Shame on me – Stigma and addiction in treatment

I keep hearing that back in the old days of addiction treatment, shame was the main motivating factor used by rehab counselors. Everyone admits that it proved to be a horrible motivator. It simply didn’t work! With all the advances in research into addiction, that must have changed, right?

I don’t think so. I see shame and stigma every time I hear an addict talk about their drug use. The shame is there in their eyes as they tell the stories of their trouble and the struggles of their recovery. Given the low rates of success in addiction treatment, the shame rests firmly in the inability to quit as well. A relapse is often seen as the ultimately shameful experience for an addict. The stigma of addicts as hopeless is rampant.

Still, we have evidence of genetic predisposition to drug abuse and addiction, we know of environmental factors that make it more likely that people will get hooked. The effect of many drugs on the brain make unsuspecting lab animals as likely to become addicted as any one of us and I’m pretty sure that shame doesn’t play a role in their process.

With all this evidence, why is the stigma of drug addicts still around? Why are they the only ones being blamed for their condition?

The evidence I cited isn’t that different from that known for cancer, yet we scarcely blame cancer patients for their disease. Even in the case of smokers who become ill, their is still sympathy for their suffering. So why are addicts different?

There are good addiction treatment options out there, as long as we don’t give up on the person and simply view their addiction as evidence of their weak character. Given the changes that long term drug use produces in the brain, it’s a miracle anyone recovers at all. We should be grateful for that.

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.

The alcoholism gene? That’s quite a long story!

If you were trying to find something to blame alcoholism on, genetics would be a good place to start: As much as 50-60% of the risk of becoming an alcoholic is determined by a person’s genes (1). We’ve discussed the genetics of addiction in general as they relate to other condition like ADHD, depression, and anxiety, but the risk that a person may become an alcoholic also depends on their sensitivity to alcohol’s effects, development of tolerance, susceptibility to withdrawal symptoms and alcohol-related organ damage, among others.

Alcohol related genes and alcoholism

The genetic causes of alcoholism are not always simple and straight-forward, especially because genes interact with one another (and the environment) in ways that can create unexpected results. However, some aspects of the genetics of alcoholism are clear, like the case of the genes that affect the speed with which liver enzymes will break down (metabolize) alcohol and its byproducts. Some people have a gene variation which produces liver enzymes that have trouble breaking down acetaldehyde (ALDH2-2, very common among Asians), a basic breakdown product of alcohol. As the levels of acetaldehyde increase, people experience flushing, nausea and rapid heartbeat which makes them less likely to consume alcohol and therefore less likely to become alcoholics. Not surprisingly, alcoholism rates have been historically low in Asian populations. However, recent increasing trends of alcoholism in Japan show that if you work at it hard enough, even a genetic predisposition that is supposed to protect you from alcoholism is no match for good old social pressures to drink.

Researchers have identified one neuropeptide (called NPY) that is located near known alcohol-related traits and indicates an alcohol preference in rats, consequently increasing response to alcohol (1). The effects of alcohol are increased with certain forms of NPY and  that gene has been linked to addiction-related, and anxiety, behaviors (2). It is also generally accepted that genes that affect the activity of serotonin and GABA (one of alcohol’s main targets in the brain and body) are likely to be involved in alcoholism risk.

It is important for everyone to remember that there is a predisposition to becoming an alcoholic and that alcoholism is a disease, not simply an outcome of poor behavior . There are ways to treat both the physical symptoms and the underlying addiction in alcoholics.

We’ve barely scraped the surface of the numerous influences on alcohol’s effects, and the predisposition to alcoholism, but hopefully this post leaves you with a slightly better appreciation of the complexity of the matter…

Co-authored by: Jamie Felzer

Citations:

1. Alcohol Alert-National Institute on Alcohol Abuse and Alcoholism. No.60. July 2003

2. Anxiety and alcohol abuse disorders: a common role for CREB and its target, the neuropeptide Y gene. Trends in Pharmacological Sciences, Volume 24, Issue 9, September 2003, Pages 456-460.

Nicotine addiction and genetics – It’s the little things that matter in smoking addiction

We’ve known for a while that genes play a role in addiction in general and that nicotine is addictive at least in part because it activates receptors for a chemical called Acetylcholine (ACh) that are found all over the brain and body. Nevertheless, finding the specific mechanism for the genetic predisposition has been difficult.

Some recent large-scale studies undertaken at the University of Colorado and other institutions  around the country have made some very exciting discoveries in this area.  It seems that up to now, researchers were focusing on the most common type of ACh receptor, but that several other types play very important roles in determining how people will respond to nicotine the first time they use it, and how much they’ll be likely to use in that early period. It should be pretty obvious that both there factors can play a huge role in nicotine addiction, and indeed, it seems they do.

So here’s a little breakdown of the findings:

  • Initially, research examining the influence of ACh receptor proteins on nicotine addiction focused on the α4 and β2 subunits. These are the most common ACh subunit proteins in the brain. Animal and human imaging studies have shown that ACh receptors consisting of two α4 and three β2 subunits are critical for the rewarding effects of nicotine.
  • The new studies focused on genes that code for less common ACh receptor proteins. Researchers have implicated the genes for the α3, α5, and β4 proteins in early initiation of smoking, the transition to dependence, and two smoking-related diseases: lung cancer and peripheral arterial disease.
  • Investigators also found that whether or not a person becomes dizzy the first time he tries smoking, as well as his or her risk of addiction, depends in part on the genes for the α6 and β3 proteins.

Taken together, the results suggest that genes for several ACh receptor proteins drive different aspects of the multi-step process of nicotine addiction.

The importance of the first time

Interestingly, the findings regarding first smoking experience seem to suggest that the intensity of it, rather than simply how pleasurable it was, are associated with the likelihood of becoming dependent later on, according to Dr. Ehringer, one of the studies’ lead author. For example, the same people that reported feeling extremely dizzy their first time were more likely to report that they became addicted to nicotine. The genetics analysis supported this same finding.

From trying to becoming addicted

Other studies revealed that additional genetic variations, including those in the the gene for the α3 ACh subunit, the β3 subunit, and the α5 subunit seem to code for the likelihood of being able to quit smoking. The α5 protein, which is present in the brain’s reward area, seems to influence the risk of smoking a pack of cigarettes a day as compared with smoking fewer than 5 cigarettes a day.

Conclusions for smoking addiction

I’ve said it before and I’ll say it again and again – no matter how much we try to ignore it, genetics play a huge role in every aspect of our being, including the likelihood that we will become addicted to a substance. By learning more about the role of specific genes and specific types of receptors, researchers can attempt to uncover possible medications that will help us in treating addiction. Still, I think that the bigger take-home message is this: There are reasons behind the development of addiction that are beyond anyone’s control. Thinking of genetic causes and relating them to morality simply makes no sense.

 Citation:

Lori Whitten (2009). Studies Link Family of Genes to Nicotine Addiction – Genes for protein constituents of nicotinic acetylcholine receptors influence early smoking responses and the likelihood of nicotine dependence. NIDA Notes, 22.

Addiction is a disorder of control, not choice – A response to Heyman’s book

I was working on the first chapter of my book today and the issue of choice plays a prominent part in it. I’m a little pissed at Dr. Heyman, whose name sounds like something a stoner might say, about his book, “Addiction – A disorder of choice”.

The thing is that at its most basic, every action we perform seems like a choice. Whenever you take a step, think a thought, or feel a feeling, you’re “choosing” that specific action rather than an almost endless number of other options.

However, when choices are involuntary, or are made below the level of consciousness, as is often the case not only with addiction but in many other instances in life, than I believe the word choice is being misused. Dr. Heyman knew that his book would cause controversy, but he also knows very well that the mere exposure to substances can cause profound changes in the way animals make choices.

Drugs alter the way the brain works, including the ways choice are made. They affect the internal value given to rewards, they alter the brain’s ability to adjust to new situations, and they change the brain’s basic neurochemistry to cause profound effects on overall function that no doubt alter many more processes.

And I haven’t even touched on the ways that different people are pre-programmed to make choice in different ways because of their genetic make-up. Whether you call it choice or not isn’t the question. Rather, the question is one of control. Addiction is a disorder of control.

About addiction: Genetics, sugar, drinking, and more.

These are some useful articles about addiction I’ve found online. While they cover some topics we’ve discussed on here, I think it’s always better to be more educated!

From Addiction Recovery Basics – Personality Vs. Genetics

From Beating Addictions – A little Q & A about sugar addiction

From Breaking the Cycles – A new online tool to assess drinking problems

From Addiction Inbox – A nice review of 2008 research findings having to do with addiction.

More links to come next week!!!