Three independent studies all lead to a conclusion that the concentration of the testosterone metabolite BaB in urine can be used to discriminate between bitches that have been administered testosterone and those have not. A proposed regulatory concentration of 10 nanograms per millilitre of BaB is most generous. It is essentially impossible for a clean bitch to record levels in excess of 10 nanograms per millilitre. Administration leads to concentrations of BaB more than ten times the limit and should be detected for several days after administration. Oestrus will not lead to levels of BaB over the proposed limit.

The odds of finding a clean bitch with 10 nanograms per millilitre of BaB or more in it are better than 1 to 800 million against.

In other words, he is saying that it is nigh on impossible.

1. Obviously, in the present case, where the actual reading is estimated to be somewhere within the range of 380 and 400 plus nanograms per millilitre, it can be said a fortiori that the only way the bitch, Sick Money, could have had such a reading would be that there had been a relatively recent administration of testosterone or a testosterone product.
2. Witnesses Zahra and Karamatic also strongly supported the view that a reading of 20 nanograms per millilitre plus means administration of testosterone must have occurred.
3. Despite some desultory efforts by the applicant to challenge the sampling and testing techniques adopted by the Stewards and RASL chemists herein, none of which amounted to anything at all, (see below for further discussion on this point) otherwise all the above-related facts and opinions are firmly established and/or uncontradicted and I unhesitatingly accept them.
4. Indeed, Mr Zahra explained in some detail in his evidence the careful manner in which RASL carries out tests in strict conformity with known and approved methods.
5. Arising from this background then, the applicant has been charged with two offences:

in that you, the trainer of greyhound Sick Money, which was nominated to compete in an event namely race 10, the Action Packed Images, grade 5 T 3, conducted by Warragul Greyhound Racing Club at Warragul on 20 June 2014 did administer or cause to be administered a prohibited substance viz 5beta-androstane-3 alpha, 17 beta-diol at a mass concentration greater than 10 nanograms per millilitre for the purpose of affecting the greyhound's condition, behaviour or performance in the event.

in that you, the trainer of greyhound Sick Money, which was nominated to compete in an event namely race 10, the Action Packed Images, grade 5 T 3, conducted by Warragul Greyhound Racing Club at Warragul on 20 June 2014, did fail on that date to present the greyhound free of any prohibited substance in that the pre-race urine sample taken from the greyhound indicated the presence of the prohibited substance '5beta-androstane-3alpha, 17beta-diol at a mass concentration greater than 10 nanograms per millilitre.

1. In essence, for respondent Greyhound Racing Victoria to succeed in proving these two charges, it must establish to my confident satisfaction (Briginshaw) the following elements:

(iv) intending to affect its condition, behaviour or performance.

(i) that on the occasion in question, the dog had a prohibited substance in it;

(ii) and that on that occasion the applicant was its trainer.

1. It is also relevant to note here the following provisions in the GAR:

Testosterone as evidenced by the presence BaB at or below a concentration of 10 nanograms per millilitre in a sample of urine taken from a greyhound will not breach the provisions of subrule two of this rule.

'Exempted substance' includes the following substances that are exempted from being a prohibited substance.

1. Ethyloestranol, when administered orally to a greyhound bitch and where it has been prescribed by a veterinary surgeon for the sole purpose of regulating or preventing oestrus in that bitch.
2. Other relevant evidence to outline before I go on to analyse the dispute between the parties includes:

(a) that the applicant had been, since late 2013 and was still on 20 June 2014, administering the exempted substance Ethyloestranol (brand name Nitrotain) to his greyhound once a day every second or third day in the form of a paste, by putting a grain-sized amount on his finger from the tube and then giving it orally to the dog. The applicant did not actually testify that it was prescribed by a vet to prevent oestrus - but he did say that he bought it from a vet supplies premises and so I will infer the rest in his favour particularly as it was not made an issue by the respondent;

(b) that the applicant fed the dog with meat, usually minced beef, or occasionally offal from Maffra Meat Supply and sometimes also some dry food;

(c) that the dog, Sick Money, had previously suffered a muscular injury but he the applicant had helped it recover. It had run 26 times for one win; he never bet on it. There was no money for it at Warragul - she started at somewhere around 20 to 1. Its one win was at Sale on 15 June 2014, only five days before the Warragul meeting;

(d) that the applicant had been a licensed trainer since 1988. He admitted to several prior substance cases with his dogs but denied that any of them were administration cases and this was not disputed by GRV;

(e) that the subject dog, Sick Money, had been swabbed (I assume by urine sample) on 4 March 2014 at Sale where it was negative for any testosterone related substance including BaB; and again on 15 June 2014 (just five days before the Warragul run) where again it was negative for any prohibited substance. I will return to these two test results later as I consider them to be highly significant;

(f) that the applicant denied emphatically ever administering testosterone or any testosterone product (such as Testroprop - another oestrus suppressant) to his dog and could give the Tribunal no explanation for the high BaB concentration in its urine.

1. Now, bearing in mind what has already been accepted by me viz that on the occasion of the Warragul races, the applicant's bitch was found to have in its urine certainly well in excess of 20 nanograms per millilitre of BaB (a prohibited substance) and probably as high as 380-400 nanograms per millilitre - what does the applicant say to prevent the Tribunal:
   • (a) in relation to charge 1 - comfortably drawing the inferences that there had been an administration of the prohibited substance BaB; that it would have been by the trainer, the applicant; and that it would have been to improve the dog's performance in the race; and
   • (b) in relation to charge 2 - simply finding the charge proven because the applicant's dog had the prohibited substance in its system at the races.
2. I will put to one side for the moment the more substantial defence points which the applicant's scientific witness, Dr Tom Astbury, dealt with in his report (Exhibit 3) and in his vive voce evidence.
3. Otherwise, then, despite his indication at the pre-trial hearing on 26 March that his defence would be limited to the Astbury points, the applicant at the trial raised as many potential defences as he possibly could.
4. As previously mentioned the applicant challenged the sampling and testing practices employed by the Stewards and RASL chemists. He put that the samples may have become degraded in transit. That the plastic containers could have been pierced by syringe and the contents interfered with. That the RASL equipment may not have been sterile. That the RASL analyst used the wrong technique in doing the analysis, namely, MS62 instead of MS85. That the MS85 method of measuring a BaB concentration in urine was inappropriate and a better method would have been the IRMS (isotope spectrometry) technique used on humans. That, in any event, there was too much uncertainty in the RASL measurement process particularly with the use of dilution techniques.
5. There was never anything from the applicant to back up any of his propositions. They were nothing more than unsupported questions and criticisms. They were all rejected and explained by the respondent's scientific witnesses - Professor Hibbert, Mr Zahra and Dr Karamatic. These witnesses supported the MS85 method as being of world-wide and NATA approved use and acceptance for greyhounds. The one reference in the certificate Exhibit G to MS62 instead of MS85 was an easily explained innocent mistake. They further explained that the IRMS technique could only be used by humans. They confirmed that the samples and equipment were unsullied and not tampered with. The testing techniques they said would provide 97-98% accuracy.
6. Next, the applicant could not come to grips with the fact that RASL practice restricted its testing conclusion so as to state no more than that the sample tested was in excess of a figure double the prescribed limit, ie, here, 20 nanograms per millilitre. Cleary, this statement would ordinarily be more than enough to prove a case. However, in oral evidence, Mr Zahra was able to amplify the testing data and conclusions by referring to spreadsheets (Exhibit O - the A Sample and Exhibit S - the B Sample), both of which were clearly testing for 5beta-androstane-3 alpha, 17 beta-diol (BaB) if one examines the internal material of the reports. On this basis, Mr Zahra testified that various dilution techniques allowed the confident conclusion that the A sample was actually at a concentration of around 377 nanograms per millilitre; and the B sample was around the concentration of 478 nanograms per millilitre. This should put paid to any concern of the applicant on this issue.
7. And the applicant also pursued a line that microbial degradation may have been responsible for the high BaB. But Mr Zahra testified that this was not a relevant factor in the testing process. Dr Karamatic testified that, if anything, microbial degradation would result in a lower BaB reading rather than a higher one.
8. And further, the applicant tried to use screening graphs and data to prove various points despite sound explanation from Mr Zahra that the screening process was a preliminary one which was never meant to measure quantification of the substances. If the screening revealed the presence of the relevant substance (here BaB), then confirmatory tests using the MS85 method were done to quantify the concentration of the substance - and this is what happened here.
9. On a different tack, the applicant put that his dog may have been 'got at' by a third party. Or that someone may have fed his dog bulls' testicles which could contain high testosterone or that there may have been testosterone in the beef meat he fed to his dog because it is a well-known practice to feed testosterone to cattle, sometimes by implant, to enhance their size and weight. He referred to some articles in vet manuals (see applicant's apps 12 and 19) which refer to the dangers of certain food contents.
10. Again, these were simply shots in the dark and Dr Karamatic testified that oral (ie, from eating), absorption of testosterone was very poor compared to injection and that it was extremely unlikely that there would be elevation of testosterone levels from eating meat and that, even if testosterone was implanted in or ingested by beef cattle, the amount of testosterone that actually ends up in the meat of the carcase is very low. Dr Karamatic pointed out that the dog in question was tested on 4 March 2014 and on 15 June 2014 and showed no sign of elevated testosterone and this put paid to any argument based on contaminated feed meat.
11. The applicant also referred to material, including Dr Cawley's report (Exhibit R), and a press article by a vet surgeon, Dr Fegan, to the effect that factors such as a dog's general health, physiology, metabolism, hydration status et al, could affect BaB or testosterone levels. Dr Karamatic and Mr Zahra agreed that there could be minor variations due to these kinds of natural phenomena but the variations were minor and the various studies on hundreds of both clean and racing bitches seldom found it to exceed 1 nanogram per millilitre, usually much less.
12. In addition to the specific puttage matters I have outlined, the applicant did, in passing, raise a number of other queries and criticisms but none were supported by any evidence or opinion and were peremptorily rejected or explained away by Professor Hibbert, Mr Zahra or Dr Karamatic.
13. In contrast to the wide-ranging 'scatter gun' attacks by the applicant upon the respondent's scientific evidence as outlined above, all of which have proven to be futile, perhaps the aspects of the applicant's defence requiring greater consideration and analysis were the points arising from the applicant's expert witness, Dr Tom Astbury.
14. In essence, Dr Astbury's opinion was that it was unsafe to conclude (as the respondent has submitted) that the high BaB reading must have resulted from a testosterone administration, because there are other possible causes of the high BaB reading, namely:
    • (a) The first theory related what he, Dr Astbury, called - the race environment excitement effect. I return to consider this later.
    • (b) The second theory was a complex biochemical one. Dr Astbury postulated that there is an endogenous process which goes on naturally in a dog's metabolism whereby cholesterol metabolises into DHEA (a steroid) which in turn metabolises into BaB which in turn metabolises into testosterone. Dr Astbury goes on to postulate that, bearing in mind that the exempted substance Ethyloestranol (Nitrotain) is also an anabolic steroid, this permitted substance acts in the dog to potentiate the naturally occurring steroid DHEA which in turn increases naturally the BaB levels which in turn increase the testosterone in the dog, ie, he puts that BaB is a precursor of testosterone, that is, converts into testosterone - as opposed to BaB being a metabolised (product) of testosterone.

I will quote a passage from Dr Astbury's report on this matter word for word from page 1 of his report:

In fact the metabolite 5beta-androstane-3alpha, 17beta-diol (BaB) is a naturally produced endogenous metabolite, termed a precursor, derived by specific enzymatic change endogenously NOT from testosterone but from an endogenous source, the steroid dehydroepiandrosterone known as DHEA (3b-hydroxy-5-androstane-17-one). This steroid has itself been created by various endogenous processes commencing with endogenous cholesterol described in the literature I am providing.

Following its formation from DHEA, so called BaB is termed a pre-cursor ion and then can be enzymatically changed endogenously into endogenous Testosterone but the process cannot be reversed.

1. On further questioning, Dr Astbury clarified - he was not saying that Nitrotain (Ethyloestranol) actually directly metabolised into BaB. But he was saying that, by reason of the introduction exogenously of another steroid (Nitrotain/Ethyloestranol) into the dog, this could well block the release of endogenous testosterone, allowing more 'bound testosterone' to accumulate in the dog's system; and in turn, this may reveal itself by the dog's urine containing higher testosterone levels.
2. This, Dr Astbury conceded, was his own opinion based on his own research - and his fall-back position was that even if not accepted as correct at face value, at the very least GRV had not done any or any adequate studies to disprove it or to otherwise enquire into, consider and reach conclusions on the effects of long-term Nitrotain/Ethyloestranol use on a greyhound's metabolism - particularly as that same body, GRV, had encouraged the use by greyhound trainers of Nitrotain/Ethyloestranol as the preferred oestrus suppressant by exempting it from the definition of prohibited substance in the Rules. This then was Dr Astbury's approach on this part of his theory.
3. The principal problem for Dr Astbury and his theories is that on his own admission he is not the appropriate expert in this highly complex pharmacological and biochemical area. He is, since 1983, a veterinary surgeon but with no further qualifications. In cross-examination he has conceded he was not an expert in this area; it was outside his area of expertise; he as an interested person consulted the internet and other sources by way of his own private research. Further, on the one hand, he is a friend or acquaintance of the applicant and was helping him with his defence; and on the other hand he has been openly critical for some years of the Greyhound Racing Authority over its decision to exempt Nitrotain from the 'prohibited substance' definition - he also being personally interested in the greyhound racing industry.
4. So, through all of this, he does not present by any means as necessarily being completely dispassionate. That is not to say that I actually formed an adverse view of his honesty. On the contrary, I felt that in his own way he was trying to be helpful. But I concluded his views were seriously misguided and erroneous. I draw this conclusion for a number of reasons:
   • (a) I have already referred to his admitted lack of expertise;
   • (b) In his report and in his reasoning and even in the course of his evidence, he completely mixed up and failed to appreciate the quite significant difference between 5alpha-androstane-3alpha, 17beta-diol (Ethinylestradiol - a BB ie, an oestrogen compound); compared with 5beta-androstane-3alpha, 17beta-diol (Ethyloestranol, BaB, an anabolic steroid and a metabolite of testosterone. This failure to differentiate between quite different substances surely calls into question his capacity to properly understand what he was studying in his private research and the conclusions he ended up drawing.
   • (c) Similarly, his report constantly drew upon and referred to biochemical and like studies on humans rather than on dogs. He then extrapolated the findings from the human studies as if they applied equally to greyhounds. As I understood him in cross-examination, he conceded that there may be differences and that human metabolic processes were not the same as in greyhounds (which accorded to the evidence of all of Messrs Zahra, Karamatic and Hibbert); but his answer to this was to rhetorically complain 'where else do I turn to?' in the absence of adequate studies on dogs. This approach is obviously flawed in science and in logic and quite unsatisfactory.
   • (d) An example of the previous flaw related to his suggestion that GRV would be better off using the scanning method known as IRMS on greyhounds to determine the amounts of testosterone present due to endogenous means as opposed to amounts present due to exogenous factors. It turns out that this technique is not adaptable for use with dogs and I refer for this to the evidence of Mr Zahra and Professor Hibbert; and the method of testing used by GRV is MS85, is approved by NATA and is in used worldwide. Dr Astbury conceded in cross-examination that IRMS was not a process for use in greyhounds.
   • (e) Dr Astbury also in his report, page 3, gave an erroneous definition and understanding of an 'isomer' and ultimately conceded this in cross-examination.
   • (f) Dr Astbury was referred to his own document (App 10) and asked if he appreciated the difference between the molecular structure of a substance he had referred to in his written opinion as androstenediol with its double carbon bonding, and BaB that has no double carbon bonding. He answered by saying he was unaware of double carbon bonds.
   • (g) Dr Astbury strongly held the view that BaB was a precursor to testosterone and not a metabolite of testosterone, ie, that the steroid DHEA metabolises into BaB which in turn metabolises into testosterone. He acknowledged that this was his own view and different from the opinion of other experts. In this latter sentence he was at least correct because all other scientific witnesses in the case had no doubt whatsoever that BaB was a metabolite of testosterone, and I include in this Professor Hibbert whom everybody seemed to respect. And I accept this broadly held view, that is, that testosterone metabolises into BaB and not the view of Dr Astbury whose conclusion on this is seriously flawed and puts him right out on a limb.
   • (h) There were other valid criticisms of Dr Astbury's views and, to his credit, Dr Astbury actually conceded a number of shortcomings in his reasoning processes. But the end result of it all is that I do not consider that I can accept any of his substantive conclusions as having any real weight or probative value.
5. By way of reminder, we are still dealing with the applicant's defence point, based on Dr Astbury's theory and upon his evidence, that the exempted Ethyloestranol in the Nitrotain could well be the cause of the high BaB reading. First, this view must be read as subject to the shortcomings and errors of Dr Astbury's reasoning listed above. Secondly, it is also contrary to the vive voce evidence of all the respondent's scientific experts and not consistent with the findings recorded in the studies exhibited by the respondent, namely, Exhibits P, Q and R; studies by Messrs Biddle and others; by Professor Hibbert, and Dr A Cawley respectively. All three scientific witnesses (Zahra, Karamatic and Hibbert) testified that, without question, BaB is not a precursor to but a metabolite of testosterone and external administration of testosterone or a testosterone product will lead to increases in BaB levels and if the BaB levels exceed 10 nanograms per millilitre in the dog's urine it was virtually certain to be due to an external administration of testosterone. This view is consistent with what is apparently the only study done on a greyhound regarding the metabolic effects of Ethyloestranol and I refer to the McKinney report of 2013, Exhibit T. Oral administration to a greyhound of Ethyloestranol showed the subsequent presence in its urine of a number of metabolites - but no BaB.
6. Witnesses Zahra and Karamatic also made the point that over some years RASL has done 3,500 tests on greyhounds for BaB elevation. Only 19 were positive and of these, in 15 cases, the trainers admitted to using testosterone, leaving only 4 cases unexplained. The witnesses reasoned that, as Nitrotain is quite a commonly used product in the greyhound industry (although they did not know with any exactness how many of the 3,500 dogs were on Nitrotain), they questioned, how come there was not a far higher incidence of elevated BaB if the hypothesis that Ethyloestranol causes high BaB is a correct one.
7. Further, witness Zahra, who was recalled in rebuttal of Dr Astbury's theory regarding Nitrotain causing accumulation and therefore high levels of 'bound testosterone' in the urine, testified that if this were so, the urine would contain high 'testosterone' as opposed to high 'BaB'; and that this is so because testosterone does not convert to BaB in the laboratory. It only does so in the greyhound's system.
8. Finally, and this point, although in my opinion of considerable anecdotal significance, was not made a great deal of, but I certainly regard it as of important evidentiary value - the two fairly recent prior tests done on Sick Money on 4 March 2014 and on 15 June 2014 (when the dog won at Warragul) were both negative for BaB - yet the applicant testified that throughout this period he had been regularly administering Nitrotain to Sick Money to keep it out of season. If Nitrotain causes high BaB, how come the negative results?
9. Therefore I must conclude comfortably that Nitrotain, which does not contain any testosterone, does not either directly or indirectly lead to any elevation of BaB levels in greyhounds.
10. I have also referred to the other defence point based on Dr Astbury's opinion - that the high BaB reading could be due to a race environment excitement effect. Again, I will quote passages from Dr Astbury's report on this matter.
11. The first at page one:

In my opinion based on evidence I include the suggestion that high levels of BaB in your sample would result from natural sources initiated by the race environment excitement effect ...

The lack of any investigation into the effects of natural endogenous production and the psychogenic effect of the race excitement on the greyhound's anabolic metabolism is a serious failing in my opinion.

1. In his evidence, Dr Astbury opined that race excitement can increase the dog's cholesterol (ACTH hormone) and in turn by a chain of metabolic processes may increase BaB. Dr Astbury conceded this was really only his theory. There were no studies on the topic. He relied on his observations of how excited greyhounds appear to get pre-race but he had no idea and measurement of how much effect this had on the dog's BaB. As with the other issue, that is, Nitrotain's effects, his fall-back position was that GRV had not done any studies on the topic to disprove the possibility of race excitement converting to certain biochemical changes.
2. Again, this unsupported view was totally dismissed by the other scientific witnesses. Dr Karamatic - a veterinary surgeon, is familiar with this topic and referred to a study he had been involved in where tests were done and no differences were found in the dogs' hydrocortisone levels pre and post-race. He also asked why the great majority of the typical random tests (many pre-race) ie, the 3,500 RASL tests, came back negative, if pre-race excitement was a factor in causing elevated BaB. Why was this dog different to other dogs? And how come there was such a high reading - because if excitement was to have an effect it would be minor?
3. Professor Hibbert in his report, Exhibit Q, refers to various studies from which he took his data. One study involved 187 clean bitches (not engaged at the time in racing) where most had no or negligible BaB and in the others it was very small. Another study involved 519 race day bitches and Professor Hibbert in his vive voce evidence said that the BaB levels in this latter cohort were virtually the same as with the non-racing cohort, hence he concluded that there was no substance to Dr Astbury's theory that race day excitement was a BaB elevating factor; and Professor Hibbert went on that the allegation on page 8 of Dr Astbury's report that this race day excitement factor had been overlooked by him (Professor Hibbert) in his research, was completely wrong.
4. Finally, Dr Karamatic again made the point that the earlier sampling 5 days before the Warragul races showed no BaB elevation - and I add that presumably the same point can be made regarding the 4 March 2014 sample which was also negative for BaB elevation.
5. Again, I am comfortably satisfied that the 380-400 nanogram per millilitre urine BaB found in the pre-race sample taken from Sick Money on 20 June 2015 at Warragul cannot be attributed to pre-race excitement.
6. In summary therefore, I reject both of what I might describe as the more substantive defences raised by the applicant and supported (as much as it could) by Dr Astbury. I have also rejected the myriad of other challenges made by the applicant himself, most of which would fall under the rubric 'flying a kite'.
7. I am left with the conclusion, heavily supported by Mr Zahra, Professor Hibbert and Dr Karamatic, based on their expertise and on their reading of the materials contained in Exhibits P, Q, R and T - that the elevated BaB in Sick Money's urine was due to an administration of a significant amount of a testosterone product which - I consider most likely would have been the readily available oestrus suppressant testroprop.
8. Notwithstanding the applicant's claim (which is a claim heard in most of these sorts of cases), that there is no (and he means no 'direct') evidence of him administering testosterone to his dog or of him having an intent to affect the race result, I nevertheless conclude comfortably by inference and in the lack of any other alternative explanation, that is was the applicant who was responsible for the administration and that it was done to affect the dog's condition behaviour or performance in the race. Therefore I find both charges proven.
9. I do acknowledge that no readily discernible motive emerged from the evidence. This is by no means uncommon in prosecutions of all kinds. But here, in view of the incontravertibility and the strength of the administration evidence, I am not swayed from my conclusion by the inability to detect a motive. I suppose also that lack of unusual betting activity rules out any realistic motive for third party involvement.
10. I also acknowledge that while finding against Dr Astbury's substantive opinions on the biochemistry of the case, I do have some sympathy with his view that it would make life easier for owners and trainers in the industry and also for those involved in any prosecution proceedings if studies had been done by the Greyhound Authority on the effects of Ethyloestranol on the metabolism of greyhounds - in view of the fact that the said Authority has, by the Rules, declared the substance to be exempted and therefore permitted to be widely used. In that event, proofs and conclusions may well have been much clearer and easier to understand and draw rather than having to rely on complex, esoteric and wholly scientific material. This criticism, however, does not of course dilute or alter the conclusion I have expressed above, which, I am more than confident, is based on sound scientific reality and is in accord with the opinions of well qualified experts - three of whom gave vive voce evidence, and others whose various studies have been referred to and exhibited as part of the evidence in the case.
11. So, as I have indicated, the applicant as a result of this is found guilty and convicted of the first charge pursuant to GAR 83(1) and the second charge pursuant to GAR 83(2), (3) and (6).

1. I repeat the fundamental conclusions that I reached in relation to the issues in the case. I found the applicant guilty and convicted him of a breach of GAR Rule 83(1), ie, the administration charge; and I have found him guilty of a breach of Rule 83(2), (3) and (6), ie, the 'presentation to the races with a prohibited substance charge'. By way of elaboration I repeat my finding that there is a high probability that the BaB readings in the urine were in the order of high 300's nanograms per millilitre which could only come about as a result of a recent and significant administration by the applicant to the dog of testosterone or a testosterone product. In view of those findings, this must be taken to be a serious pair of offences. We are not talking about something at the margins. We are talking about a gross violation of the Rules by the applicant.
2. Now the applicant does not present as a person with a clean record. He does have several prior convictions for drug offences but he validly makes the point that they were all cases of the lesser offence of the two, viz, the strict liability offence (presentation) rather than the deliberate administration offence. However, they are drug offences and I cannot by any stretch of the imagination treat him as a cleanskin in this regard. There are also some other offences showing a disregard for the propriety of the industry and its officers. In addition, the applicant can receive absolutely no credit for remorse or co-operation; as is his right, he has fought the case at every level and to every conceivable degree, without giving an inch on any of it. As I say, it is his right to do so but having done so, he can receive absolutely no credit for co-operation or remorse. On the contrary, he pursued with the help of his friend or acquaintance, Dr Astbury, a most difficult and elaborate defence which ultimately was found to be quite unmeritorious but it took three days of intense evidence, scientific evidence and understanding to enable that conclusion to be reached. The other important factors that I must bear in mind in relation to penalty include the retribution consideration to properly penalise somebody who is prepared to grossly violate the Rules by deliberate administration as I have found occurred. There is the issue of the health of the dog and there is the further important issue of the integrity of the industry and the importance in the greyhound gambling industry together with the other legs of the gambling industry (thoroughbreds and harness racing) to present to the betting public as totally clean and beyond reproach. These are all important factors that I must have at the forefront of my mind in relation to penalty.
3. Mr Vass, on his own behalf, has pointed out he is an ex-serviceman; he has been a football coach; he has done voluntary work in relation to the industry, including race-calling; he has also obviously been of assistance to Judge Gordon Lewis in relation to his inquiry concerning the industry and I note the contents of Judge Lewis' letter. The factors I have mentioned must be posited as far as the applicant is concerned. However, they do not go very far in mitigating the gravity of the offence and the other factors that I have already referred to calling for condign measures.
4. There are guidelines which in no way bind me. I can look at what happened in some of the previous cases. In fact, most of the previous cases are different relating to the lesser offence (presentation). But I can use these guidelines for what they are worth. I do accept that this is a category 4 substance. On reviewing the contents of the category 3 substances, I can see nothing there that equates to testosterone or BaB and I can clearly see anabolic steroids referred to in category 4 and Dr Karamatic certified that it was a category 4 substance and for what it is worth, in terms of guidelines, that is the way I categorise it, despite the cases handed up to the contrary. But imposing a penalty in this area is the same as it is in any other area where it has to be done. It is a matter of an intuitive synthesis on my part trying to take account of all the factors that are relevant, including the factors put forward by GRV on the one hand that called for condign punishment and the factors put forward by the applicant calling for mitigation. As I have already said, the mitigation factors in my view in this case are not a great moment but for what they are worth I take them into account. I have not mentioned the factor of deterrence, ie, deterrence generally and specifically of Mr Vass. But that is also a relevant consideration. By the way, I do recall that Mr Vass did allude on the last day of the hearing to the fact that he had no intention of returning to the industry. However, that is not really is a factor that carries any relevance at this point. I do propose to make an allowance for the 2 ½ months that has already been served towards any penalty because there is no suggestion that what Mr Vass told me about that is incorrect and indeed GRV have conceded it.
5. In relation to charge 1, I have already said that I find the applicant guilty as charged and I disqualify him for a period of 3 years, and fine him the sum of $1,000.00.
6. In relation to charge 2, again, he is found guilty as charged and I disqualify him for a period of 12 months. I do not propose to add any fine there. I will order that the two periods of disqualification be served concurrently making a total of 3 years and I declare that the period of disqualification commences from this day but is subject to an allowance of 2 ½ months which I declare to be already served.