Idiot Brain (35 page)

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Authors: Dean Burnett

BOOK: Idiot Brain
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You know when you look at something extremely bright and it lingers in your vision because it was so intense it's “burned” onto your retinas? This is the memory equivalent of that. Except it doesn't fade, it persists, because it's a
memory
. That's the point, and the memory is almost as traumatic as the original incident. The brain's system for preventing reoccurrence of trauma causes reoccurrence of trauma.

The constant stress caused by vivid flashbacks often results in numbing or dissociation, where people become detached from others, from experiencing emotions, even from reality itself. This is seen as another brain defence mechanism. Life is too stressful? Fine, shut it out, go into “standby.” While effective in the short term, it's not a good long-term strategy. It impairs all manner of cognitive and behavioral faculties.
Post-Traumatic Stress Disorder (PTSD) is the most well-known consequence of this occurrence.
12

Thankfully, most people won't experience such major traumas. Consequently, stress has to be sneakier to incapacitate them. So there's chronic stress, which is where you get one or more stressors that are more persistent than traumatic, so they affect you over the long term. A sick family member to care for, a tyrannical boss, a never-ending stream of deadlines, living on welfare and never clearing your debts, these are all chronic stressors.
*

This is bad, because when too much stress occurs over a long period, your ability to compensate suffers. The fight-or-flight mechanism actually becomes a problem. After a stressful event it typically takes the body 20–60 minutes to return to normal levels, so stress is quite long-lasting as it is.
14
The parasympathetic nervous system, which counteracts the fight-or-flight response once it's no longer needed, has to work hard to undo the effects of stress. When chronic stressors keep pumping stress hormones into our system, the parasympathetic nervous system is exhausted, so the physical and mental consequences of stress become “normal.” Stress
hormones are no longer regulated and used when needed; they persist, and the person becomes constantly sensitized, twitchy, tense and distractible as a result.

The fact that we can't counteract stress internally means we seek external relief. Sadly, but predictably, this often makes things worse. This is known as the “stress cycle,” where attempts to alleviate stress actually cause more stress and consequences, which result in more attempts to reduce stress, which in turn cause more problems, and so on.

Say you get a new boss who assigns you more work than is reasonable. This would cause stress. But said boss is not open to reason or rational argument, so you work longer hours. You spend more time working and stressed, so you experience chronic stress. Soon you start consuming more junk food and alcohol to unwind. This negatively affects your health and mental state (junk food makes you unfit, alcohol is a depressant), which stresses you out further and makes you vulnerable to further stressors. So you get more stressed, and the cycle continues.

There are numerous ways to stop the ever-increasing stress (adjusting workloads, improved healthy lifestyle, therapeutic assistance, among others), but for many this just doesn't happen. So everything builds up, until a threshold is crossed and the brain essentially surrenders; much like a circuit breaker will cut the power before a surge overloads the system, so ever-increasing stress (with associated health consequences) would be terribly damaging for brain and body, so the brain puts a stop to, essentially, everything. Many argue the brain induces a nervous breakdown to stop stress escalating to the point where lasting damage can occur.

The threshold between “stressed” and “
too
stressed” is hard to specify. There's
the diathesis-stress model, where diathesis means “vulnerability,” which describes how someone who is more vulnerable to stress requires less stress to push them over the edge, into a full breakdown where they experience a mental disorder or “episode” of some description. Some people are more susceptible: those with more difficult situations or lives; those already prone to paranoia or anxiety; even those with tremendous self-confidence can be brought low very quickly (if you're very self-confident, losing control due to stress could undermine your whole sense of self, causing immense stress).

Exactly how a nervous breakdown plays out also varies. Some people have an underlying condition like (or predisposition to) depression or anxiety, and overly stressful events can bring this on. Dropping a textbook on your toe hurts; dropping it on an already-fractured toe hurts considerably more. For some, the stress causes their mood to plummet to a point where it's incapacitating, and thus depression occurs. For others, the constant apprehension and persistence of stressful occurrences causes crippling anxiety or panic attacks. The cortisol released by stress is also known to have an effect on the dopamine systems of the brain,
15
making them more active and more sensitive. Anomalous activity in the dopamine systems are believed to be the underlying cause of psychosis and hallucinations, and some nervous breakdowns do produce psychotic episodes.

Thankfully, a nervous breakdown is typically a short-lived thing. Medical or therapeutic intervention usually sees people return to normal eventually, or just the enforced break from stress may help. Granted, not everyone sees a nervous breakdown as a helpful thing; not everyone gets over it, and
those who do often retain a sensitivity to stress and adversity that means they could more easily experience a nervous breakdown again.
16
But they can at least resume a normal life, or a close approximation of it. Hence nervous breakdowns can help prevent lasting damage from a relentlessly stress-filled world.

Saying that, many of the problems a nervous breakdown helps limit are themselves caused by the brain's own techniques for dealing with stress, which often aren't up to scratch for modern life. Appreciating the brain for limiting the damage caused by stress via nervous breakdowns is like thanking someone for helping put out the fire in your house when they were the one who left the fryer on.

Dealing with the monkey on your back

(How the brain brings about drug addiction)

In 1987, there was a televised public-service announcement that illustrated the dangers of drugs via the use of, surprisingly, eggs. An egg was shown and the viewer was told, “This is your brain.” A frying pan was then shown, with the sentence, “This is drugs.” The egg was then fried in the pan, with the words, “This is your brain on drugs.” In a publicity sense, it was very successful. It won awards, and is still referenced (and, admittedly, mocked) in pop culture to this day. In a neuroscientific sense, it was a terrible campaign.

Drugs do not heat your brain so much that the very proteins making up its structure break down. Also, it's very rare for a drug to affect every part of the brain simultaneously,
in the way that a frying pan affects an egg. Lastly, you apply drugs to the brain without removing it from its shell, aka skull. If you did, drug use certainly wouldn't be so popular.

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
dollars
17
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.

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