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Addiction

The Myth and Reality of Free Will: The Case of Addiction

How addiction robs us of free will, and how to outwit it.

The tragic death of the enormously talented actor Philip Seymour Hoffman from a drug overdose has gotten a lot of people talking about drugs and addiction. Russell Brand claims that Philip Seymour Hoffman is another victim of extremely stupid drug laws. A blogger argues that a single drink led to his untimely death by heroin.

Still another blogger draws even more sweeping conclusions that should make you sit up and take notice: Phillip Seymour Hoffman did not have choice or free will and neither do you.

Do any of us have free will when it comes to addictive substances, or do they have the power to enslave us? Is the addict to be punished, pitied, or rescued? You probably have strong opinions about this question. And so, I've decided to devote this blog post to the actual workings of addiction--how it works, what it means about human choice and free will, and how to outwit it.

Answer this question

What do all addictive substances and activities have in common?

A. They are all illegal

B. They all hyper-stimulate the dopaminergic (reward) system of the brain

C. They all eventually result in neural damage

D. B and C

The answer is D—they all hyper-stimulate the brain's reward system, eventually resulting in neural damage.

The brain’s reward circuitry consists of clusters of neurons that release the neurotransmitter dopamine. They are particularly numerous in the prefrontal cortex, and certain areas of the midbrain. Any activity we find pleasurable (from eating to sex to hearing our favorite music to seeing an attractive face to drinking coffee) activates these circuits.

The function of this reward circuitry is to enable us to remember the circumstances that led to the pleasure so we can repeat the behavior and re-experience the pleasure it brought us. Our reward circuitry is vital to our ability to learn. It is what motivates us to get up in the morning and begin another day.

Addiction is nothing more and nothing less than a high-jacking of this normal reward circuitry, a high-jacking that can eventually rob people of their free will to choose. Duke University professors of pharmacology Wilkie Wilson and Cynthia Kuhn eloquently summarize addiction this way it this way:

So addiction is far more than seeking pleasure by choice. Nor is it just the willingness to avoid withdrawal symptoms. It is a hijacking of the brain circuitry that controls behavior so that the addict’s behavior is fully directed to drug seeking and use. With repeated drug use, the reward system of the brain becomes subservient to the need for the drug.

This high-jacking occurs for three reasons. First, some substances put this reward system into overdrive, causing release of dopamine (and other neurotransmitters) at levels several times higher than the brain is designed to handle. Second, some people are particularly sensitive to the effects of these drugs, causing them to become enslaved to them in ways that others have difficulty understanding. Third, in attempting right itself, the brain becomes acutely tuned to environmental stimuli that end up feeding the addiction.

A simple but powerful model of addiction.

If electrodes are implanted in the reward circuitry of a rat's brain, and the rat can stimulate this circuitry by pressing on a bar in his cage, he will do so thousands times per hour for days on end. He will forget to eat, forget to drink, ignore opportunities to mate. He will do nothing but press the bar relentlessly until he finally collapses in exhaustion. And eventually, he exhausts himself to death, unless the experimenter intervenes and removes the rat from that environment. And most importantly, he will do the same thing if pressing the bar delivers a dose of nicotine, cocaine, or other addictive substance.

At a neurological level, this is what is happening: Like the electrodes implanted in the rat's brain, drugs stimulate the brain's reward system at a level far greater than the brain can handle, although they do it different ways. Cocaine and amphetamines block chemicals that normally remove dopamine from synapses after the neuron has been activated, thereby prolonging the stimulation of dopamine receptors. Alcohol triggers a surge of dopamine release.

Nicotine triggers dopamine release (and binds to nicotine receptors in the brain), while ecstasy stimulates the release of both dopamine and serotonin. Marijuana, opiates (like heroin, morphine, oxycodone) trigger dopamine release, and active ingredients bind to endorphin-like receptors in the brain.

The short term result of tweeking the brain's reward circuitry is intensifying and prolonging the experience of intense pleasure. You feel relaxed, buzzed, euphoric, pain-free—whatever your drug of choice causes you to feel.

But what if one "keeps the pedal to the metal"—over-stimulating dopamine receptors by continued over-use of these powerful drugs? Well, your brain doesn't take that sitting down, so to speak. It fights back. And it does so in two ways.

Adaptation #1: Destroy the machinery

Over-stimulation of dopamine receptors damages or destroys them. So the brain adapts to the overwhelming surges in dopamine by producing less dopamine or by reducing the number of dopamine receptors in the reward circuit. This means that dopamine does not exert as great an impact on the reward circuit, which in turn means that the drug addict does not get the same high from his or her usual dose.

The decrease compels addicts to increase the dose in order to attempt to bring their dopamine function back to normal or to achieve the same “high”. Eventually, the circuitry "burns out". At that point, the user no longer gets pleasure from the drug or from things that he or she used to enjoy. Instead, they feel dead, and need the drug simply to feel anything at all.

Rats can't tell us what it feels like to lose the ability to feel pleasure, to become enslaved to a miniscule dose of powder or ampule of liquid. But humans can. In his Salon.com article, blogger Seth Mnookin describes how he coasted to an Ivy League degree as a drug addict, but forever damaged the bond between mother and son.

In November of sophomore year, something snapped. I would smoke pot, and five minutes later need to smoke again. I would drink, but as Tennessee Williams so accurately described it in 'Cat on a Hot Tin Roof,' I never got the click. So, at 19, I checked into an inpatient drug detox and rehab program at McLean’s Hospital in Belmont.

And that began the revolving door of falling into the abyss of addiction, drying out in rehab, and falling into the abyss again. The emotional toll is exacted not just on the user but on anyone who loves him as well.

…my mother sat down across from me in yet another well-meaning doctor’s office in a yet another institution. She adjusted her gray glasses, played with her hands and said: "This is it. Either you go to long-term treatment, or we are going to have to cut ourselves off. I will always love you," she said. "But I will not watch you kill yourself, and I will not let you do this to my family."

Adaptation #2: Learn the cues

Why do addicts tend to relapse after leaving rehab? The answer lies in Pavlov's dogs.

The function of classical conditioning is to learn what signals what and to prepare for it. Pavlov's dogs learned that the bell signaled food and their mouths salivated in anticipation of their meal.

According to the opponent process theory of drug dependency, the brain learns to compensate for the upcoming stress of drug intake when there are environmental cues that are reliably associated with the stress. It does this by producing a response that is the opposite of the drug's effect. If the drug lowers blood pressure and pain sensitivity, then the brain temporarily raises them when the cues associated with drug use are present. So when the addict who shoots up using his usual equipment (e.g., syringe and tourniquet, mirror, rolled up $100 bill) in the same (or same kind of ) place (e.g., a bathroom, bar, bedroom), the brain triggers compensatory physical responses that blunt the effect of the drug. This is your brain's way of trying to keep the body in homeostasis. The addict tries to overcome this blunting effect but increasing the drug dose. This is called drug tolerance—it takes more to get the same kick.

But what if the addict takes the increased dose in an unfamiliar environment where the usual cues are not present? The brain does not trigger the opposite physical responses in anticipation of the hit. And so the addict gets the full brunt of the higher dose. We call that overdose. And it can be fatal. When drug addicts overdose, they typically have not taken more than their usual dose. In one study, 70 percent of heroin addicts receiving emergency treatment for overdoses had not taken more than their customary dose, but they had shot up in unfamiliar surroundings.

What if the cues are present—the mirror, the $100 bill, the syringe, the drug buddies—but the addict does not take the hit? Then he experiences the full brunt of the body's compensatory states (e.g., rise in blood pressure, shakes, increased sensitivity to painful stimuli). We call those drug cravings.

Former addicts were found to display physiological signs of narcotic withdrawal months or even years after kicking their habit when they were asked to perform their drug "cooking up" procedure while their vital signs were monitored and while they watched a videotape of heroin preparation. These former addicts also reported intense cravings while watching the film. Former alcoholics report intense cravings and evidence withdrawal symptoms when they enter bars.

The upshot is that it is much easier to get clean when the addict is removed from their usual drug-taking environments. The cues aren't there, so the cravings subside. But when they return to their old environments, the cues are there, the cravings return full force, and they succumb. We call that relapse.

We are not all alike

The effects of drugs and environmental cues are the facts that apply to all of us. But we are not all alike, and this is certainly true when it comes to drugs and addiction. There are different types of dopamine receptors, and they exist in different ratios among individuals. The upshot is that some individuals are more sensitive to the effects of dopamine, which cashes out in terms of different degrees of risk for addiction. Some people are born with fewer dopamine receptors, which renders them more prone to addictions because they cannot sense normal amounts of dopamine and consequently take larger amounts of drugs in order to feel their effects.

These differences are due to genetic variability. Non-smokers are more likely than smokers to carry a protective gene, CYP2A6, which causes them to feel more nausea and dizziness from smoking. So they avoid cigarettes, which prevents repeated exposure to nicotine. Alcoholism is rare in people with two copies of the ALDH-2 gene variation, and a variant in the dopamine receptor gene DRD2 is more common in people addicted to alcohol or cocaine. In 2008, Peking University researchers Chuan-Yun Li, Xizeng Mao, and Liping We published a meta-analysis of over 2,000 medical papers published from 1976 to 2006 linking genes and addiction. They identified 1,500 human addition-related genes, and five pathways shared by cocaine, alcohol, opioids, and smoking. In other words, people with certain gene variants are prone to addiction to those four substances.

Are you one of them?

So what should you do with all of this information? First, realize that using substances like cocaine and heroin is like playing Russian roulette: The chances of a fatal payoff in the long-run is pretty high. Second, if you are using, pay close attention to environmental cues that your brain may have linked to drug use. If those cues are not there, your risk of overdose—even at your usual dose—is higher. Third, assess whether you are at risk for addiction due to your genetic make-up. Looking at family members may offer a clue, but common environmental factors (like growing up in an environment where drug use is common) makes this source of information not entirely reliable. It is possible to have genetic testing done to discover whether you have the genes that put you at risk.

But a more practical approach is to carefully observe your own response and that of others to legal drugs like alcohol or cigarettes. A person's initial response to a drug is a clue to predicting whether that person is likely to become addicted. According to Vanderbilt University neuroscientist David Zald (p. 20)

If you give people low doses of amphetamine, you find that some people get very happy, energized, even euphoric. But some say they feel nothing. And others actually find it rather unpleasant; they get anxious, irritable, or even dysphoric.

You can see this among your friends and acquaintances at parties where alcohol is served. There are those who can knock back a few beers, and are content for the evening. But then there are those who look at alcohol the way a starving person looks at a cheeseburger, and the very idea of leaving a half empty bottle of liquor on the table is incomprehensible.

Those are the clues that the person is at risk of losing his autonomy, his free will, and even his very life, to the power of addiction. This is where exercising that free will becomes crucial--before an addictive substance gains traction in the at-risk person, turning him or her into a rat whose sole intent is pressing the bar for that next hit.

And because art can sometimes bring home a message more powerfully than scientific facts, I'll close with this powerful dance about addiction.

More about the opponent process theory of addiction can be found in Chapter 7 of my book The Other Side of Psychology: How Experimental Psychologist Find Out About the Way We Think and Act.

Copyright Dr. Denise Cummins February 9,2014

Dr. Cummins is a research psychologist, a Fellow of the Association for Psychological Science, and the author of Good Thinking: Seven Powerful Ideas That Influence the Way We Think.

More information about me can be found on my homepage.

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