Sunday, April 18, 2010

biological determinism and free will

A whole lot of energy goes into proving or refuting the  biological basis of undesirable behavior.  In large part, these are political arguments.   If it is my genes/my brain/my disease that 'made me' use drugs/kill my neighbor/be homosexual, then I should not be held accountable.  I am sick, not bad.  Not so says one of my favorite social theorists, Nikolas Rose.   In great article in the History of Human Sciences (Vol. 13:1), called Screen & intervene: governing risky behavior, Rose  notes how resoundingly biological dermininism has failed in the US courts.  He goes on to say:

"Indeed, the trend of contemporary legal thought, especially in the USA, is to operate on the premise of the inescapability of moral responsibility and culpability. On this basis, no appeal to biology, biography or society should be allowed to weaken moral responsibility for the act, let alone to diminish the requirement that the offender be liable to control and/or punishment. In this context, the argument from biology is likely to have its most significant impact, not in diminishing the emphasis on free will necessary to a finding of guilt, but in the determination of the sentence. This is unlikely to be in the direction of mitigation. For if antisocial conduct is indelibly inscribed in the body of the offender, reform appears more difficult, and mitigation of punishment inappropriate. More likely are arguments for the long-term pacification of the biologically irredeemable individual in the name of public protection."

Yikes...  So much for the argument that medicalization beats criminalization.  If our medical arguments can be used to create 'biologically irredeemable' individuals (see the post on chronic, relapsing conditions below), we may be doing more harm than good.  Rose goes on to point out the ways in which new neuroscientific technologies are being used to identify people "at risk" or predisposed to criminal behavior.  Soon, you may not even have to commit a crime to become suspect.

Saturday, April 17, 2010

Addiction = chronic, relapsing disease? Not for most...

 
So in my ever pokey quest to obtain the elusive PhD, I’ve been reading Addiction: A Disorder of Choice by Gene Heyman.  Super interesting and provocative so far.  I’m sure I’ll post more about the book later, but for now I want to mention his very helpful analysis of studies on the prevalence and natural history of addiction.  As I’ve written before on this blog, the two dominant models of addiction are (and have been for decades) a disease model and a criminal justice model.  Setting aside the criminal justice model, the disease model is generally characterized by two (not mutually exclusive) discourses: 1) addiction is a brain disease and 2) addiction is chronic, relapsing condition. 

Heyman takes a close look at the scientific literature to better understand where the ‘chronic, relapsing condition’ notion comes from and how accurate it is.  He notes that most of the studies upon which this paradigm relies are of based on samples of people in treatment.  Turns out, not surprisingly, that those in treatment are quite different from others who use drugs but do not enter treatment.  Heyman reviews several large studies based on samples of the general population, which reveal that, in sharp contrast to the rates of relapse among treatment-based samples, most folks who have been addicted to drugs quit on their own and do not relapse.  In fact, three of largest national studies suggest that almost 80% of people who were addicted at one time are able to quit drugs and stay off them.  Qualitative studies of former addicts support these data and indicate that many people quit as they mature and/or have increasing reasons to quit (e.g., job, family, health).   

Research looking at what distinguishes treatment- and non-treatment-based samples shows that the biggest difference is that those in treatment-based samples have much higher rates of psychiatric comorbidity, which could plausibly affect the natural history of addiction quite differently.  Heyman has taken a lot of heat for his primary thesis that addiction is a choice, but I think his analysis of these studies is really important.  So much of what we know about addiction is based on research samples of those in treatment (my own included), which we know to be biased.  A broader view suggests that, for a whole lot of people, addiction is not a chronic, relapsing disease.  I am not suggesting that there are no folks who experiences addiction as a disease.  I've known lot of people who do.  But, I've also met a lot of people who reject the disease model of addiction and do not feel it resonates with their own experiences of addiction or recovery.  What does seem to be true is that addiction is experienced very differently by different people.  Maybe that's why I'm so interested in how the sociology of the body might be able to help lend some insights into how and why embodied experiences of addiction and recovery are so varied.

Friday, April 16, 2010

McClellan Resigns from ONDCP

Here's some bad news in my opinion (as reported by JoinTogether.org):

Respected addiction researcher Tom McLellan has announced that he will resign as deputy director of the Office of National Drug Control Policy (ONDCP) this summer.
McLellan told Alcoholism and Drug Abuse Weekly in an interview that he was not unhappy with ONDCP's mission, its personnel, or the forthcoming National Drug Control Strategy. "There's no deep dark secret here -- I'm just ill-suited to government work," he said.
ONDCP issued a statement on April 16 confirming McLellan's plans to resign. "Tom has been a leader in helping the Obama administration fashion a comprehensive and balanced approach to drug policy that puts new emphasis on prevention, treatment, and recovery while acknowledging the important role of law enforcement," said ONDCP Director Gil Kerlikowske. "I will miss having Tom at my right hand, but we will continue to benefit from his wise counsel and knowledge."
McLellan said he would remain at ONDCP over the next several months to help implement the new drug strategy. "With the passage of health care reform and the crafting of the new drug control Strategy that will be released soon, I believe we have laid the foundation to make real progress in reducing drug use and its consequences," he said.

Saturday, April 3, 2010

This is your brain on bacon

Have you noticed lately the increasing effort by public health advocates to start regulating food in ways that are similar to tobacco and alcohol?  Building on the huge success of tobacco policies that reduced smoking rates dramatically over the past several years, public health advocates are now turning their attention to fat, salt and sugar.  The skyrocketing rates of obesity and concomitant health care costs make their case pretty compelling in my view.  In fact, my work place, The New York Academy of Medicine, is involved in campaign to tax sugar-sweetened beverages.  You can get involved by clicking here.

So I am not universally adverse to drawing parallels between food and drugs, but this new study pushes my critical sociologist buttons.  Check your animal cruelty sensibilities here and listen to the methods.  Rats were implanted with electrodes and then fed this:
The cafeteria diet consisted of bacon, sausage, cheesecake, pound cake, frosting and chocolate... 

Long story short...  the rats that had the junk food diet available to them all day, not only grew obese, but become compulsive eaters and continued to eat even when they received an electric shock for doing so.   Here's the part I object to (rat mistreatment aside):

These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.

So it's not the equation of compulsive eating to addiction that really bothers me...  it's the reduction of both to neurochemical processes.  I am sure there are biological components to addiction and maybe for addictions of all types.  But what does it mean when we tell someone with an addiction that they have a brain disease or tell someone who is obese that eating bacon down regulates your striatal dopamine D2 receptors?  And what does it mean for our social and political responses to the problem of addiction?  

Stanton Peele and others have done some interesting critiques of the disease model of addiction (of which the brain disease model is just one subset).  As Granfield and McCloud discuss in their book about people who quit drugs on their own, Coming Clean, it turns out that a lot of people don't like being told they have a chronic, relapsing disease.  Not only does that model and rhetoric belie the reality that the vast majority of people who use drugs stop on their own, it isn't an empowering message for people who are trying to quit.  The disease model is not without it's advantages, however.  Sending people to treatment sure beats locking them up, and one can argue that having a disease is less stigmatizing than the other popular construct -  addiction is a failure of will.  But surely we can come up with a more nuanced model for addiction than either of those.  While you all figure that out, I am going to have a bacon cheeseburger.