it, of course, we can't do it ourselves on the amoebic situation but we ought to support others perhaps in the endemic communities to look at that more carefully."

Later in his evidence he answered some questions put to him by a member of the Tribunal (Dr Campbell) as to any causal link between amoebic infection and colon cancer. He said that the relationship is a possible one, but that he

"would have great difficulty putting a numerical figure on it because of the very facts we have just discussed - absence of sufficient information. I personally wouldn't say that no, there is certainly no relationship. I wouldn't say that. But I would say well, there may be a possibility there. That is more like it. I couldn't put a number on it, really."

The Professor affirmed in oral evidence what he had said on page 5 of his report of 14 August 1992, namely, that it is biologically plausible that an association between the irritable colon syndrome/diverticular disease and cancer of the bowel is a factor in the development of colon cancer. He said there is biological plausibility of a connection between amoebic dysentery and the colon cancer. The Professor said that when he described something as being "biologically plausible" what he meant is that:

"It makes sense considering what we know about Mr Owens and what is our scientific knowledge currently."

The evidence of Professor Kune led the Tribunal to summarize his evidence as stating that there was a biologically plausible possibility (with a suggestion that research should be undertaken and that it is worthy of research) of a relationship between the previous amoebic dysentery or irritable bowel syndrome and cancer of the colon which arose some 40 years later.

In the present case there is evidence from two highly respected medical practitioners. Professor Kune talks of the connection between amoebic dysentery or irritable bowel syndrome and cancer of the colon of the applicant as being a possibility and something deserving further research, a connection which could not be described as fanciful or absurd. Dr Levi says, not that there could not be any such relevant connection; but in a context where the precise aetiology of carcinoma or the colon is unknown, there is good evidence that the reason for the applicant's bowel cancer is that he had a villous adenoma immediately adjacent to his bowel cancer which was known to be pre-malignant and that the cancer itself rose from this. Dr Levi's view is that this is the most plausible and scientifically recognizable explanation for the cause of his bowel cancer. The Tribunal summarized this in paragraphs 25 and 26 of this reasons. Dr Levi made what the Tribunal described as "the telling point" that the evidence of the operating surgeon identifying a villous adenoma would be conclusive of the cause of the applicant's cancer. Dr Levi's view was that the cancer was of genetic origin, namely, that he had a known inherent tendency to malignancy demonstrated by the discovery of this adenoma. In Dr Levi's view the particular cause of the applicant's cancer had been identified, and to suggest any other possible cause would be to expose a theory contrary to known facts. The villous adenoma in his opinion was the most normal and accepted way of explaining the cause of the applicant's cancer.
This is not a case, in my opinion, of two different hypotheses expressed by two different medical practitioners, each of which is supportable. The Tribunal did not consider two different professional opinions, each of which had a rational foundation, and prefer one to the other. If it had done that it would have erred in law (see Bushell and Repatriation Commission v Webb (1987) 76 ALR 131 per Beaumont J. at 135). The Tribunal recognized correctly that a hypothesis does not necessarily require proof; but I agree with the Tribunal that what is in essence merely a suggestion for research cannot be itself a hypothesis on the material before the Tribunal in this case. Professor Kune's hypothesis as to causative link between either amoebic dysentery or irritable bowel syndrome and the applicant's cancer of the colon is a "hypothesis" to him in the sense that it is a possibility and it cannot be described as fanciful or absurd; but the Professor adds there has been no systematic study to his knowledge carried out, so there is no evidence to suggest the requisite link.
The Tribunal heard the evidence and had all the material before it. It was the judge of the facts and it did in my view correctly summarize the evidence of Professor Kune. The Tribunal found that the facts of the case indicated:

"a clear and recognisable cause for the disease without resort to any suggestion or hypothesis. The fact of the demonstration of the villous adenoma has not been taken into account by the applicant in formulating his alternative hypotheses. They are therefore not based on the raised facts." (par. 31)

The Tribunal correctly stated in the same paragraph that it accepted that conflict between Professor Kune's opinion and other medical opinion is not sufficient to reject a hypothesis as unreasonable, but that was not all that was before the Tribunal (see summary of facts by Tribunal in pars 25, 26 of its reasons).
In my opinion it has not been shown that the Tribunal erred in law. The application is dismissed with costs.

[1994] FCA 827

03 NOVEMBER 1994