Loss, but not absence, of control – How choice and addiction are related

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

The toyota Prius is slow but efficientIn 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.

Citations:

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.

Science Versus Religion – Mortal enemies or hopeful friends?

The feud between religion and science can be compared to the Montague and Capulet relationship – hateful at times, dismissive often, and bridged rarely, often with tragic results for those who try.

A recent article in the journal Science (see Can Science and Religion Get Along?) discussed a controversial panel that aimed to bring together players from both sides in the hopes of starting some sort of dialog. There were cries of foul from both sides before the panel took place, but to me it seems that conversation in general is good as long as both sides come to the table with the right intention – to listen and not just talk. Continue reading “Science Versus Religion – Mortal enemies or hopeful friends?”

Understanding addiction research will require us to argue our corner but be flexible to change corners.

Hello everyone,

My name is Christopher Russell, I am a doctoral student in psychology at the University of Strathclyde in Glasgow, UK. My addiction research interests are wide and varied, but my core interests are in addiction theory (“why people do what they do”), the issue of freedom to control when using drugs, interpretations of addiction research evidence, and the use of licit and illicit drugs in the law.

Respect and rational debate of addiction research

Dr Adi Jaffe has very generously asked me to become a contributor to A3 and after reading about what A3 stood for (the mission and the abbreviation) and what Dr Jaffe is trying to achieve through A3, I am delighted to be a part of A3. Adi noted in a previous post that we do hold some different opinions about the nature and course of addiction. Above our differences, however, I respect that Dr Jaffe and I are able to debate addiction research rationally, respectfully, and vigorously without either of us resorting to ideological proclamations, disrespect for the alternative view, claiming a moral high ground or attacking each other’s moral character, or worst of all, name calling! Such people are hard to find in the academic world! The truth is that I, like Dr Jaffe, am still learning about addiction, and I’m not foolish enough to believe that my way is the way! If addiction research over the past 100 years has shown anything it is that a researcher would be foolish to hang his hat on any interpretation and proclaim it as fact – for example, for the past 200 years, masturbation was considered the most prevalent psychiatric disorder until it was replaced by drug use, and up until 1973, homosexuality was still diagnosed and treated as a form of mental illness! We must be willing to bend with the wind, to accept when addiction research evidence invalidates our beliefs, and to respond to falsifications by constructing models which stand up to our efforts to falsify them.

A3 and the fluid landscape of addiction research

The landscape of addiction research changes by about 50% each decade, as do many scientific ideas, so it is important that we all hold our beliefs about addiction lightly and be willing to consider that some dearly held addiction “truths” may not be as truthful as we had thought, perhaps hoped. Scientists are constantly revising what they thought they knew, changing their approach to measuring and conceptualising the problem, disseminating the latest findings to the public; like any good scientist, those who are involved with addiction, either personally or professionally, should always try to update their model, and sometimes, evidence can arise which causes us to question everything we thought we knew about the nature of a problem. Such evidence may require us to not merely adapt our exisitng models of the problem, but if called for, to abandon them in favour of more potent models which need not necessarily be liked or fully understood.

Hearing what addiction research is telling us, not what we want to hear

However, despite our pledges to be good scientists, our basic ways of thinking tend to get in the way of building better models of a problem. For example, a classic contribution of psychology research has been the finding that people prefer to try to discredit a new piece of evidence about a concept which doesn’t fit with their existing understanding of that concept rather than assimilate the new evidence into our understanding because it is cognitively easier to leave our belief structure as it is. This phenomenon is quite common in the addiction research community; some people just refuse to believe that addiction could be something other than what they had long thought it to be, and no amount of validated, replicable evidence to the contrary will move them to revise their beliefs. It is regrettably common that, for some, beliefs about addiction are based on an unwavering ideology rather than a science-grounded conclusion. Addiction researchers cannot afford to be this pompous, lazy, or inflexible; too many people are counting us to get the right answers to them, no matter who they come from or what form they come in. I know that my contributions to A3 are only useful to the extent to which they help get people from where they are to where they want to be. To achieve this, I must argue my corner but be willing to bend when the wind blows. We all must.

In the hope that I can be both teacher and student of A3, I believe that the value of my arguments will be measured by how well they hold up in the face of your most passionate, insightful criticism. Therefore, I invite all those who read my contributions to criticize, refute or support any of my arguments when you feel it is warranted. I will always try to give an intelligent answer and I swear to never resort to clichéd answers, bumper sticker answers, or the “it just is because it is” answer, which is in effect, no answer. And I will never resort to name calling (except when you really deserve it!).

I look forward to providing you with thought pieces, philosophical contributions, reviews of evidence, and most of all, interacting with you the readers, the lifeblood of A3.

Christopher

Why the addiction-brain connection has to be part of the addiction treatment picture

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.

Believing in Recovery: Addiction treatment and faith

Faith Hill seems to believeSarah Henderson return with another article about addiction treatment and recovery. This time, Sarah gets all philosophical with us and discusses the concept of faith in recovery. Personally, my faith is and always has been very logic-based. I’m not a very spiritual person, and the things that are most important to me are usually right around me – my family, my work, and my new baby boy Kai. I’m not against the concept of a higher power, I just don’t feel a deep need for it and it’s probably the one concept that doesn’t keep me up at night (which is weird now that I think about it). But in the addiction treatment and recovery field, faith is a common word that can take on different connotations so I think it’s important to talk about.

Believing in Recovery: Articles of faith

I have a friend who is researching the history of the Bible. He’s on a bit of a mission, searching for some verifiable proof of certain articles of faith. He and I have lengthy discussions on this, going back and forth on the nature of faith, on whether or not one needs proof to believe. His position is, wouldn’t it completely change everything if we COULD verify the existence of God? My position is, yes it would; proof would make faith irrelevant.

Think about it. If you have proof of the existence of something, then believing in it is no longer faith, is it? It’s not even belief. It’s just actuality. I believe there’s a reason that we as a species have never been given proof of the existence of a higher being. (From here on out, I’m going to refer to this being as God.) I don’t believe that we, with our tiny human brains, have the capacity to understand or conceive of God. I also think part of the wisdom in perpetuating the mystery is that it keeps us engaged, keeps us seeking, keeps us wondering.

Faith is a very common word around addiction treatment and recoveryThe character House, MD (who is an atheist) said on one episode, “I love how people are always so proud of believing in something that isn’t there, like that’s some sort of accomplishment.” Well, actually is IS an accomplishment. Believing in nothing doesn’t take a whole lot of work. But believing in God without any verifiable evidence? That takes effort, takes devotion, takes love. Faith is a difficult path, no matter what you believe in. I also think that in believing in something outside of ourselves teaches us to believe in each other. For instance, when falling in love; you have to hold out your heart with no certainty that this person will not crush it. When forgiving someone; you are risking that they will hurt you again, but trusting that they won’t. When learning something new; you may fall flat on your face, but you have to believe that you can do it. If people never took a chance on each other, no one would ever get married, move away, try a new career, or have kids. Eventually, we all have to have faith in something, even if it’s just our own capabilities.Can you imagine a world without faith? I can’t. It’s what helps us believe in the future, surrender to the moment, look up when the world is falling apart and trust that things will right themselves soon.

When it comes to recovery, faith is essential- and I’m not just talking about God or religion. While attempting to recover from an addiction or other self-destructive behavior, you must have belief. First, you need to believe in yourself. You have to have confidence in your own ability to fight, to know that you have it in you to make it. And when that belief falters, as it inevitably does, you need to have faith in something outside of yourself too. You’ve got to hold on to something- God, a friend, the stars, the color blue- some entity to turn to when your confidence in yourself is flagging. And of course, there will be times when you are overwhelmed and feel like the pain of the transition is going to last forever. You have to be loyal to the concept that if you continue on the path of recovery, eventually you will find peace; that’s the “fake it ’til you make it” part. But it doesn’t happen without faith.

The word “faith” in itself has become so loaded that I think we often lose sight of what it really means; though truthfully, I think we each have to create our own personal definitions. To me, faith mean taking chances. And in recovery, that meant everything from eating when I wasn’t sure if it wold make me gain weight to reaching out to a friend without being sure I would get a response. All of those little risks built on each other until I developed some true self-confidence. With that in hand, I was able to make more proactive choices that have helped me get to the place I am now.

No matter what you believe in or how you define faith, I think we can all agree that recovery is something that cannot be done alone. It requires both external AND internal resources. At some point we all are faced with the fact that it will probably feel worse before it feels better; and in most cases, the only thing that keep us walking across that painful bridge is having faith that we’ll reach the other side.

A final word from Adi about  faith and believing in recovery

As I mentioned above, my faith is centered the things close to me and I don’t dedicate too much time to wondering about the existence of that god everyone is fighting about. Unlike Sarah, I see belief as something different than religious faith. As a scientist, I can believe information and data about addiction without having to make any leap other than in the objectivity of science and the honesty of scientists (which has certainly proven to be wrong at times). However, while I can see why people believe in a god, from the beautiful shafts of light that bounce off an ocean after a storm to the notion that there must be a master plan to make sense of all the pain and suffering in the world, I sometimes wish that I believed in a real higher power.

That’s not to say that I can’t see any power out there as greater than my own – Nature, humanity, my family, and the love I feel for my son are all ideas who’s incredible power is easy for me to grasp. Personally, that’s enough. When it comes to addiction treatment and recovery, I’ve seen the information, I’ve read the research, and I’ve personally experienced and viewed many success stories so belief doesn’t take a leap for me. That’s why I think education is so important and anonymity can be dangerous – By making successful recovery a point-of-fact, we make it easier for active addicts, and their loved ones, to believe that a different life is possible.

Addicts’ brains depressed but normal users… normal.

A paper that’s about to be published in the journal Science has found at least part of the difference between the brains of addicted individuals and those that use recreationally.

The question as to why only some people get addicted to drugs has been a difficult one to answer. Still, there’s no doubt that only a relatively small fraction of those exposed to drugs develop the compulsive, often destructive pattern of use we associate with addiction. The pattern holds in animal research too – even though all the animals in an experiment get the same amount of drugs, delivered in the same way, only some of them develop addictive drug taking. It seems there’s something different about addicts’ brains, but what is it?

What’s different about addicts’ brains?

We’ve found quite a few things that differentiate addicts’ brains from those of normal research participants. These include lower density of a certain type of dopamine receptor (D2), reduced activity in specific brain parts like the OFC (orbitofrontal cortex) that are important in decision making and behavioral control. Still, if we start with what is supposed to be a pretty similar group of rats and give them all the same drug, for the same time, in the same amounts, why do only some get addicted?

This recent study found that a specific neuronal process called LTD (Long Term Depression), that is important in learning (or what we call plasticity) is suppressed in addicted animals for far longer than in animals that end up not not displaying addictive behavior. Even though all animals displayed this sort of deficiency in LTD right after learning to take drugs, only the addicted animals showed it when tested two months later.

Since the difference was seen in an area of addicts’ brains called the Nucleus Accumbens, a very important area for learning about rewards, it seems likely that it plays an important role in addicts’ inability to change their behavior after they’ve started using drugs. Past research has already identified this as a problem with something we call “reversal learning” but it seems we may have just found at least part of the mechanism.

Now we have to figure out why some animals show this sort of pattern and others don’t. Genetic variability seems like a good place to start here.

Citation:

F. Kasanetz, V. Deroche-Gamonet, N. Berson, E. Balado, M. Lafourcade, O. Manzoni, P. V. Piazza, Transition to addiction is associated with a persistent impairment in synaptic plasticity. Science 328, 1709–1712 (2010).

Like advancements in medical care and science? Then support animal research

There was a Pro-Test for Science rally on the UCLA Campus today.  The goal of the rally was to spread awareness about the utility of animal-research and to help combat extremists and prove to the community and world that the ethical use of animals for biomedical research is absolutely vital to the progress and success of advancements in science.

Many of the treatments that we discuss on this site are available because of extensive research with animals. In fact, many scientific discoveries have been possible largely because animal research is an available tool for researchers. Immunizations, medical treatments for Parkinson’s, Alzheimer’s, and diabetes treatments have all been advanced greatly through the use of biomedical research with animals. Of course, great care is always taken to ensure humane treatment of the animals used.  Animals prove a vital part of advancements in medicine, genetics and other research.

Biomedical scientists endure many trials in order to become experts in the type of research techniques we’re talking about here, including extensive schooling, years of training and of course many thousands of hours spent in a lab, all for the benefit of humanity.  They should not have to additionally endure the harassment of extremists and fear for their safety and the safety of their loved ones who often are caught in the middle.

Debate is healthy; discussion is good. But the harassment and terrorizing of researchers must stop if we’re to consider ourselves an open, educated, society. All biomedical researchers want is to better society by finding cures for the many things that plague our world today, so what everyone should really be doing is thanking them.

Co-authored by Jamie Felzer