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/