APPENDIX 2. BECOMING AN ADDICTION SPECIALIST. A historical-biographical note.

Just as the story of disulfiram involves an unusual amount of serendipity, so does the story of how I came to specialize in addiction treatment. The specialty was not only far from my mind when I was a medical student or during my house jobs: it did not really exist in Britain. And neither, during that period in the early 1960s, did heroin addiction except among a small – though slowly growing – community divided between native British addicts (some of them receiving heroin maintenance prescriptions since injuries sustained in the First World War) and a more exotic and younger American and Canadian group attracted by the unique British prescribing policy. Almost the only well-known alcoholism specialist was Dr Max Glatt, a refugee from Nazi Germany who, unlike his parents, only just made it to Britain in time and identified with addicts partly because they too were a persecuted and marginalized group. He edited the British Journal of Addiction to Alcohol and Other Drugs, (later, the British Journal of Addiction and later still, just plain Addiction) which had only changed its name from the more censorious and Victorian-sounding British Journal of Inebriety in 1947.

As a student, my only exposure to more than the occasional alcoholic in-patient was when I was what was still called a ‘dresser’ (i.e. a student assistant) during my ‘clerkship’ (i.e. temporary attachment) to a surgeon called Alan Hunt. He was a large, strong man and a bold operator (and the brother of the first conqueror of Everest, Sir John [later Lord] Hunt). This was just as well, since his specialty was creating a porta-caval anastomosis for patients with advanced liver cirrhosis who were otherwise at serious risk of bleeding to death.[1] In Britain at that time, before the epidemics of hepatitis B and C among injecting drug abusers, by far the commonest cause of cirrhosis was drinking too much alcohol.[2]  Several of the patients were publicans or restaurateurs. Most were just enthusiastic consumers. However, the most I can say is that this early exposure may have made me a little more aware than most doctors of just how much harm alcohol can do, even to people who don’t think that they are alcoholics and whose friends and family don’t think so either. Later, I came across similar patients on the medical wards at the Westminster Hospital but by that time, most of them were being considered for liver transplants rather than anastomoses.

My student education at St Bartholomew’s Hospital certainly wasn’t responsible for my later interest in psychiatry. Few medical schools took the subject very seriously in those days and it was not well taught. We saw a few colourful but atypical patients on our visits to the great Metropolitan asylums, each one occupying many acres of what was still fairly open country, and we sat in on a few out-patient clinics. During one of these, a new, depressed patient - an intelligent and articulate man - was being interviewed by the consultant in the presence of half a dozen students. His response to one question seemed to puzzle the interviewer and after the patient had left the room, the consultant – subsequently a president of the Royal College of Psychiatrists - said that he thought there was a psychotic element to the diagnosis, on the grounds that the answer he gave was very strange and didn’t make sense. One of my more literary contemporaries pointed out politely that the man had merely been quoting from a poem to explain the way he felt.

In our final year, many of us spent a month at a hospital abroad. These visits were arranged by one of the student organisations and quite by chance, I was allotted a hospital in Porsgrunn, a small town in the south of Norway. Although small, Porsgrunn possessed a relatively large general hospital that was also the regional neurological centre. One of my duties was to do lumbar punctures, a procedure at which I became quite proficient.[3] The purpose of some of the lumbar punctures was simply to obtain cerebrospinal fluid for laboratory testing but several of them were done as part of a now-obsolete brain x-ray technique called pneumoencephalography and it was this entirely serendipitous experience that led indirectly to my becoming an addiction specialist.

Before that, I had to become a psychiatrist but even that was unplanned and  serendipitous. My original intention, once I had got the travel bug out of my system, was to do general practice. After six months of extremely general practice as a ship’s surgeon on a big cruise liner, I did a few locums, including a month in an Oxfordshire practice so rural and remote that we dispensed our own medicines, thus giving me a unique opportunity to experiment with placebo medication before it became regarded as unethical. I soon realized that about a third of general practice patients seemed not to be suffering from any physical illness and had what were usually called psychosomatic conditions (among the less stigmatising terms). It occurred to me that general practice in a university setting might give me a more intellectually stimulating bunch of patients and a particularly varied and agreeable set of colleagues. I consulted a few student health doctors, who said that I should do some psychiatry (because many students were ‘a bit neurotic’) and some dermatology (because many students had acne). I applied for jobs in both specialties but the psychiatric one came up first. It was at Cambridge and I rather enjoyed both the work and the local culture. It quickly became clear that as well as being interesting, there was very little emergency work in psychiatry; that being part of an academic community was just as much fun as I had expected; and that it only required two years to get the psychiatric specialist qualification as opposed to at least three for the MRCP.

We saw a few student heroin addicts, Cambridge being a pioneer in this field, as in so many others. I had no particular interest in them but one of my patients was a professor’s daughter whose withdrawal symptoms were so uncomfortable that she threatened to leave. Our response was simple and humane; we increased her sedation enough to keep her asleep for most of the next few days and detailed a nurse to see that she didn’t fall out of bed. The British Medical Journal was discussing how to handle these new and challenging patients, so I contributed a letter on the advantages of withdrawal under sedation.[4]

Later that year, I moved down the road from Cambridge to Harlow, one of the post-war New Towns, where Britain’s very first psychiatric unit in a general hospital had just opened. By 1968, heroin addicts were becoming steadily less unfamiliar. NHS prescribing clinics had recently started and a single patient in his 20s, who had moved to Harlow to escape the temptations and dealers of London, came to the psychiatric ward every day, Sundays included, to inject methadone on his way to and from his job on the railway. I quickly recognized that he could inject himself intravenously at least as well as I could inject him and we let him do it routinely, though always under observation. In hindsight, it may have been Britain’s – and the world’s – first supervised injecting facility.[5]

After getting my Diploma in Psychological Medicine (the Royal College of Psychiatrists was still several years in the future) I started planning the voyage around the world that I wanted to do before settling down. It began in Australia and after a few weeks of GP locums in Melbourne and upstate Victoria (where I acted first as the anaesthetist and then as the surgeon in my last two appendicectomies) I drove to Adelaide to stay with an Australian fellow-trainee at Cambridge who had started his psychiatric practice there. There were no GP locums to be had just then but my friend said that I had a specialist diploma and therefore in Australia, that meant that I was a specialist. They needed a psychiatrist at a local general hospital. At 28, I was probably Australia’s – and perhaps even the world’s - youngest consultant in the specialty.[6]

As in many publicly funded bodies, the finances of Adelaide’s Repatriation General Hospital (an institution similar to the Veterans’ Administration hospitals in the USA) were run on the basis that if any of the departmental budget hadn’t been spent as the end of the financial year approached, something was quickly found to spend it on so that the budget wouldn’t be reduced the following year. Consequently, we lacked for nothing. One day, I lifted the cover on a desk-sized object that had stood undisturbed in a corridor for several months since I had started working at the hospital, revealing a modern EEG machine, almost unused since its last-minute purchase two or three years earlier. Reading 12-line EEG tracings is tricky and it was actually much easier to send patients to real experts but I took a short course in EEGs and even did a few myself.

I enjoyed my work. For a start, it involved no night duty, not even ‘on call’ and was well-paid by NHS standards. It wasn’t an official teaching hospital but we had some students and the post-graduate programme was excellent. There were some fine consultants and it had a medical superintendent - Tom Dearlove - who was not only efficient but also a kindly man who lived up to his surname. I had good juniors, one of whom – Bob Goldney – later became a professor of psychiatry at Adelaide and almost persuaded me to return there as a senior lecturer. The relationship of juniors to consultants was completely different from the style in the NHS. In Britain, a friendly consultant might address a junior as Bob or Jane rather than Dr Smith but a junior would never address his consultant in the same familiar way. In Australia, the first-name terms were bilateral. I think one reason for this, apart from the more egalitarian Australian tradition, was that specialists in Australia were dependent for most of their income on referrals from GPs. As in pre-NHS Britain and in many poorer countries to this day, good specialists often gave their services for free to the public hospitals, getting their income mainly from private practice. If they weren’t nice to their juniors, they might not get many private referrals when those juniors became GPs.

My patients had all the usual psychiatric conditions plus a few unusual ones. Several were survivors of terrible brutality and deprivation in Japanese POW camps. One man had gone blind after getting scrub typhus and lying unattended on the battlefield for a couple of days. Another had started getting recurrent attacks of mania after a bout of cerebral malaria. However, about half of the patients in the psychiatric ward were there because they drank too much. In most cases, this had little or nothing to do with the war but the inexorable logic of Repat policy meant that everybody had to pretend that it did. People who get a disability pension for being alcoholic arguably have little incentive to get better because it pays for their drink. It occurred to me that some of them might also have drunk themselves into a state of early dementia, for although I had not treated many alcoholics, I knew from my preparatory reading for the DPM that alcohol can rot the brain quite effectively. Every asylum had a collection of patients whose brains had been so badly damaged by alcohol that they were incapable of an independent existence, even though many had stopped drinking by then. (They still exist, even if there are no longer any asylums for them to inhabit.) If some of my patients had lost a lot of brain cells, might that be another factor in their repeated relapses? Brain damage doesn’t usually improve self-control. Finding out whether they had brain damage wasn’t easy but I reasoned that investigating the brain was very like investigating the heart – the only other large electricity-emitting organ in the body. When investigating the heart, you do an ECG to look at its electrical activity, you measure blood-pressure and various other aspects of blood flow to look at its efficiency as a pump and you use x-rays or other imaging techniques to see if its internal and external shape is abnormal. The main difference is that you don’t usually hear interesting noises from dodgy valves seventy times a minute if you put a stethoscope to the head.

Since the mid-1970s, if we want to know what a patient’s brain looks like, we order a CT, MRI or PET scan. We now get beautiful pictures of the brain, sliced radiologically in various anatomical planes and we can easily see if those little grey cells in the cortex and other equally vital bits are affected by atrophy, haemorrhage, tumours and other disease processes. Unfortunately in 1969, CT scans were still five years away from being introduced. Ultrasound or radioisotope brain scans might detect a tumour or a big bleed but gave virtually no anatomical detail. A plain x-ray shows nothing of brain structure. The only way of making the brain visible was with air- (or pneumo-) encephalography which involved doing a lumbar puncture, introducing a bubble of air into the cerebrospinal fluid, letting it float up into the brain and then turning the patient every which way so that the bubble floated into the brain’s grooves and cavities, making them visible and measurable on x-ray. Many doctors thought this an excruciating and barbaric procedure but because of my medical student experience at that Norwegian hospital where pneumos were done several times a week, I knew that most patients didn’t find the procedure very distressing. In any case, if they had a post-lumbar puncture headache, I gave them generous doses of analgesics.

Repat had an experienced neuro-radiologist, Lance Perrett, who shared my interest and was willing to do pneumos, so I started ordering them. After we had done a few, it was clear that nearly all the patients had at least some brain shrinkage and most of them also showed impairments on neuropsychological tests of brain function, for Repat was as well supplied with clinical psychologists as it was with clerks and porters. We carried on assessing them and by the time I left, we had collected 33 cases. It started out as a clinical exercise but soon turned into something that could be written up as a useful contribution to knowledge.[7] Around 70% of the patients had some atrophy and in about a fifth of those, the loss of brain tissue was more than minor.

If anyone doesn’t realise that alcoholism is not just a serious condition but often a lethal one as well, I should mention that I followed up all my patients six years later. Thanks to their need to maintain at least annual contact with Repat in order to claim their pensions, I was able to track down every single one of them – an unusual situation with alcoholics, who tend to move around or simply disappear. Of the 33, eleven had already died an average of 2.5 years after their first admission under my care at an average age of only 55 (which, among other things, is very young for visible cerebral atrophy to be so common). Apart from this high mortality, four patients – all from the group with the most marked cerebral atrophy - needed apparently permanent hospital care for alcoholic dementia or intractable alcoholic paranoia.[8] Not all the deaths were clearly due to alcohol but most were. These really horrifying figures are not very different from the results of a much earlier multi-generational survey of 500 alcoholic patients of whom 55 killed themselves, 28 “died psychotic” and 25 “died derelict”. Average longevity was 52 years and 12% died aged less than 40.[9]

When I eventually returned to Britain and became Lecturer in Psychiatry at Birmingham, my brain damage paper soon became common departmental knowledge. Equally soon, clinical conversations with my colleagues started to include suggestions that since I seemed to like alcoholics, and they on the whole did not, would I mind taking over this patient of theirs who wasn’t making much progress? I thus soon became known as the go-to clinician for alcoholics and there was absolutely no competition. Griffith Edwards reinforced this image (and self-image) by inviting me to national and international conferences to speak about my brain damage study and he also invited me to the Maudsley itself – the Vatican of British psychiatry and addiction - to advise two of his colleagues, Alwyn Lishman and Maria Ron who, in 1974, were planning to use their brand-new CT scanner to repeat my pneumoencephalograpic study on a larger number of patients with British rather than Australian drinking patterns. Their results were gratifyingly similar, with “a high incidence of cortical shrinkage and ventricular dilatation”.[10]

One of my research interests didn’t seem to have much influence at the time on my approach to addiction treatment but possibly affected it later. Among Birmingham’s surgeons was a pioneer in obesity surgery, Mike Baddeley. His patients who underwent jejeunoileostomy[11] lost large amounts of weight and we collaborated in a study[12] of the psychological consequences of massive weight loss and the changes in body-image that followed. The diminishingly-influential psychoanalytical doctrines of the time held that fat patients needed to be fat and predicted that they would get symptom-substitution if they merely lost weight without attending to the underlying problems and complexes that the doctrines required them to have.[13] In reality, the interesting thing was how quickly and easily most of them adapted to their now normal or even slimline figures. Even those with a history of previous psychiatric conditions did well with no more than simple supportive counselling. Where food was concerned, many of the patients had previously behaved like addicts to other substances. During their week-long preoperative admission and preparation, they demonstrated denial, deviousness and excessive appetites but their behaviour changed dramatically and lastingly, following a procedure that was about as un-psychological and unsubtle as one could imagine. This reinforced my support for the lessons of Griff’s ‘Treatment vs Advice’ study and similar findings revealing that many patients did well with minimal psychotherapeutic intervention.

I never really intended to do much private psychiatry. Like most NHS academics, I was flattered if GPs asked me to see the occasional private patient as a special favour but I expected to be spending the rest of my life seeing mainly NHS patients and doing clinical research. Unexpectedly, I was offered a part-time Research Fellowship which involved interesting investigations but none of the daily clinical work that was what I really enjoyed doing. I assumed that a part-time clinical job would come along soon but I was keen to make up for the drop in my income and I let it be known to Birmingham's GPs that I was available for private consultations. I really didn't expect that I would get many more than the occasional private referrals that I had already had but – serendipity again – it happened that shortly afterwards, Birmingham's two busiest private psychiatrists left the scene, one through getting a chair overseas and the other through illness. Soon I was quite busy myself. By the end of my three-year Fellowship, I didn't really need an NHS job but it didn't seem right not to work in the NHS as well. Having moved to London (I commuted twice weekly to my Birmingham practice until my growing London practice made it impossible) I did a few sessions in general psychiatry at a London hospital with a world-famous community psychiatry service until Peter Dally - a very distinguished consultant who was widely believed to service Buckingham Palace - asked me if I would be interested in reviving a moribund alcoholism service at the old Westminster Hospital a few hundred yards up the Thames from Parliament. That's how I got involved in the probation-linked disulfiram programme.

Until 1985, the Cambridge patient withdrawing under sedation and the methadone-injecting Harlow one constituted almost the whole of my experience of treating heroin addicts. In that year, a new drug became available: the opiate antagonist naltrexone, which completely blocks the effects of even very large doses of heroin. (A blockade that I tested out with several patients, including an international businessman with an enormous heroin habit who showed absolutely no opiate effects after snorting half a gram of pure diamorphine powder in my presence.)[14] I could legally prescribe it for this test because he was not snorting it as part of his addiction. The test was done because he was being treated with a new type of naltrexone implant and since I wanted to be sure that it would block even his vast doses, I took blood for naltrexone and peak diamorphine levels - as well as morphine, to which diamorphine is quickly converted in the body. When they sent the results, the laboratory asked if it was a post-mortem sample, because they had never seen such high levels in a living patient.) 

Naltrexone was actually not all that new and I had read a bit about it but because it hadn’t been available in Britain and because I wasn't treating heroin addicts, I didn't read very much. However, what I had read made me realise that it had some close and interesting therapeutic similarities to disulfiram, in the sense that it, too, was a deterrent drug. It would change the experience of using heroin from a pleasant and attractive one to an unpleasant and unattractive one. The main difference between naltrexone and disulfiram was that disulfiram deterred by the prospect of an unpleasant physical reaction to alcohol while naltrexone deterred by the prospect of an unpleasant psychological reaction to heroin, namely profound disappointment and the realisation that the user had just wasted a lot of money. The probation service were starting to see quite a few heroin related offenders as well as their usual alcoholic ones and I wondered whether naltrexone might do for the former what disulfiram had manifestly done for the latter.

I didn’t plan to start treating heroin addicts myself, but the consultant responsible for them didn’t like treating offenders, didn’t approve of probation-linked treatment, wasn’t interested in naltrexone and was near retirement, so I borrowed a few patients from her (as was easily done in those relaxed days before the monstrous and growing regiments of bureaucrats took much of the pleasure out of medical practice). Nobody else in Britain seemed interested in naltrexone either but I read everything I could about it. Soon, I amazed everyone (myself included) by confirming that supervised naltrexone not only helped people to avoid relapse in much the same way that supervised disulfiram did but also shortened opiate withdrawal from the usual week or two (and often more) to just a few days. That solved one of the main problems with naltrexone: that patients usually have to be opiate-free for a week before they can start it and most opiate detox programmes had very high drop-out rates. In 2003, the Maudsley’s very own programme managed barely a 25% completion rate in carefully selected and well-motivated patients, though you had to read between the lines to discover that. It wasn’t evident from the title of the study.[15] A third of that 25% had relapsed within a month and 10% died of heroin-related causes within a year.

The technique I learned from my reading and a quick visit to the few naltrexone experts in the USA combined detox with starting naltrexone, used varying levels of sedation to minimise the discomfort of withdrawal and had completion rates close to 100%. Westminster weren’t interested in developing the programme but news of a quick detox under sedation spread rapidly among London’s heroin addicts (who have a much better treatment grapevine than the average alcoholic). My private practice was soon even busier and I left the NHS around 1987. The clinic I set up needed a name. Most of my detoxes were done at a private hospital just off the M25 near a tiny village called Stapleford Tawney, in Essex, so I called it The Stapleford Centre. Its style was deliberately Oxford Street rather than Harley Street, Marks-and-Spencer rather than Harrods. However, as well as low-cost detoxification with mainly oral sedation, we also offered a 'de luxe' version under general anaesthesia. After doing a few cases in 1989-90 following a visit to Norbert Loimer after his pioneering study at Vienna University Hospital, we offered it routinely after 1995 and detoxified over 700 patients under anaesthesia without any significant complications. After a good night's medication-assisted sleep, most of them were well enough to return home the next day. The oldest patient in this series, an international journalist in his 60s,  had breakfasted and put on his usual well-tailored suit by 8a.m. and was anxious to get back to his newsdesk. In 1989 at London’s Barbican Centre, over 100 people attended the first of about a dozen Stapleford international conferences.

Although I have not held a formal academic post since 1982, I appear to have written not only most British papers on disulfiram for alcoholism but literally every single British paper on the very similar principles and practices that underlie the use of naltrexone in the management of opiate dependence. However, while even an unlicensed disulfiram implant is not commercially available or likely to be any time soon, primitive and unlicensed but very effective naltrexone implants, initially made in the USA, became available around 1997. They transformed heroin detox because while patients on oral naltrexone could use heroin a day or two after they stopped taking it (i.e. much sooner than most patients taking disulfiram could relapse to alcohol) implants almost guaranteed that they couldn’t relapse during the first crucial month or two when most post-detox relapses happen (as they did in the Maudsley detox programme).[16] By about 2000, I was able to use an implant made in Australia with a duration of around six months. A year or two earlier, its creator, a remarkable Australian gynaecologist called George O’Neil, had tracked me down and visited me at home around midnight before returning to Perth the next morning. We have remained good friends and collaborators despite the fact that George is a Low Church Evangelical who honed his considerable improvisatory skills as a missionary surgeon in Africa while I am a cheerful unbeliever.

As might be expected, George’s implants were even more effective because after six months without experiencing the effects of opiates, both the patients and their opiate receptors had an even better chance of regarding an opiate-free life as the new norm rather than as a novel and worrying experiment. It’s the same rationale that informed the OLITA study: the longer you stay on a medication that prevents you from enjoying your favourite drug, the less likely you are to relapse when the medication is discontinued. And the fewer decisions you have to make about having a booster dose, the fewer the opportunities for making the wrong decision. When someone gets round to doing the study, I have predicted that they will get more long-term abstinence from opiates after two implants each lasting about six months than after six implants lasting about two months and that twelve injections of Vivitrol (depot naltrexone lasting about one month) will be even less effective.[17]

As well as quick and therefore relatively inexpensive inpatient heroin withdrawal and naltrexone induction with an almost 100% completion rate, followed by supervised oral and (from 1997) implanted naltrexone treatment, I had started providing methadone maintenance. This was partly because I soon discovered that not all patients feel well even after several months of being opiate-free and that some of them do much better on long-term methadone, even if they desperately want to free themselves from opiate dependence. Other patients were not really ready to withdraw and would need several weeks, months or sometimes even years on methadone before they would be ready to make the experiment of trying to live – and live happily and successfully – without opiates. Another reason was that just around the time the first randomised controlled trials showing the effectiveness of methadone maintenance were published in 1979, followed by the unexpected and unimaginable HIV epidemic that made 60% of Edinburgh’s injecting addicts HIV-positive by the early 1980s, the British addiction Establishment bizarrely decided that methadone, other than for short-term withdrawal, was neither needed nor appropriate in Britain and strongly discouraged maintenance. Patients who had been on long-term stable maintenance and in steady employment during the 1970s suddenly found that their pharmacological lifeline was brutally withdrawn. New and very suitable patients found it almost impossible to obtain methadone maintenance in NHS addiction services. Less doctrinaire addiction physicians criticised the Establishment for their “excessive adherence” to psychological approaches to addiction.[18]  It was 20 years before the Establishment did a reluctant (and one hopes at least privately embarrassed) U-turn. Many lives must have been wrecked by this massive and evidence-free gap in British addiction services, for which the Establishment have never apologized and during which they often attacked our own maintenance programmes. My first methadone maintenance patients arrived in my waiting room en masse after Dr Ann Dally – Peter’s ex-wife, with whom he shared consulting rooms – was hounded by the Establishment for taking on some of the long-term maintenance patients they had abandoned, and lost her licence to prescribe opiates. Similar conflicts of ideology led to a similar campaign against me and my colleagues that led to what was then the longest case in the history of the GMC and is still the largest in terms of the number of doctors involved. This is not the time or place to go into the details but you can get a good idea of the political background at the time from a long article in the Daily Telegraph (a newspaper not famous for its sympathy towards heroin addicts or methadone maintenance).[19]

When in 1999, the Establishment U-turn became official policy, it turned out that GPs, rather than specialist clinics, were expected to prescribe the newly-rehabilitated and un-demonised methadone. Since the Establishment had been telling them for the previous twenty years that methadone was Bad, it was natural that the GPs did not initially embrace their new task with enthusiasm and in consequence, the doses they prescribed were often derisory. The new guidelines advised, correctly, that most patients could be accommodated within a dose range of 60-120mg/day but many patients received no more than 35mg and average doses remained below 60mg for many years.

There’s an old medical saying that if you haven’t made any mistakes, you haven’t been seeing enough patients. I have never thought myself infallible but so many distinguished addiction specialists from other countries visited the clinic that I rather assumed – as did my colleagues – that we must have been broadly doing good things and helping to improve a branch of medicine which – unlike every other field of NHS practice - had really hardly changed its treatment menu since I qualified in 1963. Several visitors also told me that they would like to do some of the things that we did but that their administrators would not allow them to do so. In trying to overcome the deficiencies of the NHS, especially long waiting lists and high failure rates for in-patient opiate withdrawal, we devised a home-detox programme using family supervision that most families could afford and which ended in most cases with a naltrexone implant that almost guaranteed no relapses in that crucial first month or two after withdrawal. After some 2000 families had used it with high success rates, one patient died, in part because our instructions were held to be insufficiently clear.

Successive reorganisations and re-reorganisations of the NHS in general and of substance misuse services in particular, together with a tendency to contract out addiction services to the lowest bidder, mean that British addiction treatment now compares unfavourably with services in many other European countries. This, combined with underfunding and low morale in the NHS generally and general practice particularly, does not bode well for the future. The clinic continues and provides most of the services that it did when I was in charge, including effective in-patient detoxification, though in response to changing patterns of addiction in Britain and more generally, it is now called the Opiate and Analgesic Dependence Clinic. It is the sole remaining private methadone clinic.[20]



[1] Alan Hunt was friendly to students and invited them to his grand house in St Johns Wood at the end of their clerkship. That was the first time I had encountered a real butler. His affability and sang-froid were tested unexpectedly during a ward round when one of my fellow students – later a distinguished surgeon himself – was describing the progress of a patient who had just been anastomosed. After recounting the various pre-operative tests, he came to the denouement. ‘And then,’ he said, ‘the patient was operated on by Mr Cunt’. Mr Hunt batted not a single eyelid. The rest of us somehow contained our merriment until the end of the round.

[2] Note for the unmedical. When the liver becomes cirrhotic or hardened, the large amount of blood in the portal vein, which takes blood and nutrients straight from the intestine to the liver, cannot flow freely and so blood pressure builds up – portal hypertension - in this anatomically and hydrodynamically separate portal circulation. The result is the appearance of large and easily injured varicose veins in unlikely places within the abdomen. If they bleed, the ensuing haemorrhage is typically torrential and still quite often fatal. The brilliant comic actor Peter Cook’s first wife described how he descended into alcoholism and died (apparently from bleeding portal varices) aged only 57  ( He politely declined my advice to take supervised disulfiram on the one occasion that he was - very reluctantly - persuaded to consult me.

[3] I have always regarded the avoidance and relief of pain as one of the primary duties and skills of a doctor. If it was not an emergency, I routinely injected a little local anaesthetic before inserting large cannulas for intravenous infusions and I injected a lot more before doing lumbar punctures. One grateful patient – a nurse who had meningitis – gave me a book inscribed: ‘To Dr Brewer with thanks for two painless LPs’.

[4] Brewer C. Treatment of drug addiction.  British Medical Journal 1967; 8 July

[5] With the solitary exception of the state of Queensland in Australia, Britain was unique at that time, among countries that permitted opiate maintenance treatment, in also allowing addicts with a strong needle fixation to have all or some of their methadone or heroin in intravenous form, so that they did not have to inject drugs that were often chemically or bacteriologically contaminated. It was not until 1994, when Switzerland (in the face of fierce US opposition) pioneered heroin prescribing for methadone maintenance patients who continued to inject compulsively that a few other countries began to emulate the ‘British System’ that dated from the Rolleston Commission of the 1920s.

[6] I think Britain produces the world’s youngest doctors. I qualified at 22 but if you had the right birthday and left school at 17, as I did, it was possible to get your medical degree at 21 after a four-and-a-half year medical course.

[7] Brewer C, Perrett L. Brain damage due to alcohol consumption: a psychometric, air-encephalographic and EEG study. British Journal of Addiction 1971;66:170-82 

[8] Brewer C. Minor brain damage and alcoholism. BMJ, 1981, 283, 671

[9] Lenere F. What happens to alcoholics? Am J Psychiat 1952, 109, 674-6.

[10] Ron MA, Acker W, Shaw GK, Lishman WA. Computerized tomography of the brain in chronic alcoholism: a Survey and follow-up study. Brain. 1982 Sep;105 (Pt 3):497-514.

[11] Note for the unmedical. Though a more extensive and more risky procedure, it is much more effective than the currently popular gastric banding, which simply reduces stomach size. It is still used if banding fails and involves rearranging the digestive system so that food by-passes most of the small-intestine and is thus mostly not absorbed. It even has some similarities with disulfiram because as well as reducine the absorbtion of calories, eating more than small amounts at a time can induce diarrhea within a few minutes, thus providing an additional deterrent mechanism.

[12] Brewer C, White H, Baddeley M. Beneficial effects of jejeunoileostomy on compulsive eating and associated psychiatric symptomsBritish Medical Journal. 1974;4:314-6

[13] The author Vladimir Nabokov described psychoanalysis as the idea that “[patients with] mental woes can be cured by a daily application of old Greek myths to their private parts”.

[14] Brewer C. Serum naltrexone and 6-beta-naltrexol levels from naltrexone implants can block very large amounts of heroin: a report on two cases.  Addict Biol 2002;7:321-323

[15] Strang J, McCambridge J, Best D, Beswick T, Bearn J, Rees S, Gossop M.  Loss of tolerance and overdose mortality  after inpatient opiate detoxification: a follow up study. BMJ; 2003.326, 959-60.

[16] Foster, J, Brewer C, Steele T. Naltrexone implants can completely prevent early (1-month) relapse after opiate detoxification: a pilot study of two cohorts totalling 101 patients with a note on naltrexone blood levels. Addict Biol 2003.8, 211-7.

[17] Brewer C, Streel E. Learning the language of abstinence in addiction treatment: some similarities between relapse-prevention with disulfiram, naltrexone and other pharmacological antagonists and intensive 'immersion' methods of foreign language teaching. Substance Abuse, 2003, 24(3) 157-173.

[18] Caplehorn J. Methadone maintenance treatment: Britain has been over-committed to psychological theories of drug dependence. Brit Med J 1995; 310: 463.

[19] Mick Brown. The needle and the damage done. Daily Telegraph. 12 May 2004

[20] For the avoidance of misunderstanding, I should make it clear that I have had no financial or other interests in the clinic for several years.