The Idiot Brain

by Dean Burnett

  What if chemicals could ‘artificially’ induce activity in the reward pathway, without us having to do anything? They’d probably be very popular. So popular, in fact, that people would go to extreme lengths to get them. This is exactly what most drugs of abuse do.

  Given the incredible diversity of beneficial things that we can do, the reward pathway has an incredibly wide variety of connections and receptors, meaning it’s susceptible to a similarly wide variety of substances. Cocaine, heroin, nicotine, amphetamines, even alcohol – these all increase activity in the reward pathway, inducing unwarranted but undeniable pleasure. The reward pathway itself uses dopamine for all its functions and processes. As a result, numerous studies have shown that drugs of abuse invariably produce an increase in dopamine transmission in the reward pathway. This is what makes them ‘enjoyable’ – particularly drugs that mimic dopamine (cocaine, for example).18

  Our powerful brains give us the intellectual capacity to quickly figure out that something induces pleasure, quickly decide we want more of it, and quickly work out how to get it. Luckily, we also have higher-brain regions in place to mitigate or overrule such base impulses as, ‘Thing make me feel nice, must get more thing.’ These impulse-control centres aren’t perfectly understood but are most probably located in the prefrontal cortex, along with other complex cognitive functions.19 Regardless, impulse control allows us to curb our excesses and recognise that descending into pure hedonism is not a good idea overall.

  Another factor here is the plasticity and adaptability of the brain. A drug causes excess activity of a certain receptor? The brain responds by suppressing the activity of the cells those receptors activate, or shutting down the receptors, or doubling the number of receptors required to trigger a response, or any method that means ‘normal’ levels of activity are resumed. These processes are automatic; they don’t differentiate between drug and neurotransmitter.

  Think of it like a city hosting a major concert. Everything in the city is set up to maintain normal activity. Suddenly, thousands of excitable people arrive, and activity quickly becomes chaotic. In response, officials increase police and security presence, close roads, buses become more frequent, bars open earlier and close later, and so on. The excitable concert-goers are the drug, the brain is the city; too much activity and the defences kick in. This is ‘tolerance’, where the brain adapts to the drug so it no longer has the same potent effect.

  The problem is, increased activity (in the reward pathway) is the whole point of a drug, and if the brain adapts to prevent this, there’s only one solution: more drug. An increased dose is needed to provide the same sensation? Then that’s what you use. Then the brain adapts to that, so you need a bigger dose. Then the brain adapts to that, and on it goes. Soon, your brain and body are so tolerant of a drug that you’re taking doses that would legitimately kill someone who had never tried it before, but all it does is provide the same buzz that got you hooked in the first place.

  This is one reason why quitting a drug, ‘going cold turkey’, is so challenging. If you’re a long-term drug user, it’s not a simple matter of willpower and discipline; your body and brain are now so used to the drug they’ve physically altered to accommodate it. Sudden removal of the drug therefore has serious consequences. Heroin and other opiates provide a good example of this.

  Opiates are powerful analgesics that suppress normal levels of pain by stimulating the brain’s endorphin (natural painkilling, pleasure-inducing neurotransmitters) and pain-management systems, providing an intense euphoria. Unfortunately, pain exists for a reason (to let us know about harm or damage), so the brain responds by increasing the potency of our pain-detection system, to cut through the blissful cloud of opiate-induced pleasure. So users take more opiates to shut it down again, and the brain strengthens it further, and so on.

  Then the drug is taken away. The user no longer has something that made them incredibly calm and relaxed. What they do have is a super-enhanced pain detection system! Their pain-system activity is strong enough to cut through an opiate high, which for a normal brain would be agonising, as it is for a drug user going through withdrawal. Other systems affected by the drug are similarly altered. This is why cold turkey is so hard, and legitimately dangerous.

  It would be bad enough if it was just these physiological changes that drugs cause. Alas, changes in the brain also alter behaviour. You’d think the many unpleasant consequences and demands of drug use should logically be sufficient to stop people using them. However, ‘logic’ is one of the first casualties of drug use. Parts of the brain may work to build tolerance and maintain normal functioning, but it’s so diverse that other brain areas are simultaneously working to ensure we keep taking the drug. For example, it can cause the opposite of tolerance; drug users become sensitised to the effects of a drug by suppression of the adaptation systems,20 so it becomes more potent, compelling the individual to seek it out even more. This is one factor that leads to addiction.†

  There’s more. Communication between the reward pathway and the amygdala serves to provide a strong emotional response to anything drug related, aka ‘drug cues’.22 Your specific pipe, syringe, lighter, the smell of the substance, all these become emotionally charged and stimulating in their own right. This means drug users can experience the effects of a drug, directly from the things associated with it.

  Heroin addicts provide another grim example of this. One treatment for heroin addiction is methadone, another opiate that provides similar (though reduced) effects, theoretically enabling users to give up gradually without going cold turkey. Methadone is supplied in a form than can only be swallowed (it looks like worryingly green cough syrup), whereas heroin is usually injected. But so strong a connection does the brain make between injection and the effects of heroin, that the act of injecting causes a high. Addicts have been known to pretend to swallow methadone, then spit it into a syringe and inject it.23 This is an incredibly dangerous act (if only for hygiene reasons) but the warping of the brain by drugs means the method of delivery is almost as important as the drug itself.

  Constant stimulation of the reward pathway by drugs also alters our ability to think and behave rationally. The interface between the reward pathway and the frontal cortex, where the important conscious decisions are made, is modified, so that drug-acquiring behaviours are prioritised above normally more important things (such as holding down a job, obeying the law, showering). By contrast, negative consequences of drugs (being arrested, getting a nasty illness from needle sharing, alienating friends and family) are actually suppressed in terms of how much they bother or worry us. Hence an addict will shrug nonchalantly at losing all their worldly possessions but will repeatedly risk their own skin to obtain another hit.

  Perhaps most disconcerting is the fact that excessive drug use suppresses activity of the prefrontal cortex and impulse-control areas. The parts of the brain that say, ‘Don’t do that’, ‘That’s not clever’, ‘You’ll regret this’, and so on – their influence is diminished. Free will may be one of the most profound achievements of the human brain, but if it gets in the way of a buzz then it’s got to go.24

  The bad news keeps coming. These drug-based alterations to the brain and all the associations made don’t go away when drug use stops; they’re just ‘not used’. They may fade somewhat but they endure, and will still be there should the individual sample the drug again, no matter how long they’ve abstained. This is why relapse is so easy, and such a big problem.

  Exactly how people end up becoming regular drug takers varies massively. Maybe they live in bleak deprived areas where the only relief from the realities of life is from drugs. They might have an undiagnosed mental disorder and end up ‘self-medicating’ by trying drugs to alleviate the problems they experience every day. There is even believed to be a genetic component to drug use, possibly due to some people having a less-developed or underpowered impulse-control region of the brain.25 Everyone has that part of them that, when offered the opp
ortunity to try a new experience, says, ‘What’s the worst that could happen?’ Sadly, some people lack that other part of the brain that explains in exquisite detail exactly what could happen. This accounts for why many people can safely dabble with drugs and walk away unchanged, while others are ensnared from the first hit onwards.

  Regardless of the cause or initial decisions that lead to it, addiction is recognised by professionals as a condition to be treated rather than a failing to be criticised or condemned. Excessive drug use causes the brain to undergo startling changes, many of which contradict each other. Drugs seem to turn the brain against itself in some prolonged war of attrition, where our lives are the battleground. This is a terrible thing to do to yourself, but drugs make it so that you don’t care.

  This is your brain on drugs. It is pretty hard to convey all this with eggs, admittedly.

  Reality is overrated anyway

  (Hallucinations, delusions and what the brain does to cause them)

  One of the most common occurrences in mental health problems is psychosis, where someone’s ability to tell what’s real or not is compromised. The most common expressions of this are hallucinations (perceiving something that isn’t actually there) and delusions (unquestionably believing something that is demonstrably not true), along with other behavioural and thought disruptions. The idea of these things happening can be deeply unsettling; losing your very grasp on reality itself, how are you supposed to deal with that?

  Worryingly, the neurological systems handling something as integral as the ability to grasp reality are disturbingly vulnerable. Everything covered in this chapter so far – depression, drugs and alcohol, stress and nervous breakdowns – can end up triggering hallucinations and delusions in the overtaxed brain. There are also many other things that trigger them, like dementia, Parkinson’s disease, bipolar disorder, lack of sleep, brain tumours, HIV, syphilis, Lyme disease, multiple sclerosis, abnormally low blood sugar alcohol, cannabis, amphetamines, ketamine, cocaine, and more. Some conditions are so synonymous with psychosis they’re known as ‘psychotic disorders’, the most well known of which is schizophrenia. To clarify, schizophrenia isn’t about split personalities; the ‘schism’ for which it is named is more between the individual and reality.

  While psychosis often results in the sensation of being touched when you’re not being, or tasting or smelling things that aren’t there, the most common are aural hallucinations, aka ‘hearing voices’. There are several classes of this type of hallucination.

  There are first-person auditory hallucinations (‘hearing’ your own thoughts, as if they’re spoken by someone else), second person (hearing a separate voice talking to you) and third person (hearing one or more voices talking about you, providing a running commentary ofnwhat you’re doing). The voices can be male or female, familiar or unfamiliar, friendly or critical. If the latter is the case (which it usually is), they are ‘derogatory’ hallucinations. The nature of hallucinations can help diagnosis; for instance, persistent derogatory third-person hallucinations are a reliable indicator of schizophrenia.26

  How does this happen? It’s tricky to study hallucinations, because you’d need people to hallucinate on cue in the lab. Hallucinations are generally unpredictable, and if someone could switch them on and off at will, they wouldn’t be a problem. Nevertheless, there have been numerous studies, focusing largely on the auditory hallucinations experienced by those with schizophrenia, which tend to be very persistent.

  The most common theory of how hallucinations occur focuses on the complex processes the brain uses to differentiate between neurological activity generated by the outside world, and activity we generate internally. Our brains are always chattering away, thinking, musing, worrying and so on. This all produces (or is produced by) activity within the brain.

  The brain is usually quite capable of separating internal from external activity (that produced by sensory information), like keeping received and sent emails in separate folders. The theory is that hallucinations occur when this ability is compromised. If you’ve ever accidentally lumped all your emails together in the same folder you’ll know how confusing this can be, so imagine doing that with your brain functions.

  So the brain loses track of what’s internal and what’s external activity, and the brain isn’t good with such things. This was demonstrated in Chapter 5, which discussed how blindfolded people struggle to tell the difference between apples and potatoes when eating them. That’s the brain functioning ‘normally’. In the case of hallucinations, the systems that separate internal and external activity are (metaphorically) blindfolded. So people end up perceiving internal monologue as an actual person speaking, as internal musings and hearing spoken words activates the auditory cortex and associated language-processing areas. Indeed, a number of studies have shown that persistent third-person hallucinations correspond with reduced volumes of grey matter in these areas.27 Grey matter does all the processing, so this suggests reduced ability to distinguish between internally and externally generated activity.

  Evidence for this comes from an unlikely source: tickling. Most people can’t tickle themselves. Why not? Tickling should feel the same no matter who does it, but tickling ourselves involves conscious choice and action on our part, which requires neurological activity, which the brain recognises as being internally generated, so it’s processed differently. The brain detects the tickling, but internal conscious activity flagged it up beforehand, so it’s ignored. As such, it provides a useful example of the brain’s ability to differentiate between internal and external activity. Professor Sarah-Jayne Blakemore and her colleagues at the Wellcome Department of Cognitive Neurology studied the ability of psychiatric patients tickle themselves.28 They found that, compared with non-patients, patients who experienced hallucinations were far more sensitive to self-tickling, suggesting a compromised ability to separate internal and external stimuli.

  While an interesting approach (and one not without flaws), please note that being able to tickle yourself does not automatically mean you’re psychotic. People vary tremendously. My wife’s university housemate could tickle himself, and has never had any psychiatric issues. He’s extremely tall though; maybe the nerve signals take so long to get to the brain from the tickling site it just forgets how they originated?‡

  Neuroimaging studies have suggested further theories about how hallucinations generally come about. An extensive review of the available evidence, published by Dr Paul Allen and his colleagues in 2008,29 suggests an intricate (but surprisingly logical) mechanism.

  As you may expect, our brain’s ability to differentiate between internal and external occurrences is derived from multiple areas acting together. There are fundamental subcortical areas, predominantly the thalamus, that provide raw information from the senses. This ends up in the sensory cortex, which is an umbrella term for all the different areas involved in sensory processing (the occipital lobe for vision, auditory and olfactory processing in the temporal lobes, and so on). It’s often subdivided into primary and secondary sensory cortex; primary processes the raw features of a stimulus, secondary processes more fine detail and recognition (for example, the primary sensory cortex would recognise specific lines, edges and colours, the secondary would recognise all of this as an oncoming bus, so both are important).

  Connecting to the sensory cortex are areas of the prefrontal cortex (decisions and higher functions, thinking), premotor cortex (producing and overseeing conscious movement), cerebellum (fine motor control and maintenance) and regions with similar functions. These areas are generally responsible for determining our conscious actions, providing information needed to determine which activity is internally generated, as in the tickling example. The hippocampus and amygdala also incorporate memory and emotion, so we can remember what we’re perceiving and react accordingly.

  Activity between these interconnected regions maintains our ability to separate the outside world from the one inside our skull. It’s when the conne
ctions are changed by something that affects the brain that hallucinations occur. Increased activity in the secondary sensory cortex means signals generated by internal processes get stronger and affect us more. Reduced activity from the connections to the prefrontal cortex, premotor cortex, and so on, prevents the brain from recognising information that is produced internally. These areas are also believed to be responsible for monitoring the external/internal detection system, ensuring genuine sensory information is processed as such, so compromised connections with these areas would mean more internally-generated information is ‘perceived’ as genuine.30

  All of this combined causes hallucinations. If you think to yourself, ‘That was stupid’, when you buy an expensive new tea set and let your toddler carry it out of the shop, this is usually processed as an internal observation. But if your brain wasn’t able to recognise that it came from the prefrontal cortex, the activity it produces in the language-processing areas could be recognised as something spoken. Atypical amygdala activity means the emotional associations of this wouldn’t be dampened either, so we end up ‘hearing’ a very critical voice.

  The sensory cortex processes everything and internal activity can relate to anything, so hallucinations occur in all senses. Our brains, knowing no better, incorporate all of this anomalous activity into the perception process so we end up perceiving alarming, unreal things that aren’t there. With such a widespread network of systems responsible for our awareness of what’s real and what isn’t, it is undoubtedly vulnerable to a wide variety of factors, hence hallucinations in psychosis are so common.

  Delusions, a false belief in something that is demonstrably untrue, are another common feature of psychosis, and again demonstrate a compromised ability to distinguish between real and not-real. Delusions have many forms, such as grandiose delusions, where an individual believes they’re far more impressive than is accurate (believing they’re a world-leading business genius despite being a part-time shoe-shop employee), or (more common) persecutory delusions, where an individual believes they’re being relentlessly persecuted (everyone they meet is part of some shadowy plot to kidnap them).