Author: Marc

In a recent reply to a reader’s comment, I waxed eloquent about whether addiction was an impulsive drive or a compulsive drive. Let’s consider the matter more closely. According to neuroscientist Trevor Robbins, impulses can be defined as urges or acts that arise from an input that you can’t inhibit. In other words, the problem is in the input stream—thoughts, perceptions, and stimuli that are just too attractive to turn off. Compulsion, says Robbins, is an urge to act that is too powerful to turn off, so you keep doing the thing again and again. Now the problem is in the output stream, and the classic case is OCD—obsessive-compulsive disorder.

Present scientific wisdom on addiction would classify it as an impulsive disorder. Because, according to neuroscientist Kent Berridge, addictive cravings are always cue-related. You don’t just crave. First, there has to be a stimulus, a cue, to make you think about the thing you want. That cue can be of any sort. It can be the runny nose of opiate withdrawal, the name of a dope connection suddenly showing up on the screen of your mind. It can be just the sight of last week’s leftovers – a few paltry grains of powder, a leftover pill, whatever. Then, suddenly, wham! you want it now. The ventral striatum, the seat of craving, is highly sensitized to drug cues through repeated exposure: based on a buildup of synaptic networks that provide a potent meaning for the drug, plus the surge of dopamine directly triggered by previous associations.

But compulsion can play a huge role in addiction as well. We feel “compelled” (not “impelled”) when we reach for the drug (or the drink or food or link to our favourite gambling site) again and again and again. Even after you’ve taken a dose of whatever it is in the last half hour, you just feel that it’s not enough, and the urge is to take more, no matter what the consequences. The consequences can be pretty severe. Coke and its cousin crack are the best examples. A coke high can last for an hour or two, but cokeheads snort more and more, sometimes minutes apart, just in case there’s not enough already inside them, and that can lead to a stroke or heart attack. With opiates, compulsive consumption can obviously lead to an OD. The source of compulsion is some kind of deep anxiety, but more on that another time.

The striatum has a component that focuses attention on the goal. That’s the ventral striatum, and it’s a key player in drug craving. But the striatum also has a motor component that generates action. The “dorsal striatum” releases actions, something like bullets from a gun. It puts the actions into effect. And there you are doing it – again! – before you’ve even thought about it. The dorsal striatum is the culprit when it comes to compulsive (repetitive) behaviour. But the close linkage between these two parts of the striatum – attention to the goal (ventral) and execution of the goal (dorsal) – is what moves us from impulse to compulsion.

That’s not good news for addicts of many stripes. But what can I say? Be careful! We have to live with the hardware in our heads, so we’d better get to know it and learn how to use it properly.

A reader recently brought up the fascinating connections between Buddhist meditation and neuroscience. There has been a lot of work in the last two decades, trying to develop a scientific foundation for meditation and also teaching science a thing or two, like how meditation changes the brain. In this post I want to suggest how meditation can reduce craving, thus potentially aiding recovery, and I want to briefly describe how this might work in the brain.

Last post, I suggested that “free will” or at least deliberate choice could be facilitated by slowing, down, relaxing, seeing the bigger perspective, and…even meditating. I was following Nico Frijda’s ideas about the importance of reflectivity in overcoming impulsive action. But how on earth do you slow down, relax, and reflect (let alone meditate) when craving is erupting throughout your consciousness. The craving for drugs (or booze, or other substances and activities) can be enormously powerful. As noted recently in a response by Mike Johnson, the dACC (dorsal anterior cingulate cortex), which is the seat of deliberate self-control, can be a leaf tossed around by a cyclone when the impulse to take drugs gets too strong.

Indeed, addicts are often caught in the cross-fire between two warring brain systems. The dACC, and its connections to the (probably left) dorsolateral prefrontal cortex, try to set up a long-range forecast, a bigger picture, a more reasoned perspective, and then use that perspective to inhibit behaviours that surely lead to failure and misery. Meanwhile, connections between the ventral striatum, which is the seat of goal-seeking, and the orbitofrontal cortex, another ventral system that anticipates the pleasure and relief of taking the drug or drinking the drink, get increasingly activated by dopamine, as the possibility, no, likelihood, no, GIVE IT TO ME NOW! gets closer and closer. The craving builds on itself in a self-reinforcing feedback loop in the ventral (lower) regions of the prefrontal cortex. While efforts to control the craving activate the dorsal (upper) regions of the prefrontal cortex, trying their best to hold the feedback in check. What’s a poor brain to do?! Or in human terms, how do you slow down enough to choose tomorrow, and the day after tomorrow, instead of the few hours’ relief promised by the drug?

Research into the neuroscience of meditation often uses practiced meditators, or else they compare people following a course of meditation against those who’ve taken some other form of instruction (the control group). These people are placed in an fMRI scanner or other brain-imaging system, and their brain activity is recorded, either while they are meditating or while they are engaged in other activities (such as looking at pictures designed to induce empathy). It’s difficult to sum up this entire branch of research in a few sentences, and results are not always consistent. But one finding from several studies (here’s an example) is that meditation causes increased activation in the dACC and/or in the (left) dorsolateral prefrontal cortex—the exact regions that support insight, reflection, and long-range perspective.

So it looks like meditation builds muscle, so to speak, in brain regions that can win against impulsive (e.g., addictive) thoughts and actions. How can addicts, recovering or not, use this information to their advantage? I’m no expert on treatment and recovery. But maybe we can think of these insight-generating brain regions as muscles, that are weakened by excessive use (trying, trying, trying not to give in) and strengthened by meditation. Then meditate whenever you can! And do it even if you’re still using. In fact, do it especially if you’re still using, or if you’ve recently stopped. Try it for 5 or 10 minutes, if that’s as long as you can last, even if you’re still thinking about getting high later in the day. But do it the next day as well. And the day after that. You can learn how in twenty minutes. Or check out this link to a talk by Jon Kabat-Zinn. As I said, I’m no expert, but meditation really helped me in the weeks and months following my last relapse. A little bit of meditation, spread over days and weeks, can gradually shift the balance between brain systems that dance to the music of craving and those that turn down the volume.

In my last post I talked about the debate between the disease model and the choice model of addiction. I argued that you need to understand a bit about the brain in order to make sense of choice in the first place, and I reviewed some of the changes in the brain brought about by addiction — changes that make it more and more difficult to choose NOT to go after the thing (drugs, booze, Facebook, whatever) that you are addicted to. But now I want to go deeper into the issue of how we make choices. This seems so important to the topic of addiction, in general, and to the immediate question: how do you tell yourself NO?

A current article in NatureNews (a science publication for the general public) reviews some recent neuroscience experiments into the nature of free will. What is free will anyway? We generally assume that we make choices out of…well out of choice. We decide, we are the decider, we are the ones who choose what we do and what we don’t do. (In which case, addicts must be real idiots!) Yet neuroscience tells a different story. There are activation patterns in the brain that foreshadow what we are about to choose, seconds before we actually decide. In a new version of a classic experiment, Bode and colleagues (2011) asked participants to lie in an extremely powerful (fMRI, 7 Tesla) brain scanner. They were told to push a button on a joystick either on the left or the right, whenever they felt like it. Meanwhile, a stream of letters went by on a screen, changing every half-second. As soon as they pressed the button, recently displayed letters appeared in a new window. Now they were asked to select the letter they saw precisely when they had DECIDED whether to press the left or right button. The results? Activity in the left “frontopolar cortex” (at the very front of the prefrontal cortex) predicted what decision they were about to make, several seconds before they were aware of making the decision!

These results suggest that the moment of choice is not free at all. It is already determined by events in the brain. The debate between free will and “determinism” has gone on for years (in fact it started way back in the 18th century, with philosopher David Hume). But the science that shows us the nature of determinism has become more and more sophisticated. Now it is hard to refute the idea that choice is a moment in a stream of biological events. It is never entirely “free”.

Maybe this should not be surprising. After all, if our brains didn’t fall into a specific pattern before choosing whether to turn right or left, whether to have a cookie or an apple, whether to buy heroin or turn on the TV, then where would the decision come from? It has to come from our brain — from our very own brain, with all its cravings and preferences — or else where would it come from? It wouldn’t be ours if it didn’t come from our brain. And brains take time to do things. So it may not be so weird to think that changes in brain activity precede the moment when we are aware of making a choice.

If you follow that argument, then the difference between deliberate choice and addictive (compulsive) choice isn’t easy to pinpoint. In which case, what should we do about our tendency to make addictive choices? Just sit back, give up responsibility, and take the consequences? No, there’s a better answer! The closest thing to free choice, says emotion theorist Nico Frijda, is to insert moments of reflection into the stream of impulses going on behind the scenes. Our brains include the machinery to reflect, as well as the machinery to act impulsively, and brain changes preceding moments of choice can call upon both. If you relax, sit back for a moment, even meditate a bit, the short-term gains of addictive behaviour start to pale next to the long-term gains of getting and staying abstinent. Yes, it’s all happening in your brain before “you” make the choice, but you can guide your brain into activation patterns that are not ruled by habit and compulsion. And the more often you do it, the easier it gets.

There may not be such a thing as pure free will. But I like to think that choices are moments in a river of brain activity that can be altered by reflection and foresight. Or as William James said, “My first act of free will shall be to believe in free will.”

Tomorrow, for my last publicity event in Toronto, I’m giving a talk at a Harm Reduction group. I don’t know that much about harm reduction as a philosophy or practice. I do know that I like the idea that there are many and varied paths to recovery, or maintenance, or whatever you want to call a relatively harm-free solution to addiction. I also recently found out that the Harm Reduction folks don’t even like the word addict. I think I get their point. The tension here seems to resolve to the ongoing debate, both in science and in clinical practice, about whether addiction is a disease or a choice. Here’s what I think.

It’s a false dichotomy. Addiction is not a disease like cancer or diabetes. No way. It’s hard to get rid of, which makes it like a disease, but that’s really just an analogy. The resemblance stops there.You can’t catch it. It’s not communicable. And you can’t cure it according to some specific formula. This idea is very much at odds with the pronouncements of the American Society of Addiction Medicine, the high church of addiction, as it were.  So is addiction a choice, is it just bad behaviour, is it the result of a genetic predisposition to self-indulgence or a low tolerance to psychological pain? All of these other definitions fall short as well. Addiction has an incredibly powerful, self-propelling momentum that takes it beyond the realm of “normal” choice or “normal” bad behaviour. If addiction is neither a choice nor a disease, then the choice vs. disease dichotomy is useless. It creates havoc and argument, it’s confusing, and it takes our minds off the more important issue. Such as: What is addiction really?

The disease camp assumes that the brain is important for understanding addiction. Addiction, they claim, is a brain disease. But the choice people paint themselves into the opposite corner. They claim that the brain is not important for understanding addiction. Rather we need to understand how difficult circumstances — trauma, rejection, economic hardship, and so on — affect substance-taking behaviour. What’s that got to do with the brain?

It’s got everything to do with it! Choices are not some magical puff of our spirit selves. Choices come from the brain. And the choice to take drugs, or booze, or cigarettes, again and again, comes from a brain that has been altered by a series of similar choices in the past. It just takes a moment of reflection to realize that choices are rarely “free”. And while philosophers debate the very existence of free will, we can be much more practical about it. Choices involve an exchange between the part of your brain that wants something (the ventral striatum and related areas) and the part of your brain that thinks about consequences and directs behaviour accordingly (dorsal and lateral regions of the prefrontal cortex). That exchange takes place in the synapses (connections) that join these regions. And those connections are altered by so many aspects of experience: hardship, success, self-image, trauma, and very clearly by the spiralling of wanting and relief that results from substance-taking itself. No two people have the same brain to work with, but there are features of addicts’ brains that neuroscientists can describe in detail: high levels of dopamine continue to strengthen the feelings of craving that spring from the striatum, while the satisfaction of those pernicious goals continue to reinforce the circuits that give substances their meaning and value. And the regions responsible for self-control are themselves weakened by excessive demands for impulse control. So their connections to the regions of craving shrivel because they’ve lost their potency.

Understanding the brain is essential for making sense of the kinds of choices that addicts repeatedly make. But that doesn’t make addiction a brain disease. It makes it an aspect of the biology of being a sensitive human being in an often difficult world.

People have asked me how I feel about the Insite issue. Insite is a clinic in downtown Vancouver that provides a safe environment for junkies to shoot (their own) dope. The Supreme Court of Canada just overruled Harper’s attempt to shut it down. Did they do the right thing? Should we make it easier or harder for junkies to shoot up safely?

Easier is right. When opportunities are present, addicts will take them. And Vancouver is full of heroin. The brains of hungry animals can guide our thinking here. When a starving animal holds any hope of finding food, its brain shifts from a balanced stew of neuromodulators to a dopamine-spiked frenzy. Chemicals like acetylcholine, which usually plays a big part in alertness and action, are shut off at the tap when dopamine takes over. Gouts of dopamine spurt into the ventral striatum, so that all of the animal’s goal-seeking behaviour is directed at one goal only: and that’s food. It’s the same for junkies. When they are in need, there is only one goal anywhere of any value worth pursuing. Need more. Get some. Want it now.

So whether you get a clean needle or a used one just doesn’t occupy much space. Sure, it’s better to be safe, to take no chances, but you’ve taken so many chances in your life, and you’re still here, you’re still in one piece. So one more chance is no big deal. And really, for those minutes and hours between now and the next hit, its importance pales beside the real goal.

I know. I’ve been there. I once found myself in a room with four or five  junkies in downtown Oakland. I was scared. This was the ghetto. I wasn’t even physically addicted at that time. I didn’t know if they were going to include me or knife me, so when one guy offered me the cotton (the leftover heroin at the bottom of the spoon), I said I’d take it.  And I could see that the guy’s eyes were yellow–a common symptom of hepatitis. That’s what kills me when I look back on it. Yet I did it anyway. I was young and stupid. I’d like to think that, a year or two later, I wouldn’t have taken such a chance. But that would depend on how badly I wanted it.

If you can make it so that no heroin is available in Vancouver or its surrounds, then do it Mr. Harper. Otherwise, the Supreme Court did the right thing.