Idiot Brain

by Dean Burnett

  This isn’t to say drugs are necessarily good for the brain; it’s just the truth is far more complicated than egg-based metaphors can allow for.

  The illegal drug trade is estimated at nearly half a trillion dollars17 and many governments spend countless millions finding, destroying, and discouraging the use of illegal drugs. Drugs are widely assumed to be dangerous; they corrupt users, damage health and ruin lives. This is fair because drugs often do exactly that. Because they work. They work very well, and do so by altering and/or manipulating the fundamental processes of our brains. This causes problems such as addiction, dependence, behavioral changes and more, all of which stem from how our brains deal with drugs.

  In Chapter 3, the dopaminergic mesolimbic pathway was mentioned. It’s often called the “reward” pathway or similar, because its function is refreshingly clear: it rewards us for actions perceived as being positive, by causing the sensation of pleasure. If we ever experience something enjoyable, from a particularly pleasant satsuma to the climax of a certain bedroom-based activity, the reward pathway provides the sensations that make us think, “Well, wasn’t that pleasant?”

  The reward pathway can be activated by things we consume. Nutrition, hydration, alleviating appetite, providing energy; edible substances that do these things are recognized as pleasant because their beneficial actions trigger the reward pathway. For example, sugars provide easily utilized energy for our bodies, so sweet-tasting things are perceived as pleasant. The current state of the individual also plays a part: a glass of water and slice of bread would usually be considered the most uninspiring meal, but would be divine ambrosia to someone just washed up after months adrift at sea.

  Most of these things activate the reward pathway “indirectly,” by causing a reaction in the body that the brain recognizes as a good thing, thus warranting a rewarding sensation. Where drugs have the advantage, and what makes them dangerous, is they can activate the reward pathway “directly.” The whole tedious process of “having some positive effect on the body that the brain recognizes” is skipped, like a bank employee handing over bags of cash without needing boring details like “account numbers” or “ID.” How does this happen?

  Chapter 2 discussed how neurons communicate with each other via specific neurotransmitters, including noradrenaline, acetylcholine, dopamine, serotonin. Their job is to pass signals between neurons in a circuit or network. Neurons squirt them into synapses (the dedicated “gap” between neurons where communication between them occurs). There they interact with dedicated receptors like a specific key opening a specific lock. The nature and type of receptor the transmitter interacts with determines the activity that results. It could be an excitatory neuron, which activate other regions of the brain like someone flicking a light switch, or it could be an inhibitory neuron, which reduces or shuts down activity in associated areas.

  But suppose those receptors weren’t as “faithful” to specific neurotransmitters as hoped. What if other chemicals could mimic neurotransmitters, activating specific receptors in their absence? If this were possible, we could feasibly use these chemicals to manipulate the activity of our brains artificially. Turns out, it is possible, and we do it regularly.

  Countless medications are chemicals that interact with certain cell receptors. Agonists cause receptors to activate and induce activity; for example, medications for slow or irregular heartbeats often involve substances that mimic adrenalin, which regulates cardiac activity. Antagonists occupy receptors but don’t induce any activity, “blocking” them and preventing genuine neurotransmitters from activating them, like a suitcase wedged in an elevator door. Antipsychotic medications typically work by blocking certain dopamine receptors, as abnormal dopamine activity is linked to psychotic symptoms.

  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 centers 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 recognize 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 agonizing, 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 legit
imately dangerous.

  It would be bad enough if it was just these physiological changes that drugs cause. Alas, changes in the brain also alter behavior. 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 sensitized 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 behaviors are prioritized 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 opportunity 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 led to it, addiction is recognized by professionals as a condition to be treated rather than a failing to be criticized 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 behavioral 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 tumors, 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 of what 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 wh
at’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 gray matter in these areas.27 Gray 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 recognizes 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 to 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 college roommate 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?‡