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Posts Tagged ‘bupropion’

Quitting smoking without help is hard: Effects of motivation and other personality factors

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?

Citation:

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?

Citation:

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
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A new candidate for ADHD medication: Amantadine and the rise of non-stimulants

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.

Amantadine may soon offer a new non-stimulant medication option for ADHD treatmentThe 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.

Citation:

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
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The genetics of quitting smoking- Bupropion and nicotine metabolism

October 18th, 2010

If you’ve been reading A3 for a while, you know that we’re big supporters of scientific progress in addiction treatment. While it may be true that addicts need to want recovery in order to truly turn their lives around, the choice is hardly ever that simple and if we can tip the balance in the favor of treatment, or a better way of life, I say let’s go for it. When it comes to genetics and addiction, I’ve normally talked only about the fact that a person’s genetic code may predispose them to addiction or to other related conditions (like depression, anxiety, and so on). Aside from a single mention of pharmacogenomics, I don’t think I’ve spoke much about the way genetics can help us tailor addiction treatment to individual needs. We’re about to fix that.

Replacement therapies and quitting smoking

You’ve heard of nicotine patches and gums, right? In the research community, those are all known as Nicotine Replacement (NR) therapy and they’ve proven to be some of the most helpful tools for those who are quitting smoking. By allowing smokers to still get the nicotine their body craves (even though there are thousands of other chemicals in cigarettes that likely make them even more satisfying) without having to light up, these NR methods let cigarette addicts get their NIC fix while slowly lowering their dose and getting away from the habit of putting a cigarette in their mouth. Like methadone, buprenorphine, and other replacement therapies, the idea is to move addicts one step away from the actual addictive behavior and allowing them to begin adopting a healthier way of living. Replacement therapies are very successful, even if some people hate the idea of giving drugs to drug addicts, and nicotine replacement works well by itself for some people (though only about 20%).

But when it comes to nicotine, like with many other drugs, different people metabolize the stuff at different rates. The individual variability in the internal processing of nicotine greatly affects how many cigarettes individuals smoke and also the probability that they will become addicted to tobacco (people who metabolize nicotine more quickly smoke more and are more likely to become addicted to smoking). Fast metabolizers are also half as likely to be able to use nicotine replacement alone to quit smoking (1). However, when you put all of the addiction research together, it becomes pretty obvious that the same variability in nicotine metabolism can also help us determine the best course of treatment for tobacco addiction.

Metabolism, treatment, and the best way to quit smoking

Bupropion helps fast metabolizers increase their quitting chancesFortunately for smokers, the only research finding in this area hasn’t been that slow metabolizes have a much better chance of quitting smoking with nicotine replacement therapy. The same group of addiction researchers (led by Caryn Lerman of University of Pennsylvania), also found that buporopion, the smoking cessation medication everyone knows as Zyban (and the antidepressant called Wellbutrin), could help those fast metabolizers catch up with the slow metabolizers when it came to quitting (see the figure on the left taken from the actual study – you see that the dark bars, who are the bupropion patients, do as well as the white bars regardless of their metabolism rate, which is on the bottom). The researchers found that while slow matabolizers of nicotine did much better with simple smoking cessation therapy and fast metabolizers did very poorly (30% versus 10% quit respectively in each of the groups), adding bupropion made all groups look essentially the same (2). The moral? While those slow metabolizers don’t really get much of a benefit from using bupropion since they do pretty well with talk therapy or nicotine replacement alone, the fast metabolizers really need it to even their chances of quitting – and once they get bupropion, they do pretty well!

Genetics and addiction treatment – is this just the beginning?

Hopefully you’re now convinced that genetics can really help us determine what treatment course will best suit a specific person over another. There’s little question that this sort of approach is in its infancy, and you certainly can’t go to a doctor right now and get your metabolism rate for a drug analyzed (unless you’re part of a research study), but this sort of work shows great promise in improving the outcomes of addiction treatment. When you look back at that original paragraph, and the quite common thinking that addicts need to WANT to be better – I would argue that those fast metabolizers probably wanted to quit smoking as much as anyone else in the study, and their physical makeup just made it that much more difficult for them. I think that if you look at the science of addiction closely, you’ll find that this supposed lack-of-motivation is sometimes more of a myth than a reality. Many addicts want to get better, they want to stop behaving in ways that specifically mess up their lives but they just find it incredibly difficult. My hope is that this is where science can truly make a difference, by making it just a little bit easier…

Hopefully one day we’ll be able to specifically adjust addiction treatment programs according to individual patients’ needs, including the use of medications, specific behavioral treatments, and more.

Citations:

1) Robert A. Schnoll, Freda Patterson, E. Paul Wileyto, Rachel F. Tyndale, Neal Benowitz, & Caryn Lerman. Nicotine metabolic rate predicts successful smoking cessation with transdermal nicotine: A validation study (2009).

2) F Patterson, RA Schnoll, EP Wileyto, A Pinto, LH Epstein, PG Shields, LW Hawk, RF Tyndale, N Benowitz & C Lerman1. Toward Personalized Therapy for Smoking Cessation: A Randomized Placebo-controlled Trial of Bupropion (2008).


Posted in:  Education, Medications, Treatment
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NIDA and ONDCP – American policy on addiction research

June 20th, 2010

At this year’s College on Problems of Drug Dependence (CPDD) Annual Meeting, I got to hear, and talk to, some of the most influential players in the American addiction research field. Here are a few highlights from their talks and our discussion:

Dr. Nora Volkow of NIDA talked about a shift from Genome Wide Association Studies (GWAS), which have been the most recent popular advance in genetics addiction research and into more Deep Sequencing work. The hope is that this will allow us to begin untangling some of the GWAS findings that have seemed counter-intutitive or puzzling. Deep sequencing should let us see what genes really are associated with addiction specifically, not just as markers.

Dr. Volkow also brought up the numerous issues of medications for addictions including the Nabi Nicotine Vaccine, Vivitrol (a Nalexone depot that helps opiate users who wouldn’t take it otherwise), and a host of new medications that are being developed or considered. An interesting idea here was the use of drug combinations which are showing great promise in providing enhanced treatment results (similar to HIV treatment that benefited greatly from drug cocktails). These include combining vernicline and bupropion for smoking and naltrexone and buprenorphine for cocaine (that’s not a type even though both have been typically thought of for opiate addicts).

Dr. Tom McLellan, who I personally believe is one of the most informed and thoughtful people we have when it comes to addiction research in this country, talked about our need to expand the reach of treatment to the drug abuse earlier in the problem cycle. While about 25 million people are considered drug addicts in this country, more than 65 million are drug abusers. By finding ways to reach those people in primary care (as in doctor offices) settings before they develop the full blown addiction we’re used to talking about we can do better. He also mentioned the idea of anonymity in recovery playing a role in the continued stigmatization of addiction, a topic I’ve written about recently.

Stay on the lookout for more amazing new addiction research knowledge!


Posted in:  Drugs, Education
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How it doesn’t work – the dogma of the 12 steps

May 23rd, 2010

Imagine being diagnosed with cancer, going through a regimen of chemotherapy only to have the cancer return within months, and being told by your doctor that there must be something wrong with you and that he can’t treat you unless you let the chemo do its work.

Absurd right?

12-Step dogma

Everyone wants to know if they can become addicted

Unfortunately, if you replace the cancer above with addiction, the chemotherapy with the 12-steps, and the doctor with 12-step dogma, you have what we know as the ________ Anonymous model (fill in your favorite blank). It’s even written in what 12-steppers call The Big Book (officially called “Alcoholics Anonymous”) and often read as part of the “How it Works” section.

“Those who do not recover are people who cannot or will not completely give themselves to this simple program, usually men and women who are constitutionally incapable of being honest with themselves… They are naturally incapable of grasping and developing a manner of living which demands rigorous honesty.”

Well, as far as I’m concerned, this is where the 12 steps lose credibility with me. In any other field, if one treatment doesn’t work, another one is tried, and another. Different people with different conditions may need slightly different approaches. If no known treatment works, experimental ones are attempted. This is how medical science advances. Still, the notion of a physician blaming the patient for a treatment not working is ridiculous. There’s an entire field built around intervention research and I’m pretty sure that simply dismissing the patient as constitutionally dishonest isn’t a common technique.

Treating chronic conditions

In diabetes, like in addiction, there is a rate of compliance with prescribed treatment. And just like among addicts, that rate is relatively low, averaging around 30% or less. Relapse is also pretty common in other chronic conditions like diabetes, asthma, and hypertension, and rests around 50%-60%, not far from estimates for addiction.

Some patients are better at following one regimen while others do better with a different schedule, different doses, or different treatment methods altogether. Similarly, while some addicts respond beautifully to CBT, it seems to help some very little. The same is true for the 12-steps, religion, and a host of other practices. As far as I’m concerned, this means that when an addict seeks treatment, their provider should take a good assessment of the issues, prescribe the treatment that seems to fit best, but if that one doesn’t work, try another method, not throw them out because the favorite approach didn’t cut it.

12-step Dogma Vs. Progress

And therein lies the problem with the 12-steps, whether supporters acknowledge the religious nature of the program or not is tangential, the important thing is that they cling to a book written decades ago much like believers hold onto a bible. Both are collections of stories and messages passed on that no one is willing to re-examine and, if needed, change. Medical texts, and indeed any textbook seeking to stay relevant, stay current by issuing new editions that incorporate new knowledge, but the 12-steps haven’t been touched since 1939, or since the beginning of world war II!!!

Advancement requires flexibility

1939 was an important year, with the 3rd Reich beginning its exploits, Steinbecks’s “Grapes of Wrath” seeing its first publication (another book without major edits since), the first stocking ever sold, and the emerging use of penicillin. I think many of us would agree that there have been some serious advances since that time.

When it comes to addiction, those advances include our vastly improved understanding of the neuroscience, genetics, and general brain function involved. Additionally, the development of very effective treatment modalities, like Motivational Interviewing (MI), Cognitive Behavioral Therapy (CBT), and Contingency Management (CM), has given providers a much more complete toolbox with which to deal with addiction problems. Unfortunately, many within the 12-step community have never heard of any of these methods, or of the use of medications (like Bupropion) to help with cravings. Personally, I think that’s just sad.

How it works. Really.

It’s time to dust off the covers, and incorporate the 12-steps into the bigger picture of addiction treatment. When 12-steppers wonder why people can’t just see the value of the program, I automatically think of the preacher who sat in on of my addiction class and kept yelling that if only addicts accepted Jesus into their lives, they would be saved. Laugh all you want, but not only did the 12-steppers dismiss him, they missed an opportunity. He had a point- those who accept Jesus into their lives fully may succeed in recovering from addiction on that basis alone – but those who fail to do so should be given every other treatment tool available so that they may also.

This is supposed to be the age of inclusion, a time for Change with a capital “C.” Let’s make ourselves proud and help those suffering by making sure that we’re offering every treatment option possible.


Posted in:  Education, Opinions
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Quitting smoking: Quitlines success

May 22nd, 2010

In the world of extremely difficult smoking-cessation (quitting smoking), telephone-based programs are apparently having some real success.

Quitting smoking with quitlines

According to a recent summary-analysis (we call these meta-analyses) of research done on Smoking Cessation Quitlines (CSQs), smokers who call and participate are 1.5 times more likely to quit! These are roughly the same numbers we see for people who use nicotine replacement therapies (NRTs, like the nicotine patch, gum, or lozenge), which are the most successful therapies we’ve got. Not bad when you consider that most quitlines are free to users.

What do quitlines do?

Once a user interested in quitting contacts a CSQ, they are taken through an assessment procedure. The California one is apparently pretty long, lasting 30-40 minutes. Don’t worry, the first call is the longest. Past this point, the lines’ activities vary greatly depending on the specific provider. Some offer phone-based counseling only, others also mail materials, and some offer recorded messages, on-demand counseling, counselor callback, and even access to medication (like patches, gum, or bupropion). Since state-based ones are free, it’s a good idea to make the call and see what your state offers. If you’re an addiction professional, or a psychologist with clients that want to quit smoking but can’t seem to shake it, this might be a great suggestion for them.

Can quitlines be used for other addictions?

Phone-based interventions have already been used for some addiction problems (mostly problem drinking), but usually as a supplement to face-to-face treatment. Still, given the relatively low cost associated, it seems that establishing such a tool for problem drinkers that doesn’t include a face-to-face interaction could be a viable option. Since it was state-based public health officials that made CSQs happen through lobbying, it seems that any addiction, or mental health, problem that is prevalent enough to warrant such attention (and such expenditures) may benefit from a little quitline love.

Citation:

Lichtenstein, E., Zhu, S.H., Tedeschi, G.J. (2010). Smoking cessation Quitlines: An underrecognized intervention success story. American Psychologist, 65, 252-261.


Posted in:  Drugs, Education
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ADD and ADHD medications: Lessons from a crystal meth experiment

April 11th, 2010

I’ve recently completed a study that I presented at the Society For Neuroscience (SFN) meeting in DC. The study was actually aimed at looking at the usefulness of two medications in interfering with the rewarding qualities of methamphetamine. The thinking was the if we could figure out a way to interfere with crystal meth being perceived as rewarding by the brain, we may be able to help addicts from continued use after a relapse.

Two prescription stones but only one hits crystal meth

The two medications are atomoxetine and bupropion, though you may know them as Strattera and Wellbutrin or Zyban. Their mechanisms of action are similar, but distinct enough that we wanted to test them both. The results of the study, in one sentence, were that atomoxetine (or Strattera), but not bupropion (or Zyban) succeeded in eliminating animals’ preference for meth if given along with it. The implication is that in the future, these, or other, similar, medications, may be given to newly recovering addicts. The hope would be that by taking the drug, they may be somewhat protected in the case of a relapse. If they don’t enjoy the drug during the relapse, they may have a better chance of staying in treatment.

More to these medications than meets the eye

I learned some other interesting things while preparing, and then carrying out, the study. While Zyban could, by itself, be liked by the animals, Strattera did not seem to produce any sort of preference. Given the common use of these drugs in the treatment of ADHD, the difference may be very important. As you may recall, I’ve talked before about the connection between impulse control problems and being predisposed to developing addiction. Given this relationship, it would seem that we’d want to be especially careful about using drugs that can cause abuse with this population. Many of the stimulants used to treat ADD and ADHD can indeed lead to abuse, as their effects are very similar to speed, or crystal meth (Adderall and Ritalin come to mind). Zyban’s abuse liability is definitely lower, given the greatly reduced preference animals develop for it. Still, it seems that Strattera’s abuse potential is almost zero. In trial after trial, animals given atomoxetine fail to show a preference for the drug.

To my mind, this means that as long as it’s successful in treating the attention problems, atomoxetine is the better candidate. All in all, I’d think the first choice should be the one that helps the symptoms of ADHD while having a reduced likelihood of dependence. Obviously, if the drug is not able to treat the problem, other options should be selected, but it seems to me that given the known relationship between attention deficit problems and addiction, the question of abuse liability should play a significant role in the selection of medication.

Once again, this doesn’t mean that all users of Adderall, Ritalin, or the other stimulant ADHD medications will develop an addiction to their prescription. In fact, we know that rates of addiction to prescriptions are generally relatively low. Nevertheless, I’d consider ADHD patients a vulnerable population when it comes to substance abuse so I say better safe than sorry.


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