The Trip to Echo Spring. Olivia Laing

of the playwright.

      I lay awake most of that first night at the Elysée, dreaming in a small window of sleep of a cat with raspberries tangled in its fur. The next morning I had two unprecedented appointments. The first was to visit a psychiatrist and the second was to attend an AA meeting. My cab driver had only just arrived in the city too, and together we muddled out a route to St. Luke’s-Roosevelt Hospital on 10th Avenue and 58th Street. The Addiction Institute was on the ninth floor, down a run of corridors that seemed to spiral inward like a snail’s shell. By the time I was ushered into the director’s office I was thoroughly disorientated. I thought I was deep inside the building and the presence of a window startled me. The books were arranged according to colour, lavender to violet, turquoise to green; a buttress assembled in praise of order.

      Back in the day, the Addiction Institute was called the Smithers Alcohol Treatment and Training Center. It’s where John Cheever and Truman Capote went to dry out, though only the former was successful in his labours. At that point, in the spring of 1975, it was located in a brownstone at 56 East 93rd Street. ‘The house is palatial and not at all shabby,’ Cheever wrote in a letter during his voluntary incarceration. ‘The tenants are forty-two drug addicts and clinical alcoholics.’ He shared his room with a con man, a ballet dancer, a sailor and the owner of an unsuccessful German deli, who talked in his sleep, asking all night long: ‘Haff you been taken care of? Haff you been waited on?’ He was intensely miserable (hardly the place for such a distinguished Yankee as a Cheevah) and complained vociferously throughout his twenty-eight-day internment, but it got him sober and in all probability also saved his life.

      In order to understand how an intelligent man could end up in such a place, it’s necessary first to know what a shot of Smirnoff or Scotch does to the human body. Alcohol, also known as ethanol, is both an intoxicant and a central nervous depressant, with an immensely complex effect upon the brain. In simple terms, it works by interfering with the activity of neurotransmitters, the chemicals by which the nervous system relays information around the body. Its effects can be divided into two categories. Alcohol activates the pleasure-reward pathways by way of dopamine and serotonin. In psychological terms this effect is known as positive reinforcement, since continuing to ingest the substance leads to pleasure.

      But alcohol also works by way of negative reinforcement. In the brain, there are two types of neurotransmitters: inhibitory and excitatory. Inhibitory neurotransmitters depress activity in the central nervous system, while excitatory neurotransmitters stimulate it. When alcohol is ingested, it interacts with the receptor sites of an inhibitory neurotransmitter called gamma-aminobutyric acid or GABA, mimicking its effects. The result is sedative, reducing activity in the brain. In addition, alcohol blocks the receptor sites of an excitatory neurotransmitter: N-methyl-D-aspartate or NMDA (a subset of glutamate, the major excitatory neurotransmitter), preventing its activity. This also causes a reduction in excitation, albeit by a different route.

      These sedative effects are what makes alcohol so adept at reducing tension and anxiety. Both positive and negative reinforcement drive alcoholism, but as the addiction progresses it is negative reinforcement that tends to take the larger role. ‘The click’, Brick calls it in Cat on a Hot Tin Roof. ‘This click that I get in my head that makes me peaceful. I got to drink till I get it. It’s just a mechanical thing . . . I just haven’t got the right level of alcohol in my bloodstream yet.’

      The realisation that alcohol is capable of alleviating anxiety means that for susceptible individuals it can quickly become the preferred method of managing stress. There’s more than a hint of this in a letter John Cheever wrote about an early experiment with drinking. Intimidated by a social gathering, he discovered alcohol’s powerful knack for obliterating nerves. ‘The next engagement that threatened to arouse my shyness,’ he wrote, ‘I bought a bottle of gin and drank four fingers neat. The company was brilliant, chatty and urbane and so was I.’ In Memoirs, Tennessee Williams takes up the same refrain, noting that after a mezzo-litro of Frascati, ‘you felt as if a new kind of blood had been transfused into your arteries, a blood that swept away all anxiety and all tension for a while, and for a while is the stuff that dreams are made of’.

      For a while. The problem is that over time the brain begins to adjust to the presence of alcohol, compensating for its effects on the central nervous system. In particular, it increases the production of excitatory neurotransmitters, so that normal activity can be maintained. This neuroadaptation is what drives addiction, eventually making the drinker require alcohol in order to function at all.

      In the current edition of the Diagnostic and Statistical Manual of Mental Disorders (known universally as DSM-IV-TR), alcohol dependence is categorised as a form of substance dependence, which is defined as:

      A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period:

      1.Tolerance, as defined by either of the following:

      –A need for markedly increased amounts of the substance to achieve intoxication or desired effect.

      –Markedly diminished effect with continued use of the same amount of the substance.

      2.Withdrawal, as manifested by either of the following:

      –The characteristic withdrawal syndrome for the substance.

      –The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms.

      3.The substance is often taken in larger amounts or over a longer period than was intended.

      4.There is a persistent desire or there are unsuccessful efforts to cut down or control substance use.

      5.A great deal of time is spent in activities necessary for obtaining the substance, using the substance or recovering from its effects.

      6.Important social, occupational, or recreational activities are given up or reduced because of substance use.

      7.The substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance (e.g., continued drinking despite recognition that an ulcer was made worse by alcohol consumption).

      As it gathers momentum, alcohol addiction inevitably affects the drinker’s physical and social selves, visibly damaging the architecture of their life. Jobs are lost. Relationships spoil. There may be accidents, arrests and injuries, or the drinker may simply become increasingly neglectful of their responsibilities and capacity to provide self-care. Conditions associated with long-term alcoholism include hepatitis, cirrhosis, fatty liver, gastritis, stomach ulcers, hypertension, heart disease, impotence, infertility, various types of cancer, increased susceptibility to infection, sleep disorders, loss of memory and personality changes caused by damage to the brain. As an early researcher into alcohol addiction wrote in the American Journal of Psychiatry back in 1935: ‘The striking and inescapable impression one gets from a review of acute alcoholic intoxication is of the almost infinite diversity of symptoms that may ensue from the action of this single toxic agent.’

      Not everyone who drinks alcohol, however, becomes an alcoholic. This disease, which exists in all quarters of the world, is caused by a multitude of factors, among them genetic predisposition, early life experience and social influences. In a 2011 paper entitled ‘The role of early life stress as a predictor for alcohol and drug dependence’, Mary-Anne Enoch, a long-term researcher in the field, wrote:

      It is well established that the hereditability of alcoholism is around 50% . . . Therefore, genetic and environmental influences on the development of addictive disorders are equally important, although the proportions of risk may vary according to societal groups.

      Later, when I was transcribing my interview with Dr. Petros Levounis, the Addiction Institute’s director, I realised that I’d asked the question of what causes alcoholism several times over, in varying formulations, and that each time his answer was slightly different. This isn’t