The Fix
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There’s something wrong with this methodology, however, as Gene M. Heyman, a hospital research psychologist and lecturer at Harvard University, points out.
‘Most research is based on addicts who come to clinics,’ he says. ‘But these are a distinct minority, and they are much more likely to keep using drugs past the age of 30 – probably because they have many more health problems than non-clinic addicts. They are about twice as likely to suffer from depression, and are many times more likely to have HIV/AIDS. These problems interfere with activities that can successfully compete with drug use. Thus, experts have based their view of addiction on an unrepresentative sample of addicts.’10
Heyman went looking for large-scale studies of addiction in the US based on more representative samples of addicts in the general population, not just in clinics. He found four of them, carried out by leading researchers and funded by national health institutes.11 Yet, mysteriously, the clinical texts and journal articles spreading the message of a ‘primary, chronic, relapsing disease’ fail to mention these epidemiological studies. Why?
Could it have been because none of the surveys found that most addicts eventually relapse? What they suggested, inconveniently, was that between 60 and 80 per cent of individuals who met the criteria for lifetime addiction stopped using drugs in their late twenties or early thirties. In short, high remission rates would seem to be a stable feature of addiction.12
In 1970 there was a shockingly sudden burst of heroin addiction among GIs in Vietnam. As Alfred McCoy describes in his book The Politics of Heroin, until 1969 the ‘Golden Triangle’ of south-east Asia was harvesting nearly a thousand tons of raw opium annually – but there were no laboratories capable of turning it into high-grade heroin. That changed when Chinese master chemists from Hong Kong arrived in the region. Suddenly South Vietnam was full of fine-grained No. 4 heroin instead of the impure, chunky No. 3 grade.
‘Heroin addiction spread like the plague,’ writes McCoy. ‘Fourteen-year-old girls were selling heroin at roadside stands on the main highway from Saigon to the US army base at Long Binh; Saigon street peddlers stuffed plastic vials of 95 percent pure heroin into the pockets of GIs as they strolled through downtown Saigon; and “mama-sans”, or Vietnamese barracks’ maids, started carrying a few vials to work for sale to on-duty GIs.’13
By the summer of 1970, virtually every enlisted man in Vietnam was being offered high-quality heroin. Almost half of them took it at least once; between 15 and 20 per cent of GIs in the Mekong delta were snorting heroin or smoking cigarettes laced with it. Ironically, heroin use soared after the Army cracked down on the much more easily detectable habit of smoking pungent marijuana. But the key factor, argues McCoy, is that drug manufacturers could make $88 million a year from selling heroin to soldiers; no wonder that ‘base after base was overrun by these ant-armies of heroin pushers with their identical plastic vials’. Rumours spread that the North Vietnamese were behind this intense marketing campaign – what better way to immobilise the enemy? But the truth was that South Vietnamese government officials were protecting the pushers.
In any case, combat troops avoided heroin use in the field: being stoned, especially on a drug as soporific as heroin, was more likely to get them killed. But they made up for it when they returned to base. One soldier came back from a long patrol of 13 days; his first action was to tip a vial of heroin into a shot of vodka and knock it back.14
Panicky headlines about the ‘GI epidemic’ started appearing in American newspapers. The Nixon administration was terrified of a crime wave caused by the return of thousands of desperate junkies to American cities. But it never materialised. Instead, the addicted soldiers cleaned up their act – fast.
We know this because the US government, anticipating disaster, commissioned a medical study that recruited more than 400 returning soldiers who snorted, smoked or injected heroin and described themselves as addicted (making it possibly the largest ever study of heroin users). To researchers’ surprise, back in the United States only 12 per cent of these addicts carried on using heroin at a level that met the study’s criteria for addiction.15
This is really powerful evidence that changes in social environment can dramatically affect people’s drug-taking habits. As Professor Michael Gossop, a leading researcher at the National Addiction Centre, King’s College, London, explains: ‘The young men who served in Vietnam were removed from their normal social environment and from many of its usual social and moral constraints. For many of them it was a confusing, chaotic and often extremely frightening experience and the chances of physical escape were remote except through the hazardous possibilities of self-inflicted injury.’16 Gossop uses the phrase ‘inward desertion’ to describe what heroin offered the soldiers: a cheap trip to another world.
The scared, disorientated soldiers in Vietnam were being offered a chemical fix to relieve their fear. The social and psychological pressure to do something they would never dream of doing in America – take heroin – was intense: one in five slid all the way into addiction. But, once home again, they weren’t scared any more. They weren’t mixing with other users. The drug was expensive, hard to find, low-grade and highly illegal. The pressure went into reverse. In other words, the same combination of social and psychological factors that turned these men into addicts explains why they were able to stop.
True, these were remarkable circumstances. So we might expect other addicts, whose initiation into drug use was less dramatic and more gradual, to recover at a slower rate. And that’s precisely what those four big epidemiological studies show: they paint a picture of users slowly changing their behaviour when their circumstances changed. They don’t support the progressive disease model. The Vietnam statistics, meanwhile, directly undermine it. The US government went to a lot of trouble to make sure that the soldiers it was testing were addicts. Are we supposed to believe that the 88 per cent who later kicked the habit were misdiagnosed? Or that being drafted to fight in heroin-saturated Vietnam ‘doesn’t count’ because it was such an unusual situation?
The Vietnam survey identifies a key factor in addiction: availability. To quote Michael Gossop: ‘Availability is such an obvious determinant of drug taking that it is often overlooked. In its simplest form the availability hypothesis states that the greater the availability of a drug in a society, the more people are likely to use it and the more they are likely to run into problems with it [my italics].’17
This hypothesis might seem like a statement of the obvious. Actually, as Gossop says, the question of availability is often treated as a secondary factor, less important than any predisposition to a so-called ‘disease’.
Gossop identifies different dimensions of availability. There’s physical availability, obviously, but also psychological availability (whether someone’s personality, background and beliefs increases their interest in using particular drugs), economic availability (whether the drugs are affordable) and social availability (whether the social context encourages use of the drugs). In the case of Vietnam, he points out, many soldiers found that all the boxes were ticked. Troops in Thailand, by contrast, could easily get hold of heroin – but their lives were not in danger, they were free to move among a friendly population and their peers were not using it. Less than one per cent of military personnel took the drug.18
Availability doesn’t offer a comprehensive explanation for addiction, but it reminds us that we cannot hope to understand why people engage in addictive activities – be it shooting up heroin in the jungle or gorging on muffins in Starbucks – unless we take account of what that activity means in its social setting.
No one who has watched The Wire, the magnificent television epic of life in drug-saturated districts of Baltimore, can seriously propose that it depicts a black population afflicted by chronic disease. The characters in the show who smoke heroin do so, basically, because they live in districts where everyone does. If I lived there, I’d be a smack addict. Since I’m an addict, perhaps that goes without saying. But I have a sneaking feeling that even my local vicar would be hooked on the stuff.
Gossop, who has advised the British government on drug policy, is unusual among addiction experts for the bluntness with which he dismisses the disease theory. He describes addiction as a ‘habit’. That may sound less scary than an irreversible disease, but it isn’t. In a society overflowing with abundance, the implications of a habit of addiction driven by availability are every bit as alarming as those of a disease that strikes only individuals with malfunctioning brains.
This isn’t to deny that some people are naturally more vulnerable to addiction than others. And we can’t ignore recent discoveries in neuroscience, which show how the brain’s natural reward systems are being hijacked by newly available substances and gadgets. In the next chapter, we’ll look at what the brain does and doesn’t tell us about addiction.
But I want to end this chapter by stressing, yet again, the inadequacies of the disease model. If the word ‘disease’ is at all useful in this context, it’s as a metaphor for addiction, not as a diagnosis. And I can think of another vivid metaphor that works just as well. Modern consumers are like soldiers drafted to Vietnam – disorientated, fearful and relentlessly tempted by fixes that promise to make reality more bearable. You don’t have to be ill to give in; just human.
3
WHAT THE BRAIN TELLS US (AND WHAT IT DOESN’T)
Imagine the embarrassment. You are a retired civil servant with Parkinson’s disease. You are industrious and introverted, like many sufferers from the condition. (We don’t know for sure why it often strikes people with this type of personality, but the correlation was noted as long ago as the 19th century.1) You’re a regular at your local pub, where you’re known as a modest, affable chap who orders half-pints rather than pints. Occasionally you while away 20 minutes by pushing a few coins into the slot machine, accepting your losses with a philosophical shrug.
Then something odd happens. Without warning, you develop an obsession with playing the machine. You stand in front of it from opening time until last orders, much to the bemusement of the other regulars. You know that the pub’s fruit machine is programmed to return only 80 per cent of the money you put into it, but one day you hit multiple jackpots that earn you £50. The thrill of this experience – and the possibility of it happening again – reinforces your new preoccupation. You are no longer thinking rationally.
Eventually the teasing from other patrons turns to alarm as they see you pouring away your pension. The pub landlord has ‘a quiet word’ and asks you to stop playing. You’re mortified and stop going to the pub – but, instead of finding another place to drink, you slip into your local betting shop, where the jackpots are bigger. Then a newspaper article about online gambling catches your eye and before long you are shutting yourself away in your study, steadily building up credit card bills as you accrue greater and greater losses. Your wife still doesn’t have a clue.
But your problems don’t end there. Somewhere along the line, much to your own surprise, you discover a taste for internet pornography. Under normal circumstances, porn would have no appeal – you’re 70 years old, after all. But even before you stumbled across these sites you had noticed that your sexual appetite had mysteriously reawakened.
This story sounds implausible, but something very much like it happened to several Parkinson’s patients recently. They developed gambling urges out of nowhere, and in certain cases these were accompanied by a revived sex drive. There were other permutations: patients experienced a revved-up sex drive without the gambling urges, or started binge eating. Some began shopping obsessively, perhaps combining it with other risk-taking activities. The common thread was the startling change in the behaviour of people who, until recently, had devoted most of their leisure time to tending their begonias.
But the culprit wasn’t the disease. It was the medication designed to reverse its symptoms. The medicine wasn’t supposed to produce those results, but the fact that it did so provides us with vital information about the strange, self-defeating behaviours that we call addictions.
These Parkinson’s patients had been given drugs that mimicked the action of dopamine. This is a neurotransmitter, or chemical messenger, that affects our experience of pleasure and also has the ability to map out new reward pathways in the brain – in other words, to rewire it.
That’s a trendy way of describing complex changes in the brain. This is arguably the most impenetrable subject human beings have ever tried to understand. Scientists who have devoted their careers to it admit that they have only pieced together a tiny section of the jigsaw. That’s frustrating – but bear with me, because what they have discovered has fascinating implications. Dopamine is an ancient mechanism: it’s found in lizards and every other animal along the evolutionary tree. It has been called the ‘pleasure chemical’ because it is released whenever we eat good food, enjoy sex or take pleasure-enhancing drugs.
Recently, scientists have refined their understanding of dopamine. They now think that it has more to do with desire than pleasure – or, to use the refreshingly simple terms that now loom large in scientific discussions of addiction, with wanting rather than liking.
In a series of experiments on the brains of rats, the psychologist Kent Berridge of the University of Michigan came to the conclusion that ‘wanting’ (desire) and ‘liking’ (pleasure) are separate urges controlled by different brain circuits in humans as well as animals. That is an important discovery that we need to keep at the back of our minds whenever we think about how and why we are behaving addictively.
Dopamine is involved in both brain circuits, but its main function is to stimulate wanting; liking is more affected by the opioid system, which contains endorphins, the brain’s natural morphine-like compounds.2 Of the two urges, wanting is more powerful. ‘The brain seems to be more stingy with mechanisms for pleasure than for desire,’ says Berridge.3
This helps us understand another apparently simple distinction made by scientists that we came across in Chapter 1 – between the Stop and Go impulses in the brain. The Go impulse tells us to reach out for an immediate reward; it’s ancient, it’s powerful and it’s shared with animals. As you might expect, it goes into overdrive at the prospect of food and sex. Dopamine and ‘wanting’ are central to this urge – but different levels of ‘liking’ also determine the strength of the Go message.4
The Stop impulse is highly developed only in humans. It helps us manage our Go impulse by spelling out the consequences of immediate reward. You could call it the voice of reason; it comes from the frontal lobes of the human brain. These are not fully developed in adolescents, who are therefore poor at managing the Stop impulse. This will not come as a surprise to the parents of teenage children.
Let’s return to the traumatic experience of those Parkinson’s patients. Their disease drains the brain of dopamine. Indeed, it may begin to do so decades before more obvious symptoms become apparent. That could explain why Parkinson’s seems to disproportionately affect people with introverted personalities: those self-effacing traits may not be signs of natural, life-long introversion but, rather, the first symptoms of the disease, appearing years before diagnosis.
The patients who developed sudden gambling or other impulsive habits had been given dopamine agonists, which, by boosting dopamine, usually slow down the progression of the disease. They are a common treatment and can be remarkably effective. An aunt of mine with Parkinson’s was given one of these drugs. The brightening of her personality and her fresh pleasure in everyday experiences, such as looking at her garden, seemed almost miraculous. For some patients, however, the same chemical that restored my aunt’s joie de vivre was psychological poison.
Alan Burrows, a pensioner from Queensland, was one of 100 Australians who sued the drug company Pfizer after taking its dopamine agonist medication Cabaser. He claims that it caused him to start binge gambling on ‘pokies’ (Australian slang for slot machines). Eventually, he had to sell his house to pay off his $300,000 gambling debts. ‘Once I started I had to keep going, by withdrawing money every hour, until I couldn’t get any more money,’ he said. ‘It was a compulsion to do it. You became really devious, disgusting.’5
It’s probably no consolation to Mr Burrows, but what happened to him and to the other Parkinson’s sufferers who developed compulsive habits helps us to draw the boundaries of addiction. Their ordeal suggests that dopamine is a common factor in habits that society has been slow to label ‘addictions’ because they don’t involve drugs.
After the stories of bad reactions to Parkinson’s drugs surfaced, Dr Valerie Voon of the US National Institutes of Health led a study of patients given dopamine agonists. She found that 13 per cent exhibited ‘a constellation of pathological behaviours, including gambling, shopping, binge eating and hypersexuality’.6 They did so because they were being over-supplied with dopamine.
The inference we can draw from this is valuable. It seems that people who don’t have Parkinson’s disease but engage in the same pathological habits are also having problems with their dopamine levels. Gambling, obsessive shopping, binge eating, hypersexuality – note how those Parkinson’s patients found themselves caught up in the sort of activities where wanting overwhelms liking. Also, they were being driven by repetitive urges. This is typical of dopamine at work, laying down new patterns in the brain as it takes effect. As the psychiatrist Norman Doidge explains: ‘The same surge of dopamine that thrills us also consolidates the neuronal connections responsible for the behaviours that led us to accomplish our goal.’7
In other words, the more we experience dopamine-induced pleasure, the more we want to repeat the experience. But, thanks to levels of tolerance that have been raised by rewiring, the harder we have to work to repeat it to our satisfaction. That is why addicts always seem to be looking for a bigger and bigger hit.
All substance abusers experience surges of dopamine, often accompanied by craving – that is, very strong feelings of wanting. Alcohol, amphetamine, cocaine, heroin, marijuana and nicotine all increase the supply of dopamine to the nucleus accumbens, a pleasure centre buried deep in the brain that has been called the final destination of the reward pathway.8
This does not mean that addicts are people born with naturally high or low levels of dopamine, nor that they have inherited cravings that force them to keep stimulating the rush of dopamine into their nucleus accumbens. If any of these things could be proved, then the study of addiction science wouldn’t involve so much infuriating guesswork.
Different recreational drugs do different things to the brain. They produce different rewards – and different punishments. You don’t have to take them to know that; you just have to observe the behaviour of their users. It’s a bit like visiting the zoo.
Coke-heads and speed freaks gabble excitedly as they are swept along on a tide of dopamine. When that tide pulls out, they experience a particular sort of come-down. ‘Coke is the drug we save for the time after we get back from clubbing,’ says Olly, 27, a graphic designer. ‘It runs out pretty quickly. Presuming we don’t order more, by 4 a.m. everyone is getting jittery and anxious. You see people’s eyes flicking around the room wondering if anyone’s got any left. A group of four chatty and gobby friends suddenly becomes four individuals chewing the insides of their cheeks. The next morning we go for brunch to cure our hangovers but everyone’s coming down off the coke, snapping at each other. Some people feel blue for days.’
Heroin users don’t inflict logorrhea on their friends: their drug is forcing the brain to over-produce endorphins, those natural euphoria-inducing and painkilling neurotransmitters. Heroin suppresses neurotransmission in the central nervous system, which can produce an exquisitely calm feeling, particularly if your nerves were shot to pieces in the first place. This can take people to the gates of paradise, but also to hell: the come-down is long and usually profoundly depressing, because the nucleus accumbens is extremely sensitive to opioid withdrawal.9
Also, the brain’s self-regulatory process means that junkies quickly need to increase their doses to slow down neurotransmission; in severe cases, they inject themselves hourly in order to maintain a state of mental paralysis. William Burroughs, writing about his last year of addiction in North Africa, said he could look at the end of his shoe for eight hours. And if a friend had visited him and died on the spot, ‘I would have sat there looking at my shoe waiting to go through his pockets’.10
Ecstasy releases serotonin, a neurotransmitter associated with happiness; hence its users’ indiscriminate declarations of affection. ‘One of the reasons I don’t do pills is seeing how fucking annoying people are when they’re “loved up”,’ says Ollie. ‘MDMA [a purer form of Ecstasy] is even worse. You see groups of heterosexual men hugging and kissing each other. There’s this idiotic bear hugging that goes on for hours, and I’m afraid it makes me laugh when I see them at work on Monday, looking sheepish and sad.’ The sheepishness is self-explanatory; the sadness is pure dopamine deprivation.
Alcohol, meanwhile, has been called the most ruthless of all brain-hijackers. Looking back on my drinking, I now have some idea of what was happening to my body; I just wish I’d known at the time, if only to avoid some hangovers of apocalyptic proportions.
Alcohol molecules are quite unlike those of other addicting drugs. They have the ability to speed up the transmission of chemicals that excite us and also, later, those that relax us, sometimes to the point of stupor. We’re talking about a fiendishly complicated neurochemical dance that releases inhibitions and twists moods over the course of an evening. I reckon my own dopamine would peak around the third glass of red wine, which was the moment when – if I was on form – I was most fun to be around. By the third bottle the flow of mood-enhancing chemicals would have slowed down and the inhibitory neurotransmitter GABA would be in the ascendant. My voice would become slurred and my thoughts confused – but I’d be chasing the vanishing high by drinking even faster. And my friends, sensibly, would have made their excuses and left.
As for the hangovers – well, if ever I feel like going back on the sauce after 18 years I have only to cast my mind back to any of the thousand or so I inflicted on myself. Perhaps it was the ability of the alcohol molecule to insinuate itself into so many different functions of the brain that produced such all-encompassing misery. But, as we’ll see later, I eventually discovered an effective but fabulously stupid pharmaceutical remedy for those feelings.
All intoxicating experiences involve a cocktail of brain chemicals that are mixed quite differently depending on the nature of the behaviour. But dopamine is still the master drug that, in the words of the research psychiatrist Morten Kringelbach, ‘appears to encode desire’ and can make us chase after something long after we’ve ceased to derive much pleasure from it.11 To quote Dirk Hansen, ‘dopamine is part of the reason why we remember how much we liked getting high yesterday’.12