Smoking habits in bipolar and schizophrenic outpatients in southern Israel.

BACKGROUND: Although rates of cigarette smoking have been found to be higher in schizophrenic and depressed patients than in the general population, data regarding rates in bipolar patients are limited. This study further examines the relationship between bipolar disorder and smoking and compares the rate of smoking in bipolar disorder patients with rates in schizophrenic patients and in the general population. METHOD: Seventy bipolar patients and 64 schizophrenic patients (diagnosed using DSM-IV criteria) treated at the largest specialized public bipolar and schizophrenia clinics in southern Israel were interviewed regarding their smoking habits. The interview included a questionnaire relating to personal information, past and present smoking, and drug abuse and the Fagerstrom scale for nicotine dependence. Data from these patients were also compared with data from the general Israeli population. RESULTS: Data indicate that the rate of smoking does not appear to differ between bipolar (43.0%) and schizophrenic (45.0%) patients, whereas the rate for both patient groups is higher than that for the general Israeli population (27.5%). Smoking intensity was not found to be different between the 2 groups of patients. CONCLUSION: Smoking in patients with schizophrenia was suggested to be related to nicotine cholinergic dysfunction, but this suggestion cannot explain the equally high rates of smoking in bipolar patients. Schizophrenia, bipolar disorder, and smoking may all be related to dopamine transmission, and, therefore, dopaminergic interactions may provide a better explanation for the results.

Augmentation of lithium's behavioral effect by inositol uptake inhibitors.

Lithium inhibits the enzyme inositol monophosphatase and thus obstructs the enzymatic degradation of inositol triphosphate (IP3) to inositol in the phosphate-phosphoinositide (PIP) cycle. This inhibition may result in reduced availability of the second messengers IP3 and DAG that are derivates of the PIP cycle, and this action is currently a leading hypothesis regarding lithium's therapeutic and prophylactic effect in affective disorders. Inositol is also available to the cell by uptake from the intercellular matrix, and therefore it is possible that compounds that block the uptake may have lithium-like effects. To test this hypothesis, the present study evaluates the effects of two inositol uptake inhibitors, the carbohydrate L-fucose and the cyclodepsipeptide nordidemnin, in a behavioral model of pilocarpine-induced seizures known to be enhanced by lithium. We tested the possibility that L-fucose produces lithium-like effects, or that L-fucose or nordidemnin augment lithium's behavioral effects. Results indicate that acute ICV treatment with L-fucose did not by itself have a lithium-like effect in the behavioral model, but significantly augmented lithium's effect when combined with lithium treatment. Nordidemnin treatment showed similar effects. The results suggest that when inositol monophosphatase is inhibited by lithium, further restriction of cellular inositol availability may result in an augmentation of lithium's behavioral effects. It is possible that such manipulations may be applicable in the treatment of patients with affective disorders, especially patients who are poor responders to lithium monotherapy.