Addiction and Free Choice

Nora Volkow, in the first two sentences of this post, provides more clarity than I think I’ve every seen on the matter of choice and the brain disease of addiction:alg-model-brain-jpg

Choices do not happen without a brain—it is the mechanism of choice. The quality of a person’s choices depends on the health of that mechanism. However much we may wish that a person’s choices were free in all instances, it is simply a fact that an addicted person’s failures in the realm of choice are the product of a brain that has become greatly compromised—it is readily apparent when we scan their brains. Even if taking a drug for the first time is a “free” choice, the progression of brain changes that occurs after that involves the weakening of circuits in the prefrontal cortex and elsewhere that are necessary for exerting self-control and resisting the temptations of drug use. Once addiction takes hold, there is greatly diminished capacity, on one’s own, to stop using. This is why psychiatry recognizes addiction as a disease of the brain, and why professional intervention is needed to treat it in most instances.

via Nora’s Blog Addiction and Free Choice | National Institute on Drug Abuse (NIDA).

More on choice and addiction

why oh why by larryosan
why oh why by larryosan

From Kevin McCauley:

The argument against calling addiction a disease centers on the nature of free will. This argument, which I will refer to as the Choice Argument, considers addiction to be a choice: the addict had the choice to start using drugs. Real diseases, on the other hand, are not choices: the diabetic did not have the choice to get diabetes. The Choice Argument posits that the addict can stop using drugs at any time if properly coerced.

As evidence, the Choice Argument offers this scenario: a syringe of drugs is placed in front of an intravenous drug addict and the offer is made to “Spike up!” When the addict picks up the needle and bares his arm, a gun is placed to his temple and the qualifier is added that if the addict injects the drug his brains will be blown out. Most addicts given this choice can summon the free will to choose not to use drugs. The Choice Argument claims this proves that addiction is not a disease. But in real diseases – diabetes, for instance- a gun to the head will not help because free will plays no part in the disease process. So the Choice Argument draws a distinction between behaviors – which are always choices – and diseases.

This is a powerful argument. It is also wrong.

While it is true that a gun to the head can get the addict to chose not to use drugs, the addict is still craving. The addict does not have the choice not to crave. If all you do is measure addiction by the behavior of the addict – using, not using – you miss the most important part of addiction: the patient’s suffering. The Choice Argument falls into the trap of Behavioral Solipsism.

Just as a defect in the bone can be a fracture and a defect in the pancreas can lead to diabetes, a defect in the brain leads to changes in behavior. In attempting to separate behaviors (which are always choices) from symptoms (the result of a disease process), the Choice Argument ignores almost all of the findings of neurology. Defects in the brain can cause brain processes to falter. Free will is not an all or nothing thing. It fluctuates under survival stress.

Hat tip: Matt Statman


NA gives its members opioids?

Marc Lewis discusses an important role of endogenous opioids.

Some very prominent emotion scientists have theorized that opioids (made inside our brains) are at the root of human attachment. Mother’s milk is rich with opioid molecules. In other words, nature found a surefire way to soothe the baby with its mother’s milk, using the same chemical formula that’s responsible for the soothing feeling of heroin. Jaak Panksepp theorizes that all social attachment is based on the release of opioids within the brain.

Then about research finding endogenous opioid production may be activated by had holding.

The brain regions that got calmed down by hand-holding (including regions of the ventral ACC, ventral prefrontal cortex, striatum, and insula) are the same brain regions that have a high density of opioid receptors! The authors speculate (and I think it’s very likely) that opioid release is what causes the deactivation of these emotional hot spots. The subjects also reported less unpleasantness when they were holding hands while anticipating the shock. And, get this, the reduction in unpleasantness was correlated with the reduction in brain activity in these hot spots.

Then he suggests these findings may explain some benefits of 12 step meetings.

In a recent debate on this blog, I argued that a supportive group like NA makes sense as a primary treatment for addiction–not a secondary one. Certainly members of NA or AA see their group experience — with or without hand-holding — to be the most powerful antidote to their feelings of anxiety, stress, loneliness, and all the other negative variants that can lead to relapse. Now we can point to a very concrete, biological mechanism responsible for the soothing function of the group: when you are in close contact with people who care about you (even a little), your own brain releases opioids. And, in a sense, those opioids replace the opioids you’d otherwise be buying on the street.

This begs a question about medications that interfere with pleasure responses to drugs and alcohol.  Do these meds also interfere with endogenous opioid responses? I had a friend who was going research on it nearly 20 years ago. He told me that he was frequently approached after presentations by people who were on the drug and reported weird effects like no longer liking cheesecake.

I found one study on the issue and it found no adverse effects, however is was funded by the manufacturer of the drug. It’s worth noting that researchers use naltrexone to “disrupt opioid neurotransmission in mouse pups and their attachment relationships with the mother.”

So…might this medication, and others like it, interfere with the benefits of 12 step groups? It seems like a question worth asking.

Response to Why Addiction is NOT a Brain Disease

English: Magnetic resonance imaging (MRI) of t...

In a thoughtful post, Marc Lewis questions the disease model of addiction.

He doesn’t dismiss it out of hand. He seems to look for ways in which it’s right and useful.

It’s accurate in some ways. It accounts for the neurobiology of addiction better than the “choice” model and other contenders. It explains the helplessness addicts feel: they are in the grip of a disease, and so they can’t get better by themselves. It also helps alleviate guilt, shame, and blame, and it gets people on track to seek treatment. Moreover, addiction is indeed like a disease, and a good metaphor and a good model may not be so different.

He offers two objections.

Spontaneous Recovery

First the existence of spontaneous recovery:

What it doesn’t explain is spontaneous recovery. True, you get spontaneous recovery with medical diseases…but not very often, especially with serious ones. Yet many if not most addicts get better by themselves, without medically prescribed treatment, without going to AA or NA, and often after leaving inadequate treatment programs and getting more creative with their personal issues.

My first reaction is that we’re not very good at distinguishing misuse, dependence and addiction. These studies include people who met diagnostic criteria for alcohol dependence in college and reduced their use as they moved into other stages of life. The other frequently cited group are heroin dependent Vietnam vets. Again, it’s important to distinguish between dependence and addiction.

So, I think, the problem is not the disease model, but rather, our diagnostic categories and their application. I suspect that if those studies finding high rates of natural recovery limited subjects to those with true loss of control (addiction), the prevalence of spontaneous remission would drop dramatically.

Further, I’m not sure this this is a strong argument at all. Wouldn’t this exclude hundreds of viral and bacterial diseases? These are generally acute illnesses, but don’t other diseases have acute and chronic forms?

Dopamine responses are normal

His second objection is that addiction uses natural brain mechanisms that are shared by many other life experiences.

According to a standard undergraduate text: “Although we tend to think of regions of the brain as having fixed functions, the brain is plastic: neural tissue has the capacity to adapt to the world by changing how its functions are organized…the connections among neurons in a given functional system are constantly changing in response to experience (Kolb, B., & Whishaw, I.Q. [2011] An introduction to brain and behaviour. New York: Worth). To get a bit more specific, every experience that has potent emotional content changes the NAC and its uptake of dopamine. Yet we wouldn’t want to call the excitement you get from the love of your life, or your fifth visit to Paris, a disease.

I have a couple of thoughts about this. First, lots of diseases are characterized by natural body processes turning against the body, many cancers for example. Second, when we’re talking about addiction, we’re not talking about one brain mechanism. (He focused on dopamine release.)

Several brain mechanisms have been identified and, I suspect, better understandings of these will lead to better typologies for AOD problems. Some people may have only one or two of these neurobiological factors, while others have ten.  Some factors may be associated with a more chronic form, others may be associated with a more severe loss of control and overall severity may be associated with the number of factors the person has. (Also, some might be primary to addiction, others secondary.)

What is a disease, anyway?

I think the biggest barrier to responding is that the writer did not offer a definition or boundaries for understanding “disease.” Merriam-Webster offers this definition:

a condition of the living animal or plant body or of one of its parts that impairs normal functioning and is typically manifested by distinguishing signs and symptoms

WebMD offers Stedman’s Medical Dictionary’s definition as:

A morbid entity ordinarily characterized by two or more of the following criteria: recognized etiologic agent(s), identifiable group of signs and symptoms, or consistent anatomic alterations.

Is the writer arguing that addiction does not meet these definition? I’m having a hard time seeing how. And, why does the idea of classifying addiction as a disease bother people so much?


Methadone’s cognitive effects


English: Methadone structure, animation
English: Methadone structure, animation (Photo credit: Wikipedia)

Another study on methadone’s cognitive effects:

In one study, on the day after the last exposure to methadone, there was a significant reduction (around 70 per cent) in the level of a signal molecule which is important in learning and memory, in both the hippocampus and in the frontal area of the brain. This reduction supports findings from a previous study (Andersen et al., 2011) where impaired attention in rats was found at the same time. At this time, methadone is no longer present in the brain. This indicates that methadone can lead to cellular changes that affect cognitive functioning after the drug has left the body, which may be cause for concern.

The study was done on rats, not people, but it’s findings aren’t isolated.

Patients and their loved ones may decide that the potential benefits outweigh the costs, but they should be made aware of the costs and know the alternatives.

Revenge and the reward system

A chimpanzee brain at the Science Museum London
(Photo credit: Wikipedia)

I’ve often wondered about all of AA’s emphasis on resentment and whether research will end up provide an evidence-base for all the attention it receives in the steps, literature and discussion.

I found this, from a recent episode of On Being, very interesting:

Mr. McCullough: And if you look at the brain of somebody who has just been harmed by someone, right, they’ve been ridiculed or harassed or insulted — we can put those people into technology that allows us to see what their brains are doing, right? So we can look at sort of what your brain looks like on revenge. It looks exactly like the brain of somebody who is thirsty and is just about to get a sweet drink to drink or somebody who’s hungry who’s about to get a piece of chocolate to eat.

Ms. Tippett: It’s like the satisfaction of a craving?

Mr. McCullough: It is exactly like that. It is literally a craving. What you see is high activation in the brain’s reward system. So, the desire for revenge does not come from some sick, dark part of how our minds operate. It is a craving to solve a problem and accomplish a goal.

Emotional pain without context

MRI coronal view of the hippocampus
MRI coronal view of the hippocampus (Photo credit: Wikipedia)

Siddhartha Mukherjee provides a brief history of the serotonin hypothesis of depression, its demise and why dismissing serotonin may be an “overcorrection.”

Part of this story is an emerging theory of depression:

A remarkable and novel theory for depression emerges from these studies. Perhaps some forms of depression occur when a stimulus — genetics, environment or stress — causes the death of nerve cells in the hippocampus. In the nondepressed brain, circuits of nerve cells in the hippocampus may send signals to the subcallosal cingulate to regulate mood. The cingulate then integrates these signals and relays them to the more conscious parts of the brain, thereby allowing us to register our own moods or act on them. In the depressed brain, nerve death in the hippocampus disrupts these signals — with some turned off and others turned on — and they are ultimately registered consciously as grief and anxiety. “Depression is emotional pain without context,” Mayberg said. In a nondepressed brain, she said, “you need the hippocampus to help put a situation with an emotional component into context” — to tell our conscious brain, for instance, that the loss of love should be experienced as sorrow or the loss of a job as anxiety. But when the hippocampus malfunctions, perhaps emotional pain can be generated and amplified out of context — like Wurtzel’s computer program of negativity that keeps running without provocation. The “flaw in love” then becomes autonomous and self-fulfilling.

He proposes an alternative understanding of the role serotonin may play:

An antidepressant like Paxil or Prozac, these new studies suggest, is most likely not acting as a passive signal-strengthener. It does not, as previously suspected, simply increase serotonin or send more current down a brain’s mood-maintaining wire. Rather, it appears to change the wiring itself. Neurochemicals like serotonin still remain central to this new theory of depression, but they function differently: as dynamic factors that make nerves grow, perhaps forming new circuits.

This still doesn’t explain the variation in responses to psychotropics. He acknowledges as much and alludes to the need for new typologies of depression. (Remember the dark ages when we talked about endogenous vs. exogenous depressions?)

The layers of speculation can obscure or illuminate just how crude our understandings of depression and the brain are. This, along with the history of psychiatric fads and abuses, makes one wonder if we should proceed a little more cautiously and work a little harder to capitalize on non-pharmacological tools like exercise and social support.

How Exercise Can Prime the Brain for Addiction


This makes sense, but is a weird thing to think about. Drug addiction may be more difficult to kick if it became habitual while exercise if part of your routine:


It does indicate that shedding an addiction acquired when a person has been exercising could be extra challenging, he says.

“But, really, what the study shows,” he continues, “is how profoundly exercise affects learning.”

When the brains of the mice were examined, he points out, the runners had about twice as many new brain cells as the animals that had remained sedentary, a finding confirmed by earlier studies. These cells were centered in each animal’s hippocampus, a portion of the brain critical for associative learning, or the ability to associate a new thought with its context.

So, the researchers propose, the animals that had been running before they were introduced to cocaine had a plentiful supply of new brain cells primed to learn. And what they learned was to crave the drug. Consequently, they had much more difficulty forgetting what they’d learned and moving on from their addiction.

That same mechanism appeared to benefit animals that had started running after becoming addicted. Their new brain cells helped them to rapidly learn to stop associating drug and place, once the cocaine was taken away, and start adjusting to sobriety.

“Fundamentally, the results are encouraging,” Dr. Rhodes says. They show that by doubling the production of robust, young neurons, “exercise improves associative learning.”

But the findings also underscore that these new cells are indiscriminate and don’t care what you learn. They will amplify the process, whether you’re memorizing Shakespeare or growing dependent on nicotine.


Top Posts of 2011 #4 – Acquiring addiction?

download (2)Nora Volkow suggests that it is possible to acquire cocaine addiction from a combination of stress and exposure to cocaine:

Dr. Nora Volkow, director of the National Institute on Drug Abuse, has shown in several brain-imaging studies that people addicted to such drugs as cocaine, heroin and alcohol have fewer dopamine receptors in the brain’s reward pathways than nonaddicts. Dopamine is a neurotransmitter critical to the experience of pleasure and desire, and sends a signal to the brain: Pay attention, this is important.

When Dr. Volkow compared the responses of addicts and normal controls with an infusion of a stimulant, she discovered that controls with high numbers of D2 receptors, a subtype of dopamine receptors, found it aversive, while addicts with low receptor levels found it pleasurable.

This finding and others like it suggest that drug addicts may have blunted reward systems in the brain, and that for them everyday pleasures don’t come close to the powerful reward of drugs. There is some intriguing evidence that there is an increase in D2 receptors in addicts who abstain from drugs, though we don’t yet know if they fully normalize with time.

But people are not brains in a jar; we are heavily influenced by our environments, too. The world in which Ms. Winehouse traveled appears to have been awash in illicit drugs and alcohol whose use was not just accepted but encouraged. Even people who aren’t wired for addiction can become dependent on drugs and alcohol if they are constantly exposed to them, studies have found.

Drug use changes the brain. Primates that aren’t predisposed to addiction will become compulsive users of cocaine as the number of D2 receptors declines in their brains, Dr. Volkow noted. And one way to produce such a decline, she has found, is to place the animals in stressful social situations.

A stressful environment in which there is ready access to drugs can trump a low genetic risk of addiction in these animals. The same may be true for humans, too. And that’s a notion many find hard to believe: Just about anyone, regardless of baseline genetic risk, can become an addict under the right circumstances.