Showing posts with label Marc Lewis. Show all posts
Showing posts with label Marc Lewis. Show all posts

Wednesday, September 26, 2012

Does Brain Research Obscure Addiction’s Root Causes?


Did Dickens Get It Right?

Breathe the polluted air, foul with every impurity that is poisonous to health and life; and have every sense, conferred upon our race for its delight and happiness, offended, sickened and disgusted, and made a channel by which misery and death alone can enter. Vainly attempt to think of any simple plant, or flower, or wholesome weed, that, set in this foetid bed, could have its natural growth, or put its little leaves forth to the sun as God designed it. And then, calling up some ghastly child, with stunted form and wicked face, hold forth on its unnatural sinfulness, and lament its being, so early, far away from Heaven—but think a little of its having been conceived, and born, and bred, in Hell!

That’s how Charles Dickens chose to put the generational question, in his 1848 novel, Dombey and Son. Poverty and bad mothering (there was hardly any fathering) stunted a child’s “natural” inclinations toward normalcy and love. As the reed is bent, and so on. It is a forceful and memorable literary case for the debilitating effects of childhood deprivation, illness, and trauma. And quite timely, given the ongoing backlash against the “disease model” of addictions and mental illnesses. Did Dickens have it right, more than 150 years ago? Has the research associated with the disease model—the brain breakthroughs, the MRI scans, and the neurotransmitter studies—all been giant detours away from root causes?

You would think so, listening to the cacophony of voices seeking to discredit the notion of addictions and mental illnesses as medical diseases. Medical and psychiatric opinion appear to be revolving away from a strict study of mechanisms of the brain, and back toward the study of society and the environment as root causes of conditions like schizophrenia and drug addiction.

Assuming that we avoid the drastic road of looking beyond the brain entirely for addiction causes—which would represent a true return to the past—what seems to be called for is some sort of “third way” of threading between the determinism of DNA and the fuzzy humanism surrounding the question of social causation, even as many researchers and commentators have become frustrated with the pace of new drug discovery for treating addictive disease, and are threatening to throw out the baby with the bathwater.

Recently, during a lively dinner in Amsterdam, I raised some of these questions with neuroscientist Marc Lewis, Professor of Human Development and Applied Psychology at Radboud University in Nijmegen, The Netherlands, and author of Memoirs of an Addicted Brain: A Neuroscientist Examines his Former Life on Drugs.

“Addictive drugs convert the brain to recognize only one face of God, to thrill to only one suitor,” Lewis wrote in that excellent book. Dopamine becomes “specialized, stilted, inaccessible through the ordinary pleasures and pursuits of life, but gushing suddenly when anything associated with the drug comes into awareness…. I wish this were just an exercise in biological reductionism, or neuro-scientific chauvinism, but it’s not. It’s the way things really work.”

Nonetheless, even Dr. Lewis is unhappy with the idea of calling drug addiction a “disease.” But why? Dopamine, says Lewis, is about craving and attraction, and not just about pleasure. There is too much going on with addictive behavior to fit neatly into the disease category, Lewis believes. Lewis doesn’t argue that brain structure is not causal—much of his book is devoted to proving that it is—but rather that the early brain, in the first two years of life, is so malleable that parent-child experiences shape the style of that young brain, so to speak. “There must be neural correlates to addiction,” he said, “ but this can occur in early childhood, and not from innate genetics.”

This idea has sweeping ramifications. It suggests that a person could become a drug addict entirely independent of his or her inborn genetic predilections. It suggests that a biological propensity for addiction may not need to be innate in order for the disorder to develop. The neurobiological preconditions may develop in early childhood, or even in the womb, and an individual’s basic chromosomal endowment may not be as predictive or protective as we have previously concluded.

I am not yet convinced on this point. Certainly there is evidence that addicted people have often had traumatic childhoods. Or, as we now refer to them: ACEs, or adverse childhood experiences. But should we be spotlighting parents and social setting, as we did for most of the 20th Century, or should we be paying attention to the disordered central nervous system, with associated behavioral traits such as impulsivity, low harm avoidance, and difficulty imaging future consequences, that characterize the behavior and cause much of the frustration in dealing with chronically “bad” children?

The Third Way could well be epigenetics, defined as the study of how gene expression can be modified without making direct changes to the DNA. Writing in Science News, Tina Hesman Saey explains that "epigenetic mechanisms alter how cells use genes but don't change the DNA code in the genes themselves.... The ultimate effect is to finely tune to what degree a gene is turned on or off. Often the fine tuning is long-lasting, setting the level of a gene's activity for the lifetime of the cell."  From a scientific point of view, epigenetics opened the door for a new way of thinking about addiction.

 An addict, as Lewis told me, “is like a starving animal.” You cannot talk that animal out of stalking it prey. However, Lewis believes it is time to do away with the dominant role that the chase for specific genes has played in addiction science. The endeavor resembles a classic needle-in-the-haystack kind of search, and is unlikely to come up with something simple but significant. Lewis believes that in many cases “womb trauma and infant trauma during the first two years” is sufficient to create the innate biological architecture responsible for addiction. Is this true in every case? The research pictures strongly suggests that it isn’t—sorry, Dr. Maté. It seems clear that some people are hardwired for addiction in a way that transcends family environment and social circumstances. We have all heard of the perfect young man or woman, with every advantage, and a loving home life, who succumbs, mysteriously, to the lure of addictive drugs.

We also discussed an article Lewis wrote for Perspectives on Psychological Science, called “Dopamine and the Neural Now,” in which he argues that “the disease-versus-choice debate creates a false dichotomy: Neuroscience does not have to frame addiction as a disease. Rather, it can help explain how addicts make impulsive choices in the moment and distort appraisal and decision-making habits in the long run…. repeated dopamine enhancement modifies brain structures to maximize the appeal of addictive activities, minimize the appeal of competing rewards, and undermine the cognitive capacities necessary to choose between them. I conclude that addiction is not a monolithic state but a recurrent series of choices that permit negotiation, and sometimes cooperation, between immediate and long-range goals.”


Despite the growing popularity of ACE hypotheses for explaining addiction, Lewis insists that addiction is neither a disease of choice nor a genetic imperative. In some ways, it is a meta-disease, calling into question, as all “mental” illnesses do, the very notions of personhood and autonomy. But a Third Way of thinking about addiction; one that incorporates both the innate propensities of our genetic endowment and the many ways early experience can shape the expression of our DNA, may help draw the addiction field out of the “either/or” thinking that continues to shape many of the debates.

 As Saey wrote in Science News: “Such findings suggest that medicines that interrupt or reverse epigenetic changes… could one day prevent or cure addiction." Drugs to treat drug addiction are going to be a central feature of future addiction research, no matter how we rejuggle the relationship between nature and nurture.

Graphics Credit: http://news4geeks.net/

Friday, May 4, 2012

Review: Memoirs of an Addicted Brain


“I’m a drug addict turned neuroscientist.”

What’s it like to swallow 400 milligrams of dextromethorphan hydrobromide, better known as Romilar cough syrup? “Flashes of perception go by like clumps of scenery on either side, while you float along with the slow, irresistible momentum of a dream.” Marc Lewis, a former addict, now a practicing neuroscientist, further muses: “But what was Romilar? It sounded like an ancient kingdom. Would this dark elixir take me to some faraway place? Would it take me into another land? Would it be hard to come back?”

In Memoirs of an Addicted Brain: A Neuroscientist Examines his Former Life on Drugs, Dr. Marc Lewis follows his description of his gateway Romilar drug experience with the neurological basics of the matter: “The problem is that the NMDA receptors in my brain are now clogged with dextromethorphan molecules! The glutamate isn’t getting through. The receptor neurons aren’t firing, or they’re not firing fast enough…. Drugs like DM, ketamine, PCP, angel dust, and those most damaging of substances, glue and gasoline, are called dissociatives, because they do exactly what drugs are supposed to do: they dissociate feeling from reality, meaning from sense—and that’s all they do.”

Speaking of the self-reinforcing cycle “through which calamities of the mind arise from vulnerabilities of the brain,” Lewis argues that dissociatives only produce an absence. As a friend of his puts it with regard to another popular dissociative, “Nitrous oxide doesn’t give you consciousness. It takes it away.” And then, the friend adds: “Just bonk yourself on the head with a baseball bat if you want to lose consciousness.”

Lewis ultimately turns to opioids. “The emotional circuitry of the ventral striatum seems to derive its power from an intimate discourse between opioid liking and dopamine wanting.” In the end, this partnership does more than produce pleasure. It also, Lewis points out, “gets us to work for things.” And by doing that, addictive drugs demonstrate “the fundamental chemistry of learning which really means learning what feels good and how to get more of it. Yet there’s a downside: the slippery slope, the repetition compulsion, that constitutes addiction. In other words, addiction may be a form of learning gone bad. For me, this neurochemical sleight of hand promises much more pain than pleasure in the years to come.”

Lewis does a good job of capturing the feeling of existential despair brought on by uncontrolled addiction: “Contemptible. That’s what I was. Unbelievably stupid, unbelievably irresponsible: selfish, selfish, selfish! But that wasn’t quite it. What described me, what this inner voice accused me of, wasn’t exactly selfish, not exactly weak, but some meridian of self-blame that included both, and also, dirty, disgusting… maybe just BAD.”

How did heroin feel? “I feel relief from that pervasive hiss of wrongness. Every emotional wound, every bruise, every ache in my psyche, the background noise of angst itself, is soaked with a balm of unbelievable potency. There is a ringing stillness. The sense of impending harm, of danger, of attack, both from within and without, is washed away.”

And Lewis provides a memorable summation of the reward system, as dopamine streams from the ventral tegmental area to its targets, “the ventral striatum, where behavior is charged, focused, and released; the orbitofrontal cortex, where it infuses cells devoted to the value of this drug; and the amygdala, whose synapses provide a meeting place for the two most important components of associative memory, imagery and emotion.” In fact, “dopamine-powered desperation can change the brain forever, because its message of intense wanting narrows the field of synaptic change, focusing it like a powerful microscope on one particular reward. Whether in the service of food or heroin, love or gambling, dopamine forms a rut, a line of footprints in the neural flesh.”

And, of course, Lewis relapses, and eventually ends his addictive years in an amphetamine-induced psychosis, committing serial burglaries to fund his habit. “You’d think that getting busted, put on probation, kicked out of graduate school, and enduring a kind of infamy that was agonizing to experience and difficult to hide—all of that, an the need to start life over again—would be enough to get me to stop. It wasn’t.”

Not then, anyway. But Lewis has been clean now for 30 years. “Nobody likes an addict,” he writes. “Not even other addicts.”

If drugs are such feel-good engines, what goes wrong? Something big. “Because when drugs (or booze, sex, or gambling) are nowhere to be found, when the horizon is empty of their promise, the humming motor of the orbitofrontal cortex sputters to a halt. Orbitofrontal cells go dormant and dopamine just stops. Like a religious fundamentalist, the addict’s brain has only two stable states: rapture and disinterest. Addictive drugs convert the brain to recognize only one face of God, to thrill to only one suitor.”  The addict’s world narrows. Dopamine becomes “specialized, stilted, inaccessible through the ordinary pleasures and pursuits of life, but gushing suddenly when anything associated with the drug comes into awareness…. I wish this were just an exercise in biological reductionism, or neuro-scientific chauvinism, but it’s not. It’s the way things really work.”


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