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Understanding why nicotine use is so common in mental illness, is an important public health objective because it
produces serious financial and health consequences in these patients. Although high smoking rates in schizophrenia
have traditionally been assumed to represent �self-medication�, newly emerging data suggests that this comorbidity is not best
explained as a therapeutic interaction between a drug and a disease process, but instead as a synergy of 2 diseases. This talk
will outline a series of basic science investigations that combine a leading neurodevelopmental rat model of schizophrenia with
addiction paradigms involving nicotine and other drugs. This work employs prospective experimental designs, and invasive
procedures in animal models that are not ethical in human subjects but are nevertheless crucial to understanding causalbiological
relationships between mental illness and addiction. The neuro developmental syndrome of schizophrenia causes
increased vulnerability to nicotine and other drug addictions, through a host of biological changes involving circuits that are
co-implicated in addiction and schizophrenia. These events do not depend on, and do not occur with, illness-specific effect
of nicotine to act as a cognitive enhancing medication for the schizophrenia syndrome. This work suggests the inaccuracy of
self-medication hypotheses as primary explanations for high nicotine use rates in mental illness while illustrating how the
developmental psychopathology of schizophrenia involuntarily enhances addiction risk and severity. This line of neuroscience
calls for a paradigm shift in research and treatment on nicotine use in mental illness where this comorbidity is understood as
a particularly severe form of addiction, rather than it being viewed as a beneficial form of medication.
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