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
As this suggests, it’s good at fastening on to cues. One sensible piece of advice that 12-step groups dole out to their members is to avoid ‘people, places and things’ that were part of their old habits. ‘If you hang around barbers’ shops, sooner or later you’re going to get a haircut,’ is an AA saying – meaning, of course, that sitting around drinking orange juice in the pub is risky for an alcoholic. The more addicted you become to something, the more sensitive you become to these cues – even after years of abstinence. Significantly, these cues are often the ‘things’ that have come to replace people in your life.
But the link between cues and desire isn’t confined to addicts. It’s part of everyday existence for people situated all along the addictive spectrum – that is, all human beings.
You don’t need to ingest any substance at all to experience a rush of dopamine: the cue is enough. The smell or even just the sight of food increases dopamine in the nucleus accumbens, the region of the brain involved in reward and motivation. It’s why our mouths water. As the psychology professors Harvey Milkman and Stanley Sunderwirth explain, this is the same type of neurochemical response that occurs when a cocaine addict sees a video of people snorting a fat line of white powder: ‘The dopamine messenger impels the organism to action, an impulse that sheer willpower cannot easily overcome.’13
I know what they mean. For some reason, watching characters drink red wine on television is more tempting for me than seeing them do it in real life; it makes me long to nip to the supermarket for a bottle of Rioja. (I don’t, I hasten to add.) Why this should be I don’t know, but in AA meetings I quite often heard speakers complain of the same thing. Some people even ‘had a slip’, to use 12-step terminology, thanks to things they had seen on screen. Cues can be made more powerful by being detached from everyday networks. This is why many slips happen when alcoholics are on holiday, away from the company of people who know they have a problem, where the booze is presented in an exotic setting that somehow detoxifies it. One businessman I know found himself – to his own astonishment – accepting a rum and coke from a stewardess on a plane flight. ‘We were so high up that it didn’t seem to count,’ he said. And thus ended the decade of abstinence of which he’d been so proud.
Milkman and Sunderwirth have produced a list of activities that boost dopamine in the nucleus accumbens. They are: crime, eating, gambling, risk-taking, sex … and hugging your loved ones. With the possible exception of hugging, there’s an addiction (or, more accurately, a huge range of addictions) lurking in all of them.
What’s useful about this list is that it reminds us that the brain’s reward circuits don’t necessarily distinguish between supposedly innocent and supposedly dangerous pursuits. Once ‘wanting’ is out of control, previously innocuous substances or experiences can become life-threatening. A heart attack brought on by an obsession with cheeseburgers can be just as fatal as a heroin overdose. And, these days, people do become obsessed with burgers – perhaps because they are chemically engineered to be almost as addictive as heroin.
To recap: both substance addictions and ‘process’ (non-substance) addictions are associated with dopamine-related disorders of brain reward. I’m not suggesting that this is a simple explanation for addiction; clearly it isn’t. But it’s useful. We now know that addictive behaviours are accompanied by physical changes in the brain – whether or not they involve drugs. Once we delve deeper into the subject, however, things get a little harder to understand. In fact, the experts don’t understand them, because neuroscience is still in its infancy.
Here’s a question that illustrates its limitations. What do young lovers have in common with coke-snorters?
The answer, according to Norman Doidge, is that they experience a similar high. Cocaine’s special relationship with dopamine creates feelings of radiant optimism. Like love-struck couples, people on cocaine are ‘filled with hopeful anticipation and are sensitive to anything that might give them pleasure – flowers and fresh air inspire them and a slight but thoughtful gesture makes them delight in all mankind’.14
In other words, falling in love activates many of the same chemical pathways as inserting a rolled-up £20 note into your nostril. That’s amusing to know – but it also gives you some idea of how difficult it is to diagnose addiction merely by looking at someone’s brain. One recent scientific paper suggests that studying ‘normal’ people going through an intense romantic episode may help us understand the pathological vulnerability of drug addicts.15 That sounds intriguing – but it also smacks of desperation. Clearly, neuroscience isn’t even close to being able to match minuscule variations in brain reward circuits to specific patterns of behaviour. And, so far as I can tell, no two neuroscientists draw the boundaries of ‘addiction’ in the same place.
We’ve seen that different drugs boost dopamine in different ways. But that information isn’t as helpful as it sounds, because dopamine can’t tell the difference between addictive substances and rewarding but non-addictive substances.16 The brain doesn’t recognise our culturally determined categories of legal and illegal drugs, or our neat distinctions between drugs and foods, or the difference between heroic and self-destructive risk-taking.
And, as if that wasn’t complicated enough, many addicts transfer their allegiance from one habit to another. If, for example, the supply of heroin runs out in a particular city, addicts will switch to cocaine – even though the gratifications the two drugs provide are quite different and involve separate reward systems. This comorbidity, as it’s known, is a puzzle to scientists.
It’s no wonder, therefore, that neuroscientists can’t read backwards from a map of the brain’s neural pathways to the behaviour that shaped them. All they can say is that specific signs of brain damage may have been caused by a particular habit, which is a very different proposition.
Why does science have such a hard time getting to grips with the phenomenon of addiction? In a nutshell, because human brains, as opposed to animal ones, can instruct the body to perform an almost infinite number of voluntary (and therefore unpredictable) actions. And, contrary to the beliefs of disease-model advocates and the huge therapeutic industry, addictive behaviour is essentially voluntary. Addicts may be influenced by their disordered brain chemistry to make bad choices, but they are choices nonetheless.
‘I really shouldn’t.’ When you hear those three words, uttered in a resigned but excited tone of voice, what image do they conjure up? I hear the voice of my long-dead grandmother, knowing that another helping of my mother’s apple crumble wasn’t going to help her lose weight and was against doctor’s orders. She had heart disease. But my grandmother couldn’t resist – or, rather, chose not to. (In her defence, I should point out that my mother’s crumble was to die for.)
Puddings are high on the list of British I-really-shouldn’t items. Pity the poor waiters who listen in on the same ritual exchange night after night:
‘I’ll just have coffee, thanks.’
‘Me too.’
‘Well, I don’t know about you, but that tiramisu looks awfully good.’
‘Ooh, it does …’
‘Can we have one tiramisu with two – no, make that three spoons.’
These people aren’t so much exchanging thoughts with each other as with themselves. What’s going on in their brains?
The neuroscientist David Eagleman compares brains to representative democracies in which parties hold different opinions about the same issues: ‘They are built of multiple, overlapping experts who weigh in and compete over different choices. As Walt Whitman correctly surmised, we are large and we harbour multitudes within us. And those multitudes are locked in chronic battle. There is an ongoing conversation among the different factions in your brain, each competing to control the single output channel of your behaviour.’17
In essence, this is a more sophisticated way of describing the Stop and Go mechanisms. Animals can’t have these conversations with themselves. They lack a fully developed prefrontal cortex, the part of the human brain that allows us to analyse situations and make reasoned choices. When a mouse is fed a drug targeted at a particular dopamine receptor, it will go into a frenzy of cocaine consumption.18 Something very similar happens in the parts of the human brain that we share with mice. But, however intense the craving that a drug addict experiences, the decision to take the drug involves uniquely human, rational functions.
To put it another way, humans don’t respond to their ‘animal instincts’ in the way that animals do. Rather, when temptation appears, those ancient instincts are fed through higher-order cognitive processes. And it’s those rational processes – the battle between Stop and Go – that tend to decide the outcome.
A cocaine addict has the mental capacity to decide not to give in to temptation; a mouse doesn’t. Of course, it’s likely that the addict will succumb, but only after rationalising his decision to do so. (‘I really shouldn’t, but …’) We should therefore be very careful about using the world ‘compulsive’ as a synonym for ‘overwhelming’. P.J. O’Rourke once wrote that there was no agreed etiquette for declining a line of coke because no one ever had – but that was in the early 1980s when, incredibly, cocaine was being touted as non-addictive.
It would be convenient if neuroscience enabled us to identify addicts, and potential addicts, by measuring their brain activity. It does not do so. On the contrary, recent research undermines the neat distinction between addicts and non-addicts that has become so central to the therapeutic industry. We have a very incomplete picture of the relationship between addictive behaviour and the brain’s reward systems. What we do know about the action of dopamine suggests that ‘normal’ over-indulgence and addictive over-indulgence are closely related to each other – not something that the disease-obsessed therapeutic industry is prepared to admit.
The essence of that disorder is that people choose to do things that are not in their best interests. In doing so, they are choosing short-term over long-term rewards. Those are the I-really-shouldn’t moments, and they come in all shapes and sizes – from the last cupcake in the box to the impulse purchase of virtual goods in a computer game. How much harm they do depends on the context, obviously. Life would be pretty grim if we never said to ourselves ‘to hell with the consequences’. In fact, I feel uncomfortable in the company of lifelong teetotallers, as opposed to ex-drunks like me. And people who boast that they’ve never even tried a cigarette strike me as annoyingly self-righteous and risk-averse. Weren’t they at least curious?
The individuals we call addicts are those who consistently seek damaging short-term rewards. They seem to have a strong ‘wanting’ pathway in the brain. To what extent they were born with this type of pathway is difficult to say. Alcoholism runs in families, but trying to draw the line between genetic predisposition and environmental conditioning is an impossible task. This wouldn’t be the case if addiction really were an organic disease such as Huntingdon’s: scientists would stand a chance of isolating the gene that caused it. But, since addiction consists of complex sequences of voluntary acts, such neurological reductionism is a waste of time.
As we’ve seen, however, neuroscience helps explain what is going on when we behave addictively, irrespective of whether we’re addicts. The pleasures we reach out for flood our brains with dopamine, among other substances, and then drain it. Illegal drugs offer extreme examples of this phenomenon. Methamphetamine and crack cocaine, for example, induce cravings that almost anyone would find hard to resist. One of my friends, a distinguished conservative journalist, was on holiday with his wife in Jamaica in the early 1990s, when the crack epidemic in American cities was at its height. They were offered a crack pipe and thought, OK, just this once. ‘It was utter bliss,’ he recalls. ‘But my wife and I took a solemn vow never to try it again because it was just so fucking delicious and we knew we’d leave the island as crackheads.’
Most of us are never confronted by that situation. Crystal meth and crack aren’t physically, psychologically, economically or socially available to us. We are, however, confronted by gingerbread biscuits that seem to gaze pleadingly at us as we order our mid-morning latte. Manufacturers of legal goods have cottoned on to how addiction works and are now repackaging, reformulating and reimagining their products accordingly. As we’ll see, manufacturers of packaged food and internet pornography have a meticulously researched grasp of brain science.
The sorts of pleasures people chase vary enormously, from the horny thrill of an MDMA high to the gloopy indulgence of a chocolate sundae. But both these sensations can, in some people, form part of an acceleration of desire – one that requires increasing amounts of exposure in order to maintain levels of pleasure.
Once we realise this, we can see that the old distinction between ‘psychological’ and ‘physical’ addiction or dependence is misleading. There are people with eating disorders whose monstrous consumption of ice cream is powerfully reinforced by changes in their brain (which may include a serotonin high if they throw it up). They are physically addicted to it, though this addiction is perfectly reversible if they stop doing this to themselves – and is therefore not a disease in any meaningful sense.
As for the notion of dependence, it can mean many things. Some diabetics are dependent on insulin in the sense that they would die without it. Heroin addicts are dependent on the drug in the sense that they will go into withdrawal without a fix; they won’t die from it. A coffee drinker who gets through six espressos a day will also experience withdrawal if he suddenly stops – probably quite a nasty headache; is he therefore not also dependent on caffeine?
In contrast, the terms ‘wanting’ and ‘liking’, though they don’t sound scientific, can be used unambiguously because they correspond to discrete urges governed by different brain mechanisms. And we can say with some confidence that, increasingly, our wanting urge is overwhelming our liking urge. This is not good news: it tends to bring out the worst in our personalities while overloading our bodies with substances they don’t need. Perhaps it’s just me, but queuing up for a cappuccino seems like a much less pleasant experience than it was a decade ago: the smell of freshly ground coffee beans seems to sharpen elbows and shorten tempers. But that doesn’t matter to vendors whose aim, to put it bluntly, is to make us as greedy as possible.
That was always the case, of course. Presumably even the bakers in ancient Mesopotamia wanted their customers to be greedy. And salesmen have known for centuries that the key to good business lies in the environment – that is, in an artfully arranged backdrop of temptations. Now, however, corporations are learning how to manipulate that environment in order to trigger specific and damaging obsessions. And as we’ll see in later chapters, these skills are being developed in every corner of the marketplace. So, if we truly want to understand addiction, we need to examine the disorientating world around us.