October 14th, 2012
Quitting smoking is hard, but that suggestion probably isn’t terribly exciting all on its own since most of our readers probably knew it already. Still, while we’ve talked about quitting smoking using nicotine replacement and medication, we haven’t really touched the subject of all those people out there who just decide to give quitting smoking a try one day without those patches, gums, or pills.
Since something like 95% of those who try their hand at quitting smoking relapse within one year, and most of these people try to quit unaided, I think this is an important topic to touch on. Fortunately, recent research conducted in the U.K. tried to assess the personality and cognitive aspects that end up predicting who will succeed, or fail, in their quit attempt.
The effects of expectation, motivation, and impulsivity when quitting smoking
Quite a bit of research has already shown that when smokers are trying to quit (so we’re talking early on during abstinence), their brains react differently to stimuli in the environment depending on the relationship between those stimuli and nicotine. Stimuli that aren’t associated with smoking (or some other form of nicotine intake) get less attention and show overall less activation of important brain circuits while nicotine associated cues light up the brain just as if nicotine was on board (even though participants were drug free at the time). Essentially, if a stimulus predicts getting a hit, the brain gets smokers to pay attention to it so that they can do whatever is necessary and get a little drug in. Throw in some of that reduced ability to control behavior that we talk about so much (like impulsivity), and which is common not only in smokers but in users of almost every other drug (heroin might be the exception) and you have a recipe for disaster, or at least for a good bit of smoking relapse. And yet if we want to fight the horrible health consequences of cigarettes, then quitting smoking has to be made easier, which nicotine replacement and medications like bupropion have done to some extent.
As part of this equation, knowing the specific predictors of early relapse in people who are quitting smoking may be useful so that professionals planning smoking interventions can do a better job of targeting the most important factors. The study recently published the journal Psychopharmacology tried to assess the relationship between the severity of smoking, the above-mentioned personality factors, and the success of the quitting attempt.
The cool thing about this study is that the 141 people who participated were assessed on a whole set of these cognitive tests twice – once after a smoking free night and a nicotine lozenge and another time after a smoking free night followed by a nicotine-free lozenge. While they couldn’t tell which was which, the procedure gave the researchers an assessment off how different participants’ reactions were with or without nicotine on board. Following the assessments participants were directed to begin their attempt at quitting smoking. While they were asked not to use nicotine replacement options or other medications, they were allowed to use any other resource available and were given a set of information pamphlets that explained expected side effects and likely difficulties during the quit attempt. They were then followed up after 1 week, 1 month, and 3 months. Quitting was identified as minimal smoking (less than 2 cigarettes per week) and was verified both by self report and cotinine testing. There was a small financial incentive to quitting, with people who relapsed after a week getting only £40 (about $60) and those who made it through month 3 getting £150 (about $250), though I’m pretty sure that if $200 was enough to make people quit we’d have just paid up already…
The first thing to note in the results was that 24% of the participants were still not smoking at the 33 month followup. This seems to be about on par with the usually low success rates at 1 year though I’m sure this research group will try to continue following these participants at least up to the 1 year mark and hopefully produce another paper.
The overall most reliable predictor of who quit and who relapsed ended up being the level of nicotine dependence as measured by the participants’ pre-quit attempt cotinine levels and the number of cigarettes they smoked every day. Since cotinine assessments are less biased, it was the most predictive of all throughout the experiment (# of daily cigarettes was no longer predictive at 3 months). Interestingly, self reported impulsivity and smokers’ initial ratings of cravings for cigarettes didn’t end up predicting relapse at all, but those cognitive tests assessing the quitters’ reactions to nicotine associated cues told a pretty interesting story: It seems that early on during their quitting attempt smokers who had more general interference with their cognitive function relapsed sooner. These cognitive problems can be thought of as interfering with normal thinking by nicotine-related cues and maybe even more general interference with brain function. After the 1-week follow-up, at the 1 and 3 month assessment, the odds of quitting had more to do with baseline assessments of motor impulsivity as well as those initial cotinine levels assessing the degree of nicotine dependence.
The take-home: Quitting smoking is hard for different reasons in the first week and later on
If you’ve ever tried to quit you’ve been told you that the first week is the hardest and that once you make it through that the rest is a piece of cake. While this research doesn’t necessarily support that notion, since about 25% of the sample relapsed between each of the followups, it does seem to indicate that the reasons for relapse change after that first week.
It seems that the first week may be difficult because of general cognitive interference by stimuli and cues that are nicotine associated. Those cues make it hard to pay attention to much else and they interfere with normal thinking and attention process, making sticking to the quit attempt difficult. After that point, successfully quitting smoking seems to be associated more with the level of initial smoking and that damn motor impulsivity test. The finding that heavier smokers have a harder time quitting isn’t new and isn’t surprising, but the fact that cognitive effects and predictors of relapse change does suggest that the interventions likely to help smokers quit may need to be different during week 1 and afterward.
Overall, these findings suggest that the cognitive function problems associated with quitting smoking (or smoking in general) may recover faster than do some of the other physiological factors associated with quitting since the initial levels of smoking continued to be highly predictive throughout the 3 month period of followup. Another explanation could be that initial smoking levels affected brain function in ways not assessed by these researchers.
Since so many smokers relapse within the first week (more than 50%), it seems to me that interventions that really focus on the cognitive interference and the extreme attention towards nicotine associated cues and stimuli would be helpful for those quitting smoking. Maybe if we can reduce relapse numbers at 1 week we can have a more gradual fall-off for the following month resulting in significantly higher quit rates.
Interestingly, NIDA and other research organizations are getting really interested in the use of technologies like virtual reality for help in addiction training. It seems that in this context, these sorts of treatments might be useful in helping early quitters train to avoid that cognitive interference. Additionally, medications like modafinil, and maybe even other ADHD medication could be used very early on for those quitting smoking to help recover some of their ability to control their attention thereby reducing the power nicotine associated stimuli have over them. I guess we’ll have to wait and see as those who develop interventions start integrating this research. In the meantime, I’d love to hear from readers who have quit or tried to quit: Does this research seem to support your own experiences?
Jane Powell, Lynne Dawkins, Robert West, John Powell and Alan Pickering (2010). Relapse to smoking during unaided cessation: clinical, cognitive and motivational predictors, Psychopharmacology.
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The first thing to note in the results was the 24% of the participants were still not smoking at the 33 month followup. This seems to be about on track for the normally low success rates at 1 year though I’m sure this group will try to follow these individuals up at that point and hopefully produce another paper. The overall most reliable predictor of who quit and who relapsed ended up being the level of nicotine dependence as measured by the participants’ pre-quit attempt cotinine levels and the number of cigarettes they smoked every day. Since cotinine assessments are less biased, it was the most predictive of all throughout the experiment (# of daily cigarettes was no longer predictive at 3 months). Interestingly, self reported impulsivity and smokers’ initial ratings of cravings for cigarettes didn’t end up predicting relapse at all, but those cognitive tests assessing the quitters’ reactions to nicotine associated cues told a pretty interesting story: It seems that early on during their quitting attempt smokers who had more general interference with their cognitive function relapsed sooner. These cognitive problems can be thought of as interruption with normal thinking by nicotine-related cues and maybe even more general interference with brain function. After that point, at the 1 and 3 month follow-ups, had more to do with baseline assessments of motor impulsivity as well as those initial cotinine levels assessing the degree of nicotine dependence.
The take-home: Quitting smoking is hard for different reasons in the first week and later on
If you’ve ever tried to quit you’ve heard someone telling you that the first week is the hardest and once you make it through that the rest is a piece of cake. Well, this research doesn’t really support that notion since about 25% of the sample relapsed between each of the followups, but it does seem to indicate that the reasons for relapse change after that first week. It seems that the first week may be difficult because of general cognitive interference by stimuli and cues that are nicotine associated. Those cues make it hard to pay attention to much else and they interfere with normal thinking and attention process, making sticking to the quit attempt difficult. After that point, successfully quitting smoking was associated more with the level of initial smoking and that damn motor impulsivity test. The finding that heavier smokers have a harder time quitting isn’t new and isn’t surprising, but the fact that cognitive effects and predictors of relapse change does suggest that the interventions likely to help smokers quit may need to be different during week 1 and afterward. Overall, these findings suggest that the brain function problems associated with quitting smoking (or smoking in general) may recover faster than do some of the other physiological factors associated with quitting since the initial levels of smoking continued to be highly predictive throughout the 3 month period of followup. Another explanation could be that initial smoking levels affected brain function in ways not assessed by these researchers.
Since so many smokers relapse within the first week (more than 50%), it seems to me that interventions that really focus on the cognitive interference and the extreme attention towards nicotine associated cues and stimuli would be helpful for those quitting smoking. Maybe if we can bring the relapse numbers down at 1 week we can have a more gradual fall-out for the following month resulting in significantly higher quit rates. Interestingly, NIDA and other research organizations are getting really interested in the use of technologies like virtual reality for help in addiction training. It seems that in this context, these sorts of treatments might be useful in helping early quitters train to avoid that cognitive interference. Additionally, medication like modafinil, and maybe even other ADHD medication could be used very early on for those quitting smoking to help recover some of their ability to control their attention thereby reducing the power that nicotine associated stimuli have over them. I guess we’ll have to wait and see as those who develop interventions start integrating this research. In the meantime, I’d love to hear from readers who have quit or tried to quit: Does this research seem to support your own experiences?
Jane Powell, Lynne Dawkins, Robert West, John Powell and Alan Pickering (2010). Relapse to smoking during unaided cessation: clinical, cognitive and motivational predictors, Psychopharmacology.
|Posted in: Drugs, Education, Tobacco
Tags: abstinence, activation, brain function, bupropion, cognitive, cognitive interference, cotinine, expectation, experiment, impulsivity, medication, motivation, nicotine, nicotine assocciated cues, nicotine associated, nicotine replacement, quit, quit attempt, quitting, quitting smoking, quitting smoking hard, relapse, research, smokers, smoking
October 5th, 2011
By Rachel Fintzy, M.A., MFT, and Adi Jaffe, Ph.D.
“You know you’re an alcoholic when you misplace things–like a decade.” (Paul Williams)
Jon Kabat-Zinn, the founder of mindfulness meditation in Western medicine, cleverly entitled one of his best-selling books on meditation, “Wherever you go, there you are.” Simple and obvious, perhaps, but easier said than done, especially when you’re struggling with an addiction, which is often an attempt to go somewhere else, emotionally and mentally. Whether the specific addiction (or attachment) is to alcohol, drugs, food, sex, or shopping, your mind is usually focused either on how to get your substance of choice, taking steps to acquire it, using it, or recovering from the effects. Very little time and energy are spent noticing the present moment, except to try and change your experience. Indeed, the present becomes little more than a constant agitated state. It thus stands to reason that the practice of mindfulness, defined as non-judgmental awareness of the present moment, would be an effective tool in addiction treatment, and in fact this has been found to be the case in many clinical studies.
First of all, although it may seem paradoxical, through increasing your ability to accept and tolerate the present moment, you become more able to make needed changes in your life. This is due to your learning to deal with uncomfortable feelings that might accompany modified behaviors, rather than reacting on automatic pilot. Also, practicing balanced emotional responses can reduce your stress level, and anxiety or stress are often a triggers for substance abuse and addictive behavior. In addition, when you choose a neutral rather than a judgmental response to your thoughts and feelings, you can increase your sense of self-compassion rather than beating yourself up, which is often associated with addictive behaviors.
Mindfulness, meditation, and breath
So, how do you practice mindfulness? One simple method involves focusing on your breath:
- Sit quietly, with a straight spine (lounging about may tempt you to fall asleep).
- Close your eyes.
- Make it your intention to be in this moment and to be open to what comes up, without judging your experience.
- Bring your attention to your breath and simply notice as you slowly inhale and exhale. You’re not trying to make anything happen but just to observe what is naturally taking place.
- If your mind begins to wander, as it inevitably will, simply notice this and gently bring your attention back to your breath. No need to judge your thoughts, as this tends to be like struggling in quicksand – you’ll just sink more quickly. Awareness and acceptance of your thoughts is paradoxically the key to detaching from them rather than identifying with them as reality.
- Try five minutes at first, and build up to 20 minutes a day or so, if possible. However, it’s better to practice mindfulness for only a few minutes a day then not at all, so no perfectionism here (or anywhere else, for that matter – but that’s another story).
Mindfulness teaches that instead of trying to avoid your experience, which has been associated with a host of mental and emotional disorders, you adopt an inquisitive and observing attitude toward your thoughts, feelings, and circumstances. In other words, instead of getting angry over being angry, you simply notice your feeling of anger and investigate its many facets. You inhabit the moment. Yes, sitting with an uncomfortable emotion may sound about as welcoming as a sharp poke in the eye, and it certainly takes some adjustment to accept what’s going on in that moment instead of taking a mental or emotional vacation. However, by changing your relationship with your thoughts, feelings, and experiences and learning to accept them as they are, rather than how you might like them to be, you can literally change your brain and create new neural networks. Over time you can develop a greater capacity for self-observation, optimism, and well-being, which can lead to better control over your addictive behavior. Mindfulness meditation has also been shown to contribute to improved self-control, and since impulsivity plays an important role in addiction and drug abuse, better self-control is always welcome.
Great websites to check out regarding on-going research in mindfulness, free downloadable mindfulness meditations, and how mindfulness benefits the brain include the following:
You can practice mindfulness on your own and also in a group setting, where you can benefit from sharing your experiences with one another and provide mutual support in continuing the practice. Just be patient and kind to yourself, as it’s the mind’s nature to be active. It may always be along for the ride, but you can learn to accept that it’s in the back seat – it just doesn’t have to drive the car.
August 16th, 2011
People who are looking for treatment for their cocaine addiction still really like cocaine, but they’ll choose money as an immediate reward if they can only get their drug of choice later.
Cocaine or money? Depends on how long the wait is
Although it might be somewhat surprising, the above finding is the result of a recent study by a team of researchers spanning the U.S. and Australia that was recently published in the journal Psychophramacology.
We’ve talked about the concept of relatively high impulsivity among addicts on A3 before and the concept isn’t a new one — Addicts make drug-focused choices in the short term even if there are larger rewards far off in the horizon. In fact, this sort of delay-discounting (considering future rewards as being worth less) is a general human phenomenon that has simply been found to be exaggerated among addicts.
Think about it – Would you prefer $50 now or $1000 in 6 year? What about $100 now?
By asking a set of similar questions researchers can determine an individuals discounting rate or the amount of discounting people put on the delay in getting the later reward. Up to now, most of this sort of research has been conducted using the same “now” and “later” rewards. People were asked to decide between money now or later, cocaine now or later, cigarettes, meth… you get it.
This recent study made things more interesting by creating a few different conditions:
- Money now Versus Money later
- Cocaine now Versus Cocaine later
- Money now Versus Cocaine later
- Cocaine now Versus Money later
The goal was to see if people discount money and drugs equally. Since one of the hallmarks of addiction is that addicts seem to undervalue everything else while overvaluing drugs, figuring out whether bringing delay into the mix was at the least interesting but at best possibly useful in treatment.
The researcher used participants who were actively looking for cocaine treatment and ended up with a relatively small sample of 47 individuals who met criteria for cocaine addiction. As is usually the case with these sorts of studies, most of the participants were men, the average education equaled high-school and the average age was early 40s.
Participants were asked how many grams of cocaine a $1000 was worth and that unique number was used for each participant as the equal point between money and drug. Then they were presented with options such as the above (X number of dollars now or X number of dollars in six months). As participants made selections, the immediate amount was changed by 50% to counter their choice (it was reduced if they chose immediate and increased if they chose delayed rewards) and the procedure repeated six times for each of seven different delay periods (1 day, 1 week, 1 month, 6 months, 1 year, 5 years, and 25 years).
So, let’s say a participant was first asked if they wanted $500 now or 20 grams of cocaine. If they chose cocaine, their next choice would be $750 now or 20 grams of cocaine later; now if they chose money, the choices became $375 now or 20 grams of cocaine later… and on the experiment went.
Cocaine addicts choose cocaine if they can get it now, but not later
First of all, it’s important to note that the research showed that different participants had pretty stable discounting characteristics. That is, if a participant preferred to get things now rather than later, that was likely true across all conditions regardless of whether the reward was drugs or money. However, the different rewards also had a large influence on this equation.
The main finding from this study was that when faced with the option, cocaine addicts chose immediate money over later cocaine even if the immediate money amount was relatively low. That finding might seem surprising at first given what we think we know about addicts. Aren’t they supposed to always choose drugs regardless of what else we put in front of them?
Apparently, what matters is not only what we put in front of them but also when. Of course, anyone who actually knows an addict (or is one themselves) already understands that trying to simplify addiction to an ability to only choose drugs is silly. Addicts would die of starvation or a host of other issues pretty quickly if that was true. Addiction is much more nuanced than that, and as I mention at the end of this piece, this finding might not be as clear as one might think.
In fact, this finding has already been greatly supported by at least one addiction treatment tactic that we’ve discussed here on A3 – Contingency Management (CM). In CM, individuals in treatment are rewarded for staying clean and doing well in treatment. They’re not given cash but instead are rewarded with vouchers that let them buy food, clothes, etc. for providing drug-free urine tests and going to their assigned group meetings. This addiction treatment method follows the basic tenant of the psychology of learning – people do what they’re rewarded to do. This study offers a fresh perspective on the matter, suggesting that one of the reasons people do well and stay longer in treatment when given CM is that the immediate money reward is thought to be worth more than the possibility of getting drugs later. It might also explain why CM has only really been shown to work well while people are in treatment and not when they leave…
I mentioned earlier that I think these findings may be a little more complicated than they first seem. One of the major issues I have with this study stems from my life as a drug dealer. The users I know quickly equate money with drugs and so it is very possible that in their minds money now also equals cocaine now, although a smaller amount of it and they’ll take whatever drug they can get now instead of having to wait for it. Most regular users I’ve met would easily choose a single gram of meth now instead of 4 or 5 in 6 months. They simply don’t want to wait that long to get high. Money holds its value much better in the long run and this research supports that idea.
Bickel, Landes, Christensen, Jackson, Jones, Kurth-Nelson, Redish (2011). Single- and cross-commodity discounting among cocaine addicts: the commodity and its temporal location determine discounting rate, Psychopharmacology
|Posted in: Education
Tags: addiction, addicts, cocaine, cocaine addicts, cocaine later, delay discounting, discounting, drug, Drugs, immediate money, impulsivity, later, later cocaine, money, money later, money later cocaine, people, treatment
February 22nd, 2011
ADHD In children and adults – Symptoms and tests
Children with attention deficit hyperactivity disorder (ADHD, formerly known also as ADD) are classically seen as the kids in class who have trouble staying in their seats and paying attention during long lessons. Underlying these problematic behaviors is a confluence of factors, with evidence pointing to genetics, neural function, and environmental factors (including parenting and lead exposure) that can all affect ADHD behavior. Many children diagnosed with ADHD seem to simply “grow out” of their symptoms. They may learn particularly effective strategies for managing inattention and disorganization (I myself am a notorious list maker), or learn to control some of the fidgeting and restlessness or channel that energy into sports or other activities. Read the rest of this entry »
|Posted in: Education
Tags: ADD, ADHD, attention deficit hyperactivity, attention deficit hyperactivity disorder, children, children adhd, high value, high value wrods, hyperactivity, hyperactivity disorder adhd, impulsivity, inattention, marijuana, memory, memory capacity, nicotine, planning, smoking, substance abuse, value, value words, words
January 27th, 2011
Here at A3, we believe in equal opportunity. We recognize that saying we have an addiction problem is not the same as saying we have a drug use problem and that just because some people abuse substances (or belief systems) doesn’t means that these have no actual value when not abused. Enter this recent paper on CB1 receptors, THC, and Huntington’s Disease.
Those of you who haven’t been reading A3 for too long (shame on you!) may not be familiar with my comparison of the cognitive (or mental) impulsivity associated with substance use disordersand the physical “impulsivity” common to Huntington Disease(HD) patients. To make a long story short – both of these dysfunctions have to do with the striatum, a brain area responsible for inhibiting and controlling unwanted brain output (as in thoughts or actions). When this area starts malfunctioning, everything goes awry. When it comes to HD, “goes awry” doesn’t really do the disorder justice. Patients with a progressive form of the condition end up flailing their limbs in a manner that’s been coined the “Huntington Dance,” a euphemism if I ever heard one. This motor flailing is closely followed by severe cognitive impairments and a premature death. Not a pretty story. Read the rest of this entry »
|Posted in: Education
Tags: addiction, cannabinoid, cannabinoid receptors, CB1, cb1 receptors, cb1 receptors thc, combined type, disease, drug use, hd, hd mice, huntington disease, huntington's disease, impulsivity, levels cb1 receptors, mice, patients, receptors, reduced levels cb1, reduced levels cb1 receptors, striatum, THC
December 23rd, 2010
It is well known that ADHD diagnoses and substance abuse problems are closely associated. It is estimated that substance abuse problems including dependence are up to twice as common among individuals with ADHD, which is not surprising given the impulsivity factor involved in ADHD. The problem is that until recently, most medications for ADHD have belonged to the stimulant category and as many, including us, have written before it is probably not the best idea ever to give drugs that have a relatively large abuse probability to people who are relatively likely to develop substance abuse problems. Right?
We’ve already written about atomoxetine and bupropion, two drugs with relatively low abuse potential (since patients don’t actually feel “high” from them) that are being successfully used in treating ADHD. But there is little doubt that the type of effect seen among patients who are using stimulants (like adderall, ritalin, etc.) isn’t being observed among patients taking non-stimulant medications. All of this means that patients on non-stimulants are getting less bang but with less risk. A dopamine agonist by the name of amantadine might change all of that according to a recent study.
Amantadine versus stimulants for ADHD treatment
Fourty children between the ages of 6 and 14 were enrolled in the study conducted in a psychiatric hospital in Iran. The kids were randomized into two groups a methylphenidate (ritalin) and amantadine group. Over a six week period the kids were assessed four times – at intake and then every two weeks -using an instrument that parents and teachers (who didn’t know what medication the kids were getting) would use to rate the child’s behavior on the 18 ADHD symptoms listed in the DSM-IV.
The final findings were very encouraging (see picture): The kids in both conditions improved greatly over the 6 weeks of the study and no difference was found between the two medications. the children in the amantadine condition actually suffered less side effects and significantly so when looking at side effects common to stimulant medication such as decrease in appetite and restlessness. While more studies are obviously needed, this randomized trial shows that amantadine is not only safe, but it may be safer than at least some stimulant medications while also providing the same effect on ADHD symptoms. Given that approximately 30% of patients don’t respond well to stimulants and that some families are afraid of giving stimulant medications to their children, at least partially because of the risk of substance abuse issues, non-stimulant medications can be an attractive alternative, and it seems like amantadine can deliver.
Final thoughts from Dr. Jaffe on ADHD medications and amantadine
One of the main reservations I have about the notion of using this medication for ADHD is that NMDA receptors are very important in learning, so it may be that we’re helping to resolve attention problems but making it more difficult to actually create memories that are crucial for learning. More research is necessary to see if these decreases in impulsivity are accompannied by improvements, and not reductions, in learning ability.
So, if you’re considering medicating a child who has been diagnosed with ADHD, I strongly support the notion given the difference that medication has made in my own life. However, I urge you to be educated and to consider non-stimulant options, especially as more are researched and as that treatment option becomes more available, less costly, and less likely to lead to abuse of the drug. With prescription drug abuse one of the fastest growing problems in the U.S., being careful is just sound advice.
Mohammad-Reza Mohammadi, Mohammad-Reza Kazemi, Ebtehal Zia, Shams-Ali Rezazadeh, Mina Tabrizi, Shahin Akhondzadeh (2010) Amantadine versus methylphenidate in children and adolescents with attention deficit/hyperactivity disorder: a randomized, double-blind trial. Human Psychopharmacology.
Some parkinson work showing effect of amantadine: http://www.springerlink.com/content/76r5wxux8wn52rq5/fulltext.pdf
|Posted in: Education, Tips
Tags: abuse, abuse problems, Adderall, ADHD, agonist, amantadine, atomoxetine, bupropion, dopamine, drug, DSM, impulsivity, medication, Medications, non stimulant, non stimulant medications, Ritalin, stimulant, stimulant medication, substance abuse, substance abuse problems
October 29th, 2010
Dr. Dodes recent article, apparently trying to blow up the myth of addiction as a neurophysiological disorder, sounded persuasive, although its underpinning was oversimplified and it’s understanding of the brain-science involved in addiction, and other associated mental health disorders, was lacking. Hopefully, by presenting a more complete picture of the evidence for a brain-aspect to addiction, I can un-bias the discussion somewhat. I, for one, don’t believe that neuroscience will ever be the only factor important in addiction – an individual’s environment, social influences, and other factors will always end up playing important parts as well – still, I think that to dismiss all of the evidence for biological factors at play in the development of addiction is foolhardy. Especially when there’s so much of it that was glossed over in Dr. Dodes’ introduction.
Pleasure center activation is only part of the picture in addiction
Firstly, supporters of the notion that addiction is, at least partly, an outcome of specific brain function point not only to pleasure center activation, but also to a whole host of findings showing genetic variability that is either protective from, or a risk factor for, dependence on drugs and likely also behavioral addiction like eating disorders, compulsive gambling, and maybe sex addiction as well (you can start out looking up ALDH2-2 variability and alcoholism and cocaine addiction, DRD4 and stimulant addiction, and many more).
While it is true that all those who consume addictive substance activate the brain similarly, there are considerable differences in the specific of that activation in reaction to drugs. Some release more dopamine while others have more “active” versions of specific important receptors; neurotransmitter recycling is quick in some, but not all, and drug metabolism is different in different individuals in ways that have been shown to be important not just for addiction risk, but also for the probability of treatment success. Just look at the nicotine and CPY26 literature for an example. It’s right there.
Additionally an entire body of literature exists that shows differential activation, as well as structural differences, between addicts and non-addicts in regions as varied as the OFC, PFC, Insula, and more. This is not to mention a slew of evidence that shows different behavioral test performance on risk-taking, impulsivity, and delay-discounting, all personality variables highly associated with addiction. If one simply ignore all of this evidence, it may be easy to believe that there is no biological explanation for these phenomena, but that’s just wrong.
To say that mesolimbic activation (what the good doctor called “pleasure centers”) is the only evidence for physiological factors in addiction is dismissive at best.
Drug addiction develops in only some drug users
The notion that not everyone who takes drugs becomes addicted is nothing close to evidence against a brain explanation for addiction. Everyone’s motor–cortex, striatum, and substantia nigra (the areas of the brain responsible for movement) activate in the same way during movement, but only a small group ends up suffering from Parkinson’s or Huntington’s disorders. One fact does not preclude the other but instead may specifically point to the fact the group which develops the disorder has somewhat different neurological functioning. Researchers aren’t concerned with explaining why all individuals can become addicted to drugs, but rather why that small subgroup develops compulsive behavior. A short reading of the literature makes that fact pretty clear. Additionally, while Dr. Dodes’ claims otherwise, imaging technology HAS produced evidence explaining this “mystery”, including differences in the ways addicted smokers respond to smoking-related triggers, and an increased dopamine response in cocaine addicts to cues, and well as to cocaine.
As mentioned in the motor disorder section above, ingestion of chemicals is not at all necessary for brain disorders to occur or indeed develop later in life. Dr. Dodes example of shifting addiction could be used as evidence for an underlying neurological difference just as well as it would serve to make his point… Or even better. If there’s a faulty basic mechanism attached to rewarding behaviors, it doesn’t really matter what the behavior is, does it? Sex addiction, gambling, and more can all be explained using a similar mechanism, though drugs of abuse may just have a more direct impact. I know, I’ve written about them all.
The Vietnam vet heroin story used by Dr. Dodes as evidence that emotional, rather than physiological, factors are responsible for addiction actually fits right in line with the notion of predisposition and underlying differences, and I’m surprised to hear a physician point to group differences as an indicator of no neurobiological basis. Indeed, when it comes to the emotional reactivity associated with drug associated cues, normal learning literature, as well as drug-specific learning research, has revealed over and over that drug-related stimuli activate brain regions associated with drug reward in the same way that natural-reward predictors do for things like food and sex. Once again, these facts are part of the basic understanding of the neuroscience of learning, with or without drug abuse involvement.
My own dissertation work shows that it is very likely that only a subsection of those exposed to nicotine will develop abnormal learning patterns associated with that drug. However, among those, learning about drug-related stimuli (as in “triggers”) continues in an exaggerated manner long after the other “normal” animals have stopped learning. That sort of difference can lead to a seriously problematic behavioral-selection problem whereby drug-related stimuli are attended to, and pursued, more so than other, non-drug-related ones. If that sounds familiar, it should, since drug users continuously pursue drug-associated activities and exposures in a way that seems irrational to the rest of the world. It just might be due to such a mechanism and others like it.
Some important points about science in Dr. Dodes’ article
One very true fact about mental health pointed out by Dr. Dodes is that diseases like schizophrenia, which used to be explained simply as demon possession and evidence of witchcraft can now be, to a large extent, explained by the study of behavioral neuroscience and cognition. The same is true for bipolar disorder, depression, ADHD, and a host of other such conditions. In fact, the study of psychology has only been able to rely on technological advances that allow us to “see” brain function for a few short decades, leading to incredible advances in the field that I think will continue. The thinking that no such advances have, or will continue to be, made in the study of addiction is, in my opinion short sighted.
As I mentioned above, I don’t for a second think that the entire explanation for drug abuse and addiction will come from neurophysiological evidence. The doctor points out that “If we could take a more accurate image of addiction in the brain, it would encompass much of the history and many of the events that make us who we are.” I agree that we need to advance our technology as well as expand our understanding, but I think that to discount neuroscientific explanations completely is a big mistake.
|Posted in: Education, Opinions
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