My Plastic Brain Page 8

  Which ties in nicely with the direction of our unconscious cognitive biases. A score of –31 means that I press a button thirty-one milliseconds faster when it follows an angry face than when it follows a smiley one. Jolyon, on the other hand, is fifty-one milliseconds faster to spot the target when it comes after a happy face. His brain automatically seeks out the good side of life—which probably explains his unusually high levels of optimism.

  If all it takes to put things right is a quick bit of computer-based training, then it shouldn’t matter how we got to be so different—but I must admit I’m curious. A glance around my close relatives makes me suspect that at least some of my neurotic tendencies might be inherited. On one side of my family it's considered unusual if you’re not anxious, prone to depression, or emotionally a bit volatile. A quick head count of my aunts, uncles, and cousins on that side of the family reveals that while the average number of people with emotional issues in the United Kingdom is one in every four, our family has roughly twice as many.5

  Elaine says she’d be happy to put me into her next study on the genetics of worry, but they probably won’t be ready to do the tests for at least another year. As a backup, she puts me in touch with the lab that does the analysis for her studies. She warns me that it’ll be expensive (at least £500, or over six hundred US dollars), but it might be possible as a one-off. It's my only hope because while some medical insurance companies in the United States will do the test under certain circumstances, commercial gene-testing companies like 23andMe—which offer off-the-shelf tests for risk genes, for everything from Alzheimer's to male pattern baldness—don’t offer it, at least not yet.

  As it happens, when I contact the lab, they are happy to help and can even chuck a few more samples in for me at no extra cost. I get a testing kit sent to Jolyon, and then we swab our cheeks, pop them in the post to the lab, and wait with bated breath to see what comes back. After several weeks of back and forth between Jolyon and the lab, where he manages to avoid getting any DNA on his first set of swabs and the second batch gets lost in the mail—and I start to wonder how he runs a successful business at all—we finally get the results. And the verdict is…not at all what I expected.

  THE WORRIER/WARRIOR GENE

  Let's not get carried away—there are most definitely lots of genes that contribute to something as complex as your outlook on life. But the serotonin transporter gene is particularly interesting because of the way that it affects the kind of implicit learning that underpins unconscious biases.

  The serotonin transporter gene makes proteins that mop up one of the brain's chemical messengers after they have been used to send a message between neurons, and recycles as much as possible, to be used again.

  Everyone has two copies (aka alleles) of this gene, and it comes in two versions: one short (the S-version) and one long (the L-version). Confusingly, there are also two versions of the L-version (LA and LG), and LG acts almost exactly like the S-version.

  This matters because the S and LG versions contain less DNA, and so they can’t produce as many transporter proteins. This leaves more serotonin hanging around between neurons, meaning there is less serotonin in the actual neuron to send more messages.

  Each of us has one of the following versions of the serotonin transporter gene: SS (short), SLA (medium), SLG (short), LALA (long), or LGLG (short), with SL being the most common and SS the rarest, at least in a UK population (it varies around the world).6

  People with at least one S or LG allele have been found to have a more reactive amygdala (involved in danger detection) than others.7 They are also more likely to have a negative cognitive bias, to have a higher score on standardized anxiety tests, and to be at higher risk of depression. Other studies have found that people with the long version are more likely to have a positive bias.

  But while it sounds like it's “case closed” for the “worry gene,” it turns out to be not quite as simple as that. While some studies have found a link between the short allele and an anxious temperament, others have found the opposite. A long-term study led by Avshalom Caspi and Terrie Moffitt in 2003 provided a crucial clue as to why.8 They looked at not only genetics but also at the number of stressful events a person had been exposed to. And they found that people with the short version were indeed more likely to become anxious or depressed, but only if they had also experienced at least one stressful life event (divorce, abuse, death of a loved one, etc.). Without life stress, they were actually less likely to become depressed than people with the long-gene type. So the same gene can be either a “worrier gene” or a “warrior gene” depending on what happens to you along the way.

  One possible explanation for this is that having the S-version gives a person a kind of super-plasticity brain, which learns and retains the lessons life throws at it unusually well. The downside is that if you learn from stressful experiences, your brain is more likely to conclude that there is a lot to fear in life and that the world is generally a dangerous place. On the upside, it quickly learns the opposite, too, if given half a chance.

  Sure enough, in Elaine Fox's lab, people with the short version were quicker to develop not only negative biases but positive biases too: “If a few bad events happen, you are more likely to develop a bias and then that gets reinforced. But by the same token, if the positive biases start developing, the people with that same genotype will be more likely to develop a positive mind-set,” she told me.

  So, the current consensus is that people with shorter versions of the serotonin transporter gene seem to be more vulnerable to the long-term effects of stress, but are also more likely to learn from life experience if it happens to be good. Given the way my brain has learned from my own stressful life events (my parents’ divorce when I was five and my father's death when I was in my late teens), I would have bet money on me being a carrier of the short version of the gene. Jolyon, I wasn’t sure about—but guessed that he was probably a super-resilient long-version carrier. We joked that if we were both short-gene carriers, it would be fantastic news for his parents and a bit of a kick in the teeth for mine.

  In fact, the genetic test revealed that he is indeed an SS carrier—born with a brain that is set up to learn from life experience unusually well. The way he describes his early life suggests he got pretty lucky: no emotional upheaval, nobody died, and he wasn’t bullied or abused in any way. This combination of genetics and experience seems to have made him super resilient to life's ups and downs, highly resistant to stress, and with an optimistic view on life.

  Me, I’m among the 50 percent or so that has one copy of the short version of the gene and one copy of the standard long version. Which basically means that I have a moderately sensitive brain: not especially resilient but not the most sensitive on the planet either.

  This might be my negative bias talking, but it seems to me that it might give me the worst of all worlds. With one copy of the short type, it does mean that my genes have made it more likely that life stress will turn into a potentially problematic negative bias. But, not having the most plastic brain possible, it might not be an easy ride to change it, either.

  THE WAY OF THE WORRIER

  At this point, it seems sensible to look at what happens in the brain to generate an anxious thought, to get an idea of what I would be changing, if I were to manage to turn things around. As it happens, this is one area where the circuitry is fairly well understood—at least in as much as anyone understands what a thought actually is. I once asked Geraint Rees, a prominent neuroscientist at University College London, to explain what happens in the brain to make a thought, and, because he is a prominent neuroscientist, I expected a concrete answer. What he actually said was, “A thought is a mental state. It is widely believed that mental states (things in the mind) correlate with neural states (things in the brain), but the mapping between the two is not well known.”

  So even top neuroscientists don’t know how brain activity turns into conscious thoughts, anxious or otherwise. The tagline
on Geraint Rees's lab website puts this rather nicely, I think, with a quote borrowed from Einstein (attributed): “If we knew what we were doing, it wouldn’t be called research, would it?”

  But this we do know: for us to notice the thing to be feared at all, it has to stimulate one of our senses. Sensory information is constantly being passed to the thalamus, which sits in the middle of the brain and acts as a switchboard cum relay center between the senses, cortex, and other important areas like the amygdala and the hippocampus (which shunts things in and out of memory).

  If there is anything around that has previously been marked as “dangerous,” it sends the information quick smart to the amygdala, the brain's burglar alarm, which snaps attention to it while readying the body for “fight, flight, or freeze” (racing heart, sweating palms, and so on). It also notifies the cortex (the thinking bit), which sets about making sense of the situation, and generates the conscious feeling of fear.

  Joseph LeDoux, a neuroscientist at New York University, was among the first to describe this basic circuitry, and since then, an overactive amygdala has become the default popular explanation for everything from panic attacks to feeling a bit stressed out. It has never really seemed to explain my experience of being a chronic worrier, at least not for all forms of worrying. It probably accounts for the sudden tension I feel when crossing the road with my son, but when I’m fretting over something—like whether my work is up to scratch or whether the thing I said earlier made me come across as a bit weird—I don’t get a surge of adrenaline and a racing heart. It's very much a slow burn, thinking-based, self-torture kind of reaction, not a primal, physical, need-to-get-out-of-here-right-now kind of feeling.

  It turns out that LeDoux now spends a lot of his time trying to explain the subtle distinction between fear and anxiety—most recently in his book Anxious. He says that these are two different, although closely related, emotions and each has a slightly different bit of brain circuitry.9 Fear—the sweaty palm bit—is a physical reaction to a threat that is happening right now, in front of you, and that might kill you if you don’t fight, run away, or hide. The emotion of fear comes later, once the slower thinking bit has come online. Anxiety and worry, on the other hand, are less to do with reacting to, or making sense of, a threat you can see but are more to do with a feeling of uncertainty about if and when something bad will happen and whether you are up to the challenge of dealing with it if it does.

  Experiments have shown that damage to the amygdala doesn’t prevent this kind of self-torture anxiety from happening. Instead, another brain area—the bed nucleus of the stria terminalis (BNST)—is in charge of processing uncertainty.10 The key difference between them is where they get their information from. While the amygdala takes information mainly from the senses, to process what is out there in the world, the BNST gets more of its information from brain areas involved in memory and other types of cognitive processing, which means that it is more than capable of making a drama out of something that is entirely in your own head.

  The BNST also seems to be the driver of hyper-vigilant threat monitoring: the keeping watch for anything that might, possibly, go horribly wrong. It does, though, put the brain in a state to react quickly if anything does happen. So the fact that I can freak out about my young son being near roads, even when he is safely tucked up in bed, should mean that I will react in super-quick time if anything actually happens. The downside is that I expend a lot of energy worrying about something that might never happen and which my lightning-fast amygdala could probably take care of anyway if it did.

  As it happens, the amygdala and the BNST are both connected to pretty much the same areas of the brain—most importantly to the prefrontal cortex, which ultimately makes the decision about whether to escalate or calm down. The subjective feeling of anxiety or calm depends on which part of the circuit is most active at any point. Electrical activity is always flowing between the two, but depending on which is shouting the loudest at any one point, we will either feel in control of the situation or not.

  If I want to take control of my worrying habit, then, I need to either reduce the number of (real or imagined) threats that get the amygdala and BNST going in the first place, and then use my thinking brain better to get out of the worry hole—or, preferably, both.

  Gaining more control of the prefrontal cortex sounds familiar. But if Elaine Fox is right, there is a stage before this one that needs to be addressed: namely, the unconscious biases that are giving my prefrontal cortex more to do than is strictly necessary.

  A trawl through the work of cognitive scientists working in this area reveals that there are three options. One is to use cognitive-bias modification training to train my attentional system to seek out positive things in an environment rather than negative ones. The most common approach to changing those biases involves flashing up a group of faces—most of them angry, and only one happy face—and asking people to click on the happy one as fast as they can (see figure 2.3).11

  Figure 2.3. Cognitive-bias training. (Courtesy of Mark Baldwin, McGill University)

  According to the people at the Baldwin Social Cognition Lab at McGill University who designed the task, the idea is, “Each time you drag your attention away from one of the frowning faces in the game in order to find a smiling, accepting face, this helps to build a mental habit. After a hundred trials or more the habit can become automatic…the mental habit generalizes beyond the visual domain of disengaging from frowning faces, to apply to disengaging from thoughts and worries.”12

  Another option, based more on the prefrontal cortex (that part of the brain above the eyebrows that keeps the more automatic impulses under control) is a different kind of cognitive-bias modification but one that is focused on practicing changing a negative interpretation of a situation. This generally comes in the form of audio of an imaginary scenario, after which you have to decide if everything is going to be okay or not. (You only get a point if you answer with a cheery “yes!”). Being forced to be positive over and over again is also meant to create a mental habit that gradually becomes ingrained in the brain's wiring, blood vessel network, and so on.

  Another option is to undergo working-memory training. Leaving aside the controversy over whether working-memory training does anything at all (that one is still being thrashed out), there are a few early studies that seem to suggest that training working memory might help to reduce anxiety—on the basis that improving working memory might provide more mental space to talk yourself out of a worry hole. Of course, it might backfire and provide more mental workspace to worry about everything that might go wrong.

  Then there's meditation—which, for me, is a work in progress. If I’m totally honest, I’m really hoping that the answer to my brain blips isn’t going to be meditation; I’m really not sure I can stick to a sitting quietly habit for very long.

  As it happened, my first bite of the cognitive brain-training cherry came not from Elaine Fox's group down the road in Oxford but from Ghent University in Belgium, where neuroscientist Ernst Koster is doing very similar work as Fox. While I am waiting for Fox to get back to me—and fretting about not having very much to write about yet—I drop Koster a line to see if he might be able to help.

  A couple of days later, we chat over Skype and he puts my fears to rest. Yes, he tells me, he could send me links to the online training they use in their studies, and he’d be happy to assess my anxiety levels before and after. It all sounds easy enough—and I wouldn’t even have to leave my sofa. But then he tells me about the experiments they’ve been doing with eye-tracking technology: measuring attentional biases by monitoring where your eyes flick to, before you even realize they have moved. Apparently, Koster and his team have had some interesting results with this, but it can only be done in the lab—which would mean a trip to Ghent. I’m intrigued, and I’ve never been to Belgium….

  Koster promised to check the lab schedule and let me know when there would be some free time over the next few weeks. A fe
w days later, I find myself on a Eurostar train to Belgium: he did get back to me as promised, but rather than, as I expected, setting a date for some leisurely time over the next month or so, I was informed that there was a rare gap in the lab schedule in just two days, and if it wasn’t too short notice—and if I could get myself to Ghent—he’d be happy to put me through my paces.

  It kind of was too short notice, but as if to prove that when there's no time for procrastination and worry I can just get on with stuff, I manage to book my travel and hotel, sort childcare and a dog-sitter, and pack a bag—in lightning-quick time. I arrive late in the evening and quickly decide against wandering the streets to find something interesting to write about my visit so far. What if I’ve accidentally booked into a hotel in the dodgy quarter? It was quite cheap…. So, with my threat-detection system very much in charge, I turn my back on the prospect of a cold Belgian beer and head upstairs to bed.

  The next morning, Jonas Everaert, one of Koster's PhD students, meets me at the hotel and walks me through the backstreets of Ghent (the not-so-pretty end—maybe I made the right decision last night) to the university. He gallantly balances my bag on the back of his bike, and we chat about all kinds of brain-changing technologies, including meditation. He tells me that brain-imaging studies with Buddhist monks have shown that their amygdala reactivity has dropped so low through constant meditation that it is no longer workable in modern life—they simply couldn’t deal with the levels of stress and threat that the rest of us do. I don’t want to take it that far, clearly, but a little more Zen might be nice. Still, it's interesting to get another insight into the pros and cons of meditation. The way most people are talking about meditation these days, you’d think it was the cure for everything.