The Symptomatic Importance of Nicotine in Schizophrenia

The tendency of people suffering from schizophrenia to consume more cigarettes and thus put themselves at a much greater risk of cardiovascular and respiratory disease is well-known. This is an obvious health consideration for people who are already more vulnerable to ill-health because of a mental illness which is notoriously difficult to manage. There is a wealth of information available detailing the importance of nicotine in the pathophysiology of schizophrenia: some important examples from this body of work will be reviewed here. Chronic Nicotine Replacement Therapy (NRT) such as with 12- or 16-hour transdermal nicotine patches are not appropriate for achieving the necessary improvements in cognitive function in schizophrenia. A better alternative is NRT which replicates the short burst of nicotinergic activity that cigarette smoking provides. Nicotine chewing gum, or more controversially, e-cigarettes, are the two clear candidates. Nicotine inhalators have been largely unsuccessful as agents for the delivery of nicotine, as the sensation that they produce is a reportedly unpleasant one. The use of nicotine gum or e-cigarettes is not something which would necessarily break the habit. In people who suffer from schizophrenia and who are supplementing their deficient endogenous cerebral nicotine with exogenous sources, delivery via gum or e-cigarettes represents a far less toxic route than tobacco cigarettes. In the latter, it is probable that the aromatic hydrocarbons in cigarette smoke also cause the increased metabolism of antipsychotic drugs due to their induction of hepatic catabolic enzymes. This adds another negative factor to tobacco cigarette consumption for people with severe mental illnesses. For a patient group which is already at risk of impaired physical health, prevention of respiratory and cardiovascular pathology is especially important. The success of clozapine and olanzapine as antipsychotic medications is in large part due to their success in improving the deficient sensory gating inherent to schizophrenia. These drugs are also associated with greater success in helping schizophrenic smokers to abstain; both of these aspects can be at least partly attributed to their involvement of cerebral nicotinic receptors. Where it is not possible for the schizophrenic smoker to abstain, then as clinicians, we are duty-bound to research acceptable alternatives to smoking. It is also possible that NRT delivered via safer methods such as gum or e-cigarettes can provide a useful adjunct to antipsychotic treatment. For these reasons, the symptomatic role of intermittent NRT in schizophrenia must be further investigated.