When I was diagnosed with a mental illness at age eleven, my doctor—soft-spoken and straitlaced, with a thick moustache—explained that I was suffering from a chemical imbalance in my brain. At the time, the medical community believed that depressive disorders were primarily caused by a deficiency of monoamine neurotransmitters, which help regulate moods and general happiness. The new drugs were thought to stall reabsorption of serotonin into nerve cells and allow it to linger instead in the synapse between cells, where over time it may help transmit the “happy” message. It sounds logical, but even today scientists have unanswered questions. Since patients were seeing improvement, doctors figured, they must have been low in monoamines.
And I did improve. A week or so after I started taking the drugs, my family took our new dog, Chester, for a walk in the Beach neighbourhood of Toronto. As we strolled along the boardwalk, he snatched a peanut butter sandwich clean out of a little boy’s hand. “It was the first time we’d seen you smile in three months,” my dad told me recently. Over the next few months, my sadness lifted. My toxic thoughts became more manageable. The nausea dissipated, and I started eating again. I switched schools, made new friends, and slowly, cautiously, returned to normal life. The drugs buoyed me up from cataclysmic depression to relatively stable, low-boiling anxiety.
The drugs came with some obsessive-compulsive side effects. I picked the skin on my face and limbs like a crystal meth addict, burrowing beneath the flesh to create welts and sores. I also developed a facial tic, wherein I’d scrunch up my nose until it ached. (Even when I think about it now, the urge to scrunch is hard to resist.) My doctor prescribed even more drugs: clomipramine and imipramine, two remnants of the old tricyclic class of antidepressants.
My parents weighed the potential risks of this cocktail against what they could only imagine would happen if I continued along my destructive path. My doctor, meanwhile, hoped that by staving off anxiety and depression at an early age, my brain might lay down permanent pathways to combat patterns of dysfunctional thinking. Really, no one knew what to expect. “We were totally in the wilderness about child and adolescent psychiatry,” explains Dean Elbe, a clinical pharmacist who specializes in child psychiatry at the BC Children’s Hospital, in Vancouver. “All we could do was extrapolate from what we saw in adults.”
We still don’t really know anything about the long-term effects of antidepressants on adolescent development. There have been no long-term studies, partly because of logistics, and because the US Food and Drug Administration and Health Canada require pharmaceutical companies to prove only that their medications are better than placebos over the short term. One study found that extended exposure to fluoxetine (the generic form of Prozac) in some young mice led to anxiety-like behavior recurring when the mice were exposed again to the drug as adults.
But the most profound and pervasive fear—among adults, among parents of affected kids, and among those kids themselves—is that antidepressants will somehow alter the patient’s essential identity. In Is It Me or My Meds: Living with Antidepressants, Boston-based sociologist David A. Karp explains, “Psychotropic drugs have as their purpose the transformation of people’s moods, feelings, and perceptions. These drugs act on—perhaps even create—people’s consciousness and, therefore, have profound effects on the nature of their identities.”
This kind of thinking taps into one of the paramount tensions of mental illness: the blurred line between pathology and personality. How much of what we feel is the result of an illness? How much is our so-called identity? Though scientists still believe neurotransmitter deficiencies affect mental health, they’ve also implicated a whack of other factors, including the environment, stress, and physical health. Together with the mysterious chemical voodoo taking place in our bodies, those factors spin in an endless feedback loop that makes it impossible to source mental illness. It stands to reason that drugs meant to treat an imbalance in serotonin might bleed beyond their reach, altering who we are as long as we’re on them.
And I did improve. A week or so after I started taking the drugs, my family took our new dog, Chester, for a walk in the Beach neighbourhood of Toronto. As we strolled along the boardwalk, he snatched a peanut butter sandwich clean out of a little boy’s hand. “It was the first time we’d seen you smile in three months,” my dad told me recently. Over the next few months, my sadness lifted. My toxic thoughts became more manageable. The nausea dissipated, and I started eating again. I switched schools, made new friends, and slowly, cautiously, returned to normal life. The drugs buoyed me up from cataclysmic depression to relatively stable, low-boiling anxiety.The drugs came with some obsessive-compulsive side effects. I picked the skin on my face and limbs like a crystal meth addict, burrowing beneath the flesh to create welts and sores. I also developed a facial tic, wherein I’d scrunch up my nose until it ached. (Even when I think about it now, the urge to scrunch is hard to resist.) My doctor prescribed even more drugs: clomipramine and imipramine, two remnants of the old tricyclic class of antidepressants.
My parents weighed the potential risks of this cocktail against what they could only imagine would happen if I continued along my destructive path. My doctor, meanwhile, hoped that by staving off anxiety and depression at an early age, my brain might lay down permanent pathways to combat patterns of dysfunctional thinking. Really, no one knew what to expect. “We were totally in the wilderness about child and adolescent psychiatry,” explains Dean Elbe, a clinical pharmacist who specializes in child psychiatry at the BC Children’s Hospital, in Vancouver. “All we could do was extrapolate from what we saw in adults.”
We still don’t really know anything about the long-term effects of antidepressants on adolescent development. There have been no long-term studies, partly because of logistics, and because the US Food and Drug Administration and Health Canada require pharmaceutical companies to prove only that their medications are better than placebos over the short term. One study found that extended exposure to fluoxetine (the generic form of Prozac) in some young mice led to anxiety-like behavior recurring when the mice were exposed again to the drug as adults.
But the most profound and pervasive fear—among adults, among parents of affected kids, and among those kids themselves—is that antidepressants will somehow alter the patient’s essential identity. In Is It Me or My Meds: Living with Antidepressants, Boston-based sociologist David A. Karp explains, “Psychotropic drugs have as their purpose the transformation of people’s moods, feelings, and perceptions. These drugs act on—perhaps even create—people’s consciousness and, therefore, have profound effects on the nature of their identities.”
This kind of thinking taps into one of the paramount tensions of mental illness: the blurred line between pathology and personality. How much of what we feel is the result of an illness? How much is our so-called identity? Though scientists still believe neurotransmitter deficiencies affect mental health, they’ve also implicated a whack of other factors, including the environment, stress, and physical health. Together with the mysterious chemical voodoo taking place in our bodies, those factors spin in an endless feedback loop that makes it impossible to source mental illness. It stands to reason that drugs meant to treat an imbalance in serotonin might bleed beyond their reach, altering who we are as long as we’re on them.
by Emily Landau, The Walrus | Read more:
Image: Adrian Forrow
