The machines that ate my life

Forget super-casinos: worry about the brash "virtual roulette" in the high street

Three days ago, I got paid and put all my money into a machine in a Coral's betting shop around the corner from where I live. I didn't mean to. I didn't want to. But I did. It's called a "virtual roulette" machine; the gaming industry calls it a "fixed-odds betting terminal", or FOBT. Walk into any bookies in the country and you'll see several, all with the sounds and effects of a real roulette wheel, usually with a crowd around them. It took less than an hour to lose my money. I walked home, sat in front of my window and wept. Occasionally, the word "probation" crossed my mind and I found myself slamming the window sill.

That is the word that our Secretary of State for Culture, Tessa Jowell, used during the second reading of the Gambling Bill in November to describe how the government views the 20,000 unregulated roulette machines that have been in betting shops up and down the country since 2001. Frankly, it was nothing more than an aside. Last month, during the third reading, she didn't even mention them. The remainder of her speech - indeed, the rest of the near-six-hour debate - concentrated mainly on the issue of deregulating casinos.

This is nothing new. Over the past several months, I have listened to politicians, journalists, editors, bishops, social workers, experts, members of the public and even a "professor of gambling" talking or writing about the consequences of relaxing the gambling regulations. Talk has centred on the so-called super-casinos and fears that this country is about to be turned into Las Vegas. The debates on the Gambling Bill have followed the same pattern.

Why is no one talking about this or showing what is happening? This government has already relaxed the gaming laws to such an extent that there are now thousands of "mini-casinos" in the country, and each one houses one or more of these roulette machines - a far more addictive and lethal game than anything you will find at a "proper" casino.

Put simply, you can now walk up any high street, in any town, on any day of the week, at ten o'clock in the morning, and be able to feed - literally feed - anything up to £500 into a machine for one spin. A few seconds later you can do it again. If you are short of ready cash, no problem, because you can use your credit card. If you find feeding £20 notes into a machine a bit laborious, just give the cashier your money and she will "top up" the machine for you, automatically. And if you find it a bit tedious having to press the start button for each game, there's an auto button, and then a repeat button. The cumulative effect is that there can be only seconds between each spin: exactly the formula for turning anyone into a potential addict. You can win or lose thousands of pounds in minutes.

Jowell calls these machines "very popular". That is an understatement. British gamblers are staking more than three times as much money on them (£290m) as they bet every week on the National Lottery (£88m).

This new betting craze, the annualised turnover of which is estimated at more than £15bn at the "big five" bookmakers, has become far and away Britain's most popular gambling product. Since the machines were introduced in 2001, betting-industry turnover has had a fourfold leap to £29.4bn. Gambling addiction has leapt, too. Only this month, GamCare, the gambling addiction charity, linked the rising number of calls to its helpline to the spread of roulette machines in betting shops.

Gambling in general has cost me dearly, but these machines especially so. A few years ago, I moved to a town that doesn't have a casino. This meant I would have to travel for miles to get to a roulette machine.

It was a good disincentive. Then the virtual roulette machines arrived and my world fell apart. I was like a heroin addict who suddenly could get a fix five hundred yards from his front doorstep.

It's what I did again this week. And it is why the debate over the Gambling Bill, again, has left me close to tears with frustration. You have got to understand that for me - and thousands like me - it's personal.

James Burton will be the subject of a 90-minute documentary special, The Confession, on BBC2 in April this year

This article first appeared in the 21 February 2005 issue of the New Statesman, Condoleezza Rice

The English patient: Britten in 1968. Photograph: Cecil Beaton Studio Archive, Courtesy of National Portrait Gallery.
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Notes from a cardiologist: Unravelling the mystery of Benjamin Britten’s heart

Cardiologist Hywel Davies describes the origins of the syphilis claim from Paul Kildea's biography of Benjamin Britten, which began as an "ordinary conversation" in a colleague's house in the late 1980s.

In 1892, William Osler published the first edition of The Principles and Practice of Medicine, in which he stated that tertiary syphilis of the nervous system, known then as general paralysis of the insane, was due to stress. Not many years later, a bacterium, called the spirochaete, was identified as the cause of syphilis and Osler was obliged to modify his textbook for the next edition. I thought of Osler’s dilemma in the context of Paul Kildea’s recent biography Benjamin Britten: a Life in the 20th Century, which claims that Britten had syphilis. The very public denials of this, some of them by people who could not possibly know one way or the other, along with the calls for revisions in the second edition, brought Osler to mind.

In assessing this, I can only gather what seems to be reasonable evidence on either side. For me, this begins with the testimony of my friend and colleague Donald Ross, the surgeon who operated on Britten’s heart on 7 May 1973 at the National Heart Hospital in London. During this procedure, he and his assistant surgeon would have inspected the heart thoroughly, at close range and from all available angles, using feel as well as vision, inside and out. Ross cut out the native aortic valve and replaced it with a homograft, which is made of tissue from a human source. This has the practical advantage of not requiring the use of anticoagulants to prevent clots forming later on the valve, as would have been the case with a mechanical prosthesis.

Ross recorded his impressions in his operative report written immediately after the surgery. This has recently been lodged at the Britten-Pears library, together with a selection of other records from Britten’s medical history, which I have been able to examine. Apart from his account of the procedure, Ross expresses clearly that when he was in theatre he was not able to tell, with any degree of assurance, exactly which disease process he was looking at, writing: “The aetiology of this valve lesion is not clear to me and certainly not characteristic of bacterial endocarditis, nor was the valve of bicuspid structure which would suggest a congenital valve.” The significance of these words is that Britten in 1968 had been treated with heavy and prolonged doses of penicillin for bacterial endocarditis, which means infection on the heart valve. There was none of the expected evidence “whatsoever” on the valve of previous infection from bacterial endocarditis. Nor were there signs of a congenitally deformed valve, since those are usually bicuspid (have only two cusps). This speaks against heart disease in infancy and childhood.

Ross adds that, on closure of the aortotomy (the initial incision in the aorta), the heart “came off bypass without difficulty”, yet: “The external appearances were those of an enlarged, bulky and flabby myocardium with a poorly contracting left ventricle.” In other words, none of the explanations given up to that point for the weakness of Britten’s heart, many of them involving assumptions that Britten had carried since childhood, appeared to be borne out. Ross proceeded to take biopsies from several parts of the heart that, together with the excised valve, were sent to the pathologists for their opinions about what the abnormal appearances might represent. He underlined the word “biopsy” each time he used it, as if to emphasise how critical the information would be to his conclusion.

In recent months, some commentators have asserted that Ross would have announced his thoughts and reservations at once in the operating theatre. On the contrary, it is extremely unlikely that he would have done this, for both intellectual and social reasons. Unclear about causes, he would never have speculated openly about such matters to what was a semi-public audience. He did, at the same time, make clear in his notes that he had been looking at something that was in his wide experience most unusual. It would have taken some weeks for the specimens to be studied and reported on before being reviewed by him. It would not – nor should it – have been a quick and hurried process. Unfortunately, if the reports of the biopsies, together with those of the relevant blood tests, were ever included in Britten’s other medical reports, they are no longer with them, but Ross would have insisted that he see them and they would have been an essential element when he came to draw his conclusions.

Over years of working with and discussing such things with Ross, I came to appreciate how keen and incisive his judgement always was in cardiac and other matters. He probably had as great an experience of assessing beating hearts as anyone before or since and a marked interest in anatomy and structure that he pursued in academic quarters. Between 1964 and 1973, 850 patients, many of them Ross’s, underwent aortic valve replacement at the National Heart Hospital and he worked elsewhere, too. As a cardiologist at Guy’s in the 1960s, I worked closely with him on the launching of his new technique of homograft valve replacement; the world’s first case, naturally in his hands, was my patient. I cared for and studied many of his homograft patients after that.         

Thus, when, during an ordinary conversation in his house in the late 1980s, Ross chose to tell me that Britten’s heart was syphilitic, I took him at his word, knowing that his opinion was that of a seasoned professional at the peak of his power in his field of expertise. I asked no further questions, except one to his assistant surgeon, present on the same occasion, as to whether he concurred with Ross’s conclusion, which he did. Beyond that, I had no particular interest in the story and did not speak to anyone about it.

Except one person. When I lived and worked in Colorado in the 1960s and again in the 1980s, one of my friends was a senior medical scientist named Basil Reeve, an Englishman who had grown up in Lowestoft with Britten, had known him well and had played the piano with him. A qualified doctor, Basil was also friendly in the Second World War with the philosopher Ludwig Wittgenstein, then working at Guy’s Hospital as a porter during the Blitz. One day in the early 1990s when I was visiting Denver again, Basil and I were having lunch in a local restaurant. He talked about these friends and, knowing his interest in Britten, I saw no reason not to mention to him what Ross had told me freely and without pledging me to silence.   

I was surprised, however, that Basil’s reaction was swift and pointed. He said: “The world should know it and we should make the information public.” I had no wish to do this and I declined to go along with his request. He repeated it a few times on the telephone during the following years and, although I realised how strongly he felt about it, I still chose to say no. Shortly after his last request, I sold my home in Switzerland and moved elsewhere. A couple of years later, I happened to call at Basil’s house during another visit to Denver. When he opened the front door, his face paled and he said, “Good God, I thought you were dead.” He explained that in the interim he had phoned again to Switzerland to repeat his request, to be told by the operator that the line had been discontinued and I could not be contacted. He drew the perhaps understandable conclusion that I was no more and accordingly felt able to speak about what I had told him. In 1999, he told the story to Kildea, the young head of music at the Aldeburgh Festival. Kildea was sceptical but, when he came to write his biography in 2008, he tracked me down to check Basil’s information. I initially told him that I was not willing to comment but over time came to realise that he was a serious scholar, interested in getting to the bottom of a puzzling case, and I decided to help him with some of the medical aspects of his book.

Based on what Ross and others wrote at the time and what Ross told me later, we may question further what this most experienced surgeon observed in the operating theatre with such puzzlement. First, Britten’s heart was much enlarged, the bulk of this consisting of a very thick left ventricle. The reason for this was ostensibly a long-standing aortic valve insufficiency – leakage backwards from the aorta into the ventricle after the aortic valve closes. The immediate reason for the enlargement and thickening (hypertrophy) of cardiac muscles is usually excessive work, as occurs in other muscles of the body. Leakage in the aortic valve results in an increase in the amount of blood the heart has to pump.

There are two conflicting descriptions of the condition and function of Britten’s ventricle that appear in the clinical notes. The first is the report on the pre-operative angiogram, which states that the left ventricle “contracts vigorously”. The second is the operation note in which Ross describes the enlarged, bulky and flabby muscle and poorly contracting left ventricle. The use of the word “flabby” speaks for itself and Ross inserted special sutures in an attempt to secure the new valve in the friable, weakened tissue. A month after the operation, Britten’s cardiologist Graham Hayward wrote to Ian Tait, Britten’s GP in Aldeburgh: “He presented us with many problems, as you know, during and after surgery as his heart was much larger and worse than one anticipated.”

The reasons for these “many problems” might not have been evident to the surgeons. They would have gone through the main possibilities, including those that the consultant physician John Paulley of Ipswich spelled out in 1960 after seeing Britten. He was the first, it appears, to make the diag nosis of aortic valve insufficiency and, in a letter to Tait, he asked the latter to arrange a WR and Kahn blood test, the standard for syphilis. He could have ordered one himself but he preferred that Tait did it. (“Reasons will probably be obvious to you?”) We must assume that the test was carried out. Paulley’s request is proof, if any were necessary, that syphilis was and still is a major diagnostic possibility in a patient with aortic valve insufficiency. Ross would have known as well as Osler that syphilis is a great mimic of other diseases and a negative blood test does not rule out the disease, especially in patients who had been treated heavily with penicillin, as Britten had.

I have taken a position in this matter largely because I find that the strongest evidence we have is that of the surgeons and I do not believe their conclusions should be cast aside lightly. (In the 1970s, the assistant surgeon passed on Ross’s conclusions to a senior colleague who repeated them to Kildea, so I was not the only route by which they reached him.) On the basis of Ross’s surgical report and his unequivocal opinion, it seems that Kildea is substantially right in what he says, though some amendments to wording, to reflect what we now know from the report, could be made before the next edition of his book. This is a sentiment with which Osler, if he were here, might well approve.

In a long career as a consultant cardiologist, Hywel Davies held posts in leading London and US hospitals before being invited by Sir Terence English to be the cardiologist to the cardiac transplant team at Papworth Hospital

This article first appeared in the 10 June 2013 issue of the New Statesman, G0