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 15th, 2011
In a recent post the notion that “loss of control” is an addiction myth was raised by our contributing author, Christopher Russell, a thoughtful graduate student studying substance abuse in the U.K. Though I obviously personally believe in control- and choice-relevant neurological mechanisms playing a part in addiction, this conversation is a common one both within and outside of the drug abuse field. Therefore, I welcome the discussion onto our pages. I’d like to start out by reviewing some of the more abstract differences between my view and the one expressed by Christopher and follow those with some evidence to support my view and refute the evidence brought forth by him.
Addiction conceptualization – Philosophical and logical differences and misinterpretations
One of the first issues I take with the argument against control as a major factor in drug addiction is the interpretation of the phrase “loss of control” as meaning absence, rather than a reduction, in control over addiction and addictive behavior. Clearly though, one of the definitions of loss is a “decrease in amount, magnitude, or degree” (from Merriam-Webster.com) and not the destruction of something. Science is an exercise in probabilities so when scientists say “loss”, they mean a decrease and not a complete absence in the same way that findings showing that smoking cigarettes causes cancer do not mean that if an individual smokes cigarettes they will inevitably develop cancerous tumors. Similarly, the word “can’t” colloquially means having a low probability of success and not the complete inability to succeed. Intervention that improve the probability of quitting smoking (like bupropion or quitlines for smoking) success are therefore said to cause improvements in the capacity for quitting.
Next, Christopher wants scientists to identify the source of “will” in the brain but I suggest that “will” itself is simply a term he has given a behavioral outcome – the ability to make a choice that falls in line with expectations. In actuality, “will” is more commonly used as a reference to motivation, which while measurable, isn’t really the aspect of addiction involved in cognitive control. Instead, what we’re talking about is “capacity” to make a choice. The issue is a significant, not semantic one, since the argument most neuroscientists make about drug abuse is that addicts suffer a reduced capacity to make appropriate behavioral choices, especially as they pertain to engaging in the addictive behavior of interest. If someone is attempting to get into a car but repeatedly fails, we say they can’t get in the car (capacity), not that they don’t want to (will). Saying that they simply “don’t” get in the car doesn’t get at either capacity or will but instead is simply descriptive. I don’t believe that science is, or should be, merely descriptive but instead that it allows us to form conclusions based on available information.
That there is a segment of individuals who develop compulsive behavioral patterns tied to alcohol and drug use and who attempt to stop but fail is, to my mind, evidence that those individuals have a difficulty (capacity) in stopping their drug use. Their motivation (will) to quit is an aspect that has been shown to be associated with their probability of success but the two are by no means synonymous. It is important to note, and understand, that the attribution for the performance should not fall squarely on the shoulders of the individuals. We humans are so prone to making that mistake that it has a name, “The fundamental attribution error,” and indeed, individuals who show compulsive, addictive, behavior do so because of neuropharmacological, environmental, and social reasons in addition to the complex interactions between them all. But no one is disputing that and in fact, the article used by Christopher to point out the notion of a “tipping point” in addiction directly points out that fact in the next paragraph (Page 4), which he chose not to reference or acknowledge.
“Of course, addiction is not that simple. Addiction is not just a brain disease. It is a brain disease for which the social contexts in which it has both developed and is expressed are critically important… The implications are obvious. If we understand addiction as a prototypical psychobiological illness, with critical biological, behavioral, and social-context components, our treatment strategies must include biological, behavioral, and social-context elements.” (Lashner, 1997)
Lastly, Christopher’s philosophical musings are interesting, but they seem to stray away from trying to find an explanation for behavior and instead simply deconstruct evidence. In a personal communication I explained that while most addiction researchers understand that addiction, like most other mental health disorders is composed of a continuum of control ranging from absolute control over behavior to no control whatsoever (with most people fitting somewhere in the middle and few if any at the extreme ends), categorization is a necessary evil of clinical treatment. The same is true for every quantitative measure from height (Dwarfism is sometimes defined as adults who are shorter than 4’10”) to weight (BMI greater than 30 kg/m²). I think it’s equally as tough to argue that someone with a BMI of 29.5 is distinctly different from an individual with a BMI of 30 as it is to argue that there is no utility in the classification. Well, the same applies for drug addiction, although some people categorically object to classification and believe it has no utility or justification.
Now for the evidence – “Choice” and “control” are not the same as “will”
Some people quit, even without help – Christopher and a number of the people he cites in support (Peele, Alexander), suggest that because some people do stop using that it can’t be said that there is a problem with any individuals’ capacity to stop. The problem with that argument is that it supposes that everyone is the same, a fact that is simply false. As an example I would like to suggest that we compare cognitive control with physical control and use Huntington’s Disease (HD or Huntington’s Chorea) as an example.
HD patients suffer mental dementia but the physical symptoms of the disease, an inability to control their physical movement resulting in flailing limbs often referred to as the Huntington Dance, are almost always the first noticeable symptoms. Nevertheless, HD sufferers experience a number of debilitating symptoms that originate in brain dysfunction (specifically destruction of striatum neurons, the substantia nigra, and hippocampus) and that alter their ability (capacity) to control their movements and affect their memory and executive function leading to problems in planning and higher order thought processes. So, while it is true that most people can control their arm movements, here is an example of individuals who progressively become worse and worse at doing so due to a neurophramacological disorder. There is currently no cure for HD but some medications that help treat it no doubt restore some of the capacity of these patients to control their movements. If a cure is found it would be difficult to say, as Christopher suggests of addiction, that the cure does not affect the capacity of HD patients to control what they once could not. I chose HD for its physiological set of symptoms but a similar example could easily be constructed for schizophrenia and a number of other mental health disorders (including ADHD and drug addiction). Importantly, cognitive control is a function of brain activity, activity that can become compromised as the set of experiment I will discuss next show.
An experiment conducted at UCLA (1) has shown that cocaine administrations reduced animals’ ability to change their behavior when environmental conditions called for it. Even more meaningful was the finding that once animals are exposed to daily doses of drugs, the way their learning systems function is altered even when the drugs themselves are no longer on board and even when the learning has nothing to do with drugs per se.
In the experiment, conducted by Dr. David Jentsch and colleagues, monkeys were given either a single dose (less than the equivalent of a tenth of a gram for a 150lb human) or repeated doses (1/8 to 1/4 of a gram equivalent once daily for 14 days) of cocaine. The task involved learning an initial association between the location of food in one of three boxes and then learning that the location of the food has changed. We call this task reversal learning since animals have to unlearn an established relationship to learn a new one.
Obviously, the animals want the food, and so the appropriate response once the location is changed is to stop picking the old location and move on to the new one that now holds the coveted food. This sort of thing happens all the time in life and indeed, during addiction it seems that people have trouble adjusting their behavior when taking drugs is no longer rewarding and is, in fact, even troublesome (as in leading to jail, family breakups, etc.).
In the experiment, animals exposed to cocaine had trouble (when compared to control animals that got an injection of saline water) learning to reverse their selection when tested 20 minutes after getting the drug, which is not surprising but still an example of how drug administration can causally affect an individual’s ability to make appropriate choices. As pointed above, the most interesting finding had to do with the animals that got a dose of cocaine every day for 14 days. Even after a full week of being off the drug, these animals showed an interesting effect that persisted for a month – while their ability to learn that initial food-box association, they had significant trouble changing their selection once the conditions changed. Remember, this effect was present with no cocaine in their system and with learning conditions that had nothing whatsoever to do with cocaine.
If that’s not direct evidence that having drugs in your system can alter the way your brain makes choices, I don’t know what is.
Another study conducted by Calu and colleagues with rats found similar (or even more pronounced) reversal learning problems after training the animals to take cocaine for themselves, clarifying that it is the taking of cocaine and not the method that causes the impairments.
Another entire set of studies has shown that stimuli (also known as cues or triggers) that have become associated with drugs can bring back long-forgotten drug-seeking behavior once they are reintroduced. This was shown in that Calu paper I mentioned above and in so many other articles that it would be wasteful to go through all the evidence here. Importantly, this evidence shows that drug associated cues direct behavior towards drug seeking in a way that biases behavior regardless of any underlying will. My own research has shown that animals who respond greatly to drugs (nicotine in our case) likely learn to integrate more of these triggers than animals who show a reduced response, indicating once again that these animals bias their behavioral selection towards drug-seeking more than usual. While we have more studies to conduct, we believe that genetic differences relevant to dopamine and possibly other neurotransmitters important for learning (like Glutamate) are responsible for this effect.
While we can’t do these kinds of experiments with people (research approval committee’s just won’t let you give drugs to people who haven’t used them before), there is quite a bit of evidence showing an association between trouble in reversal learning and chronic drug use in humans (see citation 3 for example) as well as research showing very different brain activity among addicted individuals to drug-associated versus non-drug cues (like seeing a crack pipe versus a building). All this evidence suggests that drug users are different in the way they learn generally, and more specifically about drugs, than individuals not addicted to drugs. When it comes to genetics, we know quite a bit about the association between substance abuse and specific genes, especially when it comes to dopamine function. As expected, genetic variation in dopamine receptor subtypes important in learning about rewards (D4 and D2) has been revealed to exist between addicts and non addicts. Without getting into the techniques and analysis methods involved in these genetic studies, their sheer number and the relationship between substance abuse and other impulse disorders points to a direct relationship between drug use disorders (and possibly other addictive disorders) and a reduced capacity to exert behavioral control. Less capacity for control is what researchers have found sets addict apart from non-addicts.
Summary, conclusions, and final thoughts
In closing, there are undoubtedly imperfections about the ways we diagnose addiction (drug addiction and others). It would probably be nice if we could figure out a way to incorporate what we know about the continuous nature of the disorder with the need for clinical delineation of who requires addiction treatment and who doesn’t. Addiction researchers are far from the only ones who wonder about this question though (the same issues are relevant for schizophrenia, depression, and nearly every mental health disorder) and I am certain that better and better solutions will emerge.
However, the discussion of stigma in this context needs to allow us to discuss the reality of addiction without having to resort to blaming and counter-blaming. If I describe the Toyota Prius as being slow but incredibly efficient I am no more stigmatizing than if I describe a Ferrari as being incredibly fact but wasteful in terms of fuel. The same applies, or should apply, to health and mental health diagnoses – Just because an individual is less able to exert cognitive control over impulses should not by definition call into question their standing as a human being. We are complex machines and by improving our understanding of the nuts and bolts that make us function we can only, in my opinion, improve our ability to make the best use of our capabilities while understanding our relative strengths and weaknesses. Any other way of looking at it seems to me to be either wishful (I can do anything if I want it badly enough) or defeatist (I will never be anything because I’m not good at X) and neither seem like good options to me.
1) Jentsch, Olausson, De La Garza, and Tylor (2002): Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys. Neuropsychopharmacology, Volume 26, Issue 2, Pages 183-190
2) Calu et al (2007) Withdrawal from cocaine self-administration produces long-lasting deficits in orbitofrontal-dependent reversal learning in rats. Learning & Memory, 14, 325-328.
3) Some evidence in humans from Trevor Robbins’ group: Reversal deficits in current chronic cocaine users.
|Posted in: Education
Tags: addiction, addictive, ADHD, Brain, capacity, cocaine, cognitive control, compulsive, control, depression, dopamine, drug, drug use, genetic differences, glutamate, hd, hippocampus, huntington's disease, learning, mental health, mental health disorders, motivation, obesity, peele, reversal learning, schizophrenia, science, striatum, substance abuse, substnatia nigra, treatment, triggers, UCLA, will
September 27th, 2011
Is addiction an issue of bad choices or is it a case of biological, compulsive, necessity?
If you know anything about me and my views, you know that I think little of anyone who tries to separate these. I see and talk to people all the time who are stuck in compulsive behavioral patterns but with some education and good helping of supportive tools they can begin to change these patterns and return to normal life.
But then there are those who just don’t seem to ever get better.
Be it lack of motivation, readiness, mental health issues, or a simple case of not having found a good enough reason to stop, these addiction clients can be the most frustrating and the most rewarding to work with. Any victory, no matter how small, with a difficult patient can put a big smile on my face. I love nothing more than to have someone tell me that they’re sending me a very “tough” or “resistant” client only to discover that when they’re with me, neither of these traits is really representative of their personality.
Or maybe it’s just a matter of perception, right?
Life is about choices, and compulsive or addictive behavior is certainly included in that equation. But that doesn’t mean that all choices were created equal. Indeed, all the evidence points towards the conclusion that choices are differently easy or difficult depending on a person’s experience, biology, and environment. In so many animal studies (called conditioned place preference experiments) researchers have shown that exposure to an environment in which drugs are given makes an animal much more likely to spend time there. We’re talking about 3 to 4 exposures at most and animals find it hard to leave – imagine what 3 to 4 years of that kind of exposure can. Self-administration studies (the kind where animals press levers and buttons for drugs) have revealed that animals can go through some pretty lengthy, complicated procedures to get their drugs and that their experience makes them continue pressing for a long time after the drugs have been removed from the equation. If a rat can learn to press one button, wait some time before pressing another, and finally poke his nose in a whole to get a hit, you can bet that people can do the same without needing to resort to explanations about unhealthy family environments. Family environments matter, as do friends, neighborhoods, and cultures – along with neuroscience they all create the picture we end up calling addiction.
As far as I’m concerned, there is no doubt that experience with drugs can lead to reduced self-control over activity that has been linked with drugs. Add triggers and cravings to the mix and the question of some compulsivity in addiction seems moot to me. Still, there is no doubt that compulsive or impulsive behavior can be helped when you’re not approaching the client as if they are somehow flawed but that doesn’t mean they weren’t compulsive in the first place.
Trying to make the picture simpler is like trying to draw a Picasso without being able to sketch a simple bowl of fruit – it might fool those who don’t know much but it’s far from true cubism.
|Posted in: Education
Tags: addict, addiction, case, choice, choices, compulsive, difficult, know, mental health, motivation, perception, picasso
September 2nd, 2010
My friend Patrick as SpiritualRiver reminded me of an issue that I think is somewhat obvious to many drug addiction researchers but may not be to others.
The way I see it, there is a specific reason behind much of the research into medications, or other interventions, that will help drug addicts in their transition to recovery:
If we can figure out a way to reduce the extreme hold that drugs have over addicts, we may just make it possible for a much larger proportion of them to get their life back and succeed in addiction treatment.
Long term drug use causes some serious alterations in the neurological functioning, and therefore the behavior, of substance abusers. As it stands, it requires a great deal of motivation, support, and perseverance to overcome a serious drug habit.
Still, if we can somehow make it easier, either by intervening earlier, or by somehow speeding up the brain’s recovery, or by creating the kind of functioning needed for the person to be able to make deliberate, informed decisions, we could just even the playing field a little. Right now, there are some medications out there that do just that, and as far as i’m concerned, regardless of what people say about substituting one addiction for another (which they do for methadone and buprenorphine), if we can get addiction back on the road to a functioning, contributing, life – that’s recovery too. Harm reduction is just that, a way to make people’s lives easier even if they can’t, or aren’t ready, to completely give up drugs. I for one don’t understand why so many people are insisting that it’s all or nothing. In case you haven’t figured it out, that’s not how life normally works, in recovery or anywhere else.
And by the way, that’s definitely not the only way to intervene – medication like modafinil and other pharmacotherapies that help addicts make better, less impulsive choices, also work; add to that bupropion (an antidepressant and a nicotine addiction medication that has a low abuse potential), as well naltrexone (good for opiate overdose but also for alcoholism treatment) and you begin to see that this area of treatment is getting better at providing solutions that are meant to supplement, not replace, traditional treatment modalities.
The end goal is to help the addict and as I’ve said before, I think we should use all our tools.
July 9th, 2010
If you’ve been with us for any length of time, you’ve already read about the addiction-brain effects for specific drugs. I think it’s important to understand some of the more general changes that occur in the addicted brain regardless of the specific drugs used.
One of the most common effects of long term drug use is something called tolerance, or the reduced effect of a drug dose. A lot of people know about this one, especially if they’re users and have found themselves needing to use more and more to get the same effect. However, while this is the most known, it is not the only change in the body, or brain’s, response to drugs with repeated use. The other effect, known as sensitization, is characterized by the exact opposite reaction – an increase in the response to the drug.
Tolerance & Withdrawal in the addicted brain
The exact mechanism by which tolerance occurs is different for each drug, but the overall concept is the same. With repeated drug administrations, the body adjusts its internal processes in an attempt to return to its initial level of functioning. Drug use normally causes greater quantities of neurotransmitters like dopamine, serotonin, the opioids, and adrenaline to be present in the drug user’s synapses (see here for a review). The body counters this by reducing its own release of these chemicals, reducing the numbers of receptors that can be activated by the neurotransmitters, and increasing functions known as “opponent processes” that are meant to counter their activity.
The interesting thing about tolerance is that by reducing the level of these important neurotransmitters, addicts are left with another, possibly more important effect, which is the loss of the addicted brain’s ability to respond to any reward, including natural ones like food, sex, enjoying a good football game, or anything else. Essentially, this sort of cross-tolerance leaves the addict less able to respond to rewards in general.
The reduced response to drugs, and the corresponding changes in the body and brain’s own functioning, have long been thought to be a major cause of addiction. The withdrawal that results once drug taking stops is closely linked to the development of tolerance. Still, we now know that tolerance and withdrawal are not necessary, and certainly not sufficient for the development of addiction. Nevertheless, they are referred to as the physical dependence portion of addiction and are often are part of the overall picture.
Sensitization is the term used for an increased response to the same dose of a drug. That might sound a little oxymoronic after the tolerance discussion we just had, but bare with me.
Tolerance commonly develops when drug use is constant, or ongoing. It’s an aspect of chronic, long-term, use. On the other hand, sensitization is likely to occur when a user engages in intermittent, binge-like, drug use happening either once daily, or with even greater spacing (as in once every few days) and in large quantities. When you combine chronic use with binge behavior, you can actually get both responses.
Sensitization to drugs has been shown for physiological responses like heart-rate, blood pressure, and movement in animals and humans. More importantly, sensitization plays a part in increasing the motivation for drug use. Just like sensitization increases the physical response to drugs, there is a corresponding increased response in the addicted brain in areas important for motivation (like the NAc and VTA for instance). If an addict responds more to their drug of choice after repeated use, it should come as no surprise that sensitization has also been hypothesized to play an important role in the addiction process.
Drugs cause brain changes that drive addiction
When both tolerance and sensitization develop in someone who has been using drugs, they’re left with a reward system that is less responsive to rewards in general while being more responsive to the drugs they’ve been binging on and to cues (or triggers) that are associated with those drugs. If that sounds like a recipe for disaster, it is. If you’re an addict yourself, you don’t have to imagine this, you’ve lived it – A state where nothing seems rewarding without being high.
The problem is that both tolerance and sensitization are examples of changes in response to drugs that are completely outside of the control of the user. There’s no doubt that the average drug user doesn’t think about, or even recognize, that as they continue to use drugs, their body adjusts in multiple ways that can make it that much harder for them to stop use at a later point. It should be clear that this is not an issue for everyone – both tolerance and sensitization require repeated administration of drugs that are pretty close together. But they don’t require hundreds of uses, a few days with continuous, or intermittent use, are often enough to bring about these changes in the addicted brain.
We often hear that even the first hit of a drug can cause someone to be addicted. While there’s little doubt that even a single drug administration can change brain response in important ways, I can say with absolute certainty that using a drug repeatedly cause long-lasting changes in the brain chemistry that make future drug use more likely.
|Posted in: Drugs, Education
Tags: addiction, adrenaline, binge, brain effects, dopamine, drug use, motivation, NAc, opioid, opponent processes, response, sensitization, serotonin, synapse, tolerance, VTA, withdrawal