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It has been repeatedly confirmed that persons with schizophrenia have an abnormally high risk of developing substance use disorders (that is, abuse or dependence) during the course of their lives (1). The excessive probability revealed by the Epidemiological Catchment Area (ECA) study, a general-population household survey, is 3.6 times that for alcohol, 5 times that for cannabis, 6.5 times that for opiates, and 13 times that for cocaine (2). It is also well known that persons with schizophrenia present rates of tobacco use (between 70% and 90%) that are well above those of the general population and also above the rates observed in persons with anxiety disorders or depression (although depression sufferers present the second-highest rates) (3). Risk of OccurrenceThe highest rates of addiction comorbidity are found in clinical samples gathered from outreach programs and emergency or walk-in services attending to less stable, more severely afflicted subjects (4). However, it must be noted that substance abuse frequency is not evenly distributed across demographic categories within single samples of schizophrenia patients, nor is it evenly distributed among the different locations from which the data were gathered. Rather, the prevalence profile among these individuals follows closely the age and sex differences observed in the population at large: younger and male schizophrenia sufferers outrank older and female ones (1,5). Similarly, rates reported in the US are well in excess of rates found in German (6), French (7), British (8), or Canadian (9) samples, particularly in regard to cocaine abuse. It therefore seems that, as in the general population, the risk of addiction disorders occurring among persons with schizophrenia depends on environmental conditions such as drug availability and local drug culture. Most of the US data, for instance, pertain to patients seen in public facilities. These patients come mainly from within the Department of Veterans Affairs network, which may be catering to a population preselected for high risk of illegal substance misuse. One interesting finding that emerged from a Montreal study of persons with chronic schizophrenia is that the prevalence of tobacco smoking, the most widespread drug problem in this particular population, covaries with prevalence of alcohol drinking (5). Of course, that is also the case in samples without psychosis (10). However, alcohol-abusing schizophrenia sufferers have been found to present nearly twice the rate of smoking (88.4 %) than do the single-diagnosis patients (49.5 %). This suggests that the early tobacco dependence manifested by persons with schizophrenia—it precedes alcohol abuse in nearly every case—can be considered as a precursor of a more general and indiscriminate addiction proclivity. CausationAn explanation for the excessive prevalence of substance abuse among persons with schizophrenia and the higher-than-expected rates of schizophrenic disorders in people with a lifetime history of addiction could be that the mere occurrence of one such disorder facilitates the development of the other. In other words, schizophrenia may play an etiological role in substance abuse, or substance abuse may lead to chronic psychosis. Schizophrenia may lead to addiction through self-medication behaviour (11). This is a nonspecific explanation that applies equally well to most persisting psychological disturbances, including other Axis I categories and several personality disorders, all of which are associated with elevated rates of chemical addiction. This hypothesis has 2 basic premises. The first is that substance use is perpetuated by the need to soothe or correct psychological deficits or distress. Such distress is believed to arise largely from primary self-regulation defects, or ego-function impairments, that manifest themselves as inability to tolerate negative affects, to maintain interpersonal relationships, to have a sense of personal identity, or to care for oneself. The second assumption is that substance use is not random; it is determined by a preference for drugs whose specific pharmacologic action best remedies particular individual ego-function defects. The self-medication construct thus defines addiction as the consequence of a negative reinforcement mechanism: the reward comes from impeding the occurrence of undesirable psychological states or, if they are inevitable, from decreasing the pain and discomfort they cause. Such reinforcing benefits may indeed incline schizophrenia sufferers to use drugs. This is perhaps the most convincing explanation for the high rates of tobacco smoking among this population: nicotine is likely to decrease psychological lethargy and feelings of depletion, to ameliorate negative symptoms, and to enhance cognitive functions that are diminished by the illness. Nicotine may even decrease the severity of neuroleptic drug extrapyramidal side effects (EPSEs) (12). However, schizophrenia sufferers also present excess rates of cannabis and cocaine use. These substances are known to worsen delusional and hallucinatory symptoms—untoward effects that may be caused by the drugs’ dopaminergic properties on the mesolimbic system. Of course, dopamine activation also occurs in the mesocortical projections and in the prefrontal cortex itself. This particular action potentially alleviates negative symptoms and may thus remedy what certain authors have described as “the reward-deficiency syndrome,” an anomaly believed to afflict persons with schizophrenia (13). It could therefore be postulated that the resulting lessened anhedonia, facilitated social interaction, and other such stimulating effects do constitute a reward powerful enough to counteract the aversive positive symptoms caused by these drugs. Surveys of clinical samples support this interpretation: when asked to describe their subjective experiences with each drug category, schizophrenia sufferers consistently report that cannabis and cocaine decrease “depression,” although they increase suspiciousness and distrust (14). Similarly, it is possible that activating dopaminergic function may diminish the negative mood correlates of neuroleptic-induced parkinsonism—a property that should additionally reinforce use of these drugs among schizophrenia patients receiving treatment. Lately, however, widespread acceptance of the self-medication hypothesis is being challenged by the proponents of a “primary addiction” theory of comorbidity. This theory contends that individuals with schizophrenia suffer from a nonspecific avidity for drugs that parallels their psychotic illness and may even be independent of it. According to this interpretation, the inclination of persons with dual pathology to abuse psychoactive substances is an additional symptom of the basic neuropathology underlying schizophrenia itself. In other words, both schizophrenia and substance abuse share a common pathophysiology. A review by Chambers and others details a wide range of neuroscience observations supporting the primary addiction theory (15). These authors conclude that some primary abnormalities in the hippocampal formation and in the frontal cortex exist in schizophrenia sufferers —abnormalities that facilitate the positive reinforcing effects of drug reward and reduce the individual’s ability to inhibit drug-seeking behaviour. This preexisting neuropathology is thought to lead to brain responses that facilitate the rapid development of compulsive drug use patterns, providing a shortcut in the path to addiction, as it were. Goldstein and Volkow’s report on brain-imaging studies observes that drug users experience abnormally high activation in the orbitofrontal cortex and the cingulate gyrus areas of the brain during craving and acute intoxication (16). The authors conclude that these anomalies represent the neurobiological basis of impaired inhibition, a major feature of addictive behaviour. Another explanation for the excessive co-occurrence of addiction and schizophrenia is the possibility that drugs may trigger the clinical expression of the psychotic disease. This view is supported by epidemiologic and clinical findings demonstrating that drug use among youth is associated with a higher risk of developing psychosis in subsequent years (17,18); that two-thirds of subjects with first-episode schizophrenia and comorbid addiction used drugs in the premorbid or prodromal phases, prior to the appearance of the first positive symptoms (19); and that drug use by schizophrenia patients in remission is associated with a greater risk of early relapse (20). However, incidence rates for schizophrenia have not increased in the last 30 years, whereas the prevalence of drug abuse has grown exponentially throughout the world. It therefore seems unlikely that drug abuse by itself suffices to cause the clinical manifestation of a schizophrenic disease. Other causes of comorbidity are to be found in the high-risk social settings where many persons with schizophrenia are constrained to live. The variance in prevalence rates across demographic categories suggests that such external factors also play an important role in the causation of dual disorders. Access to drugs and the environmental prompting to which many schizophrenia sufferers are exposed cannot be ignored (21). This is especially the case in urban settings, where many schizophrenia patients live in conditions of high social pathology, homelessness, and transient accommodations; that is, in settings where drug circulation is particularly heavy.
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