Effect of mirtazapine treatment on body composition and metabolism.

OBJECTIVE: Weight gain is a common side effect of psychotropic medications. Mirtazapine, a widely used antidepressant, induces adverse metabolic effects such as an increase in body weight. The aim of this study was to investigate the influence of mirtazapine treatment on body weight, body fat mass, glucose metabolism, lipoprotein profile, and leptin and its soluble receptor in a prospective, controlled study design. METHOD: Seven women who met the ICD-10 diagnostic criteria for a depressive episode (ICD-10: F31-F33) were assigned to monotherapy with mirtazapine and observed for a 6-week period. Seven mentally and physically healthy female volunteers matched for age and body weight served as a control group. Data were collected from November 2002 to December 2003. RESULTS: The mean +/- SD body weight increased from 63.6 +/- 13.1 kg to 66.6 +/- 11.9 kg during mirtazapine treatment (p = .027). Fat mass increased in study subjects from 20.9 +/- 9.6 kg to 22.1 +/- 9.3 kg (p = .018). Insulin, glucose, and the homeostasis model assessment (HOMA) index for insulin resistance and lipid parameters remained stable. Leptin concentrations increased from 23.0 +/- 17.1 ng/mL to 40.9 +/- 27.2 ng/mL (p = .018), whereas the soluble leptin receptor concentrations remained stable during mirtazapine treatment. In the control subjects, the investigated parameters remained stable. Between-group analyses of change scores revealed significant differences for body weight (p = .010), body mass index (p = .013), fat mass (p = .035), and leptin (p = .013). CONCLUSION: The antidepressant therapy with mirtazapine was associated with a significant increase in body weight, body fat mass, and leptin concentration. In contrast to other psychotropic medications inducing weight gain, such as some second-generation antipsychotics, mirtazapine treatment did not influence the glucose homeostasis.

Serum lipids and risk factors for attempted suicide in patients with alcohol dependence.

BACKGROUND: Alcohol dependence is a major risk factor for suicidal behavior. Although a number of risk factors have been suggested there is still no well-defined risk profile for attempted suicide in alcoholic patients. Alterations of serum lipids have been associated with completed as well as attempted suicide and with suicidal ideation. This study investigated potential demographic and clinical risk factors for attempted suicide in alcohol-dependent patients taking serum lipids additionally into consideration. METHODS: One-hundred ten alcohol-dependent patients who were admitted to a psychiatric university hospital department for inpatient treatment were grouped according to whether or not they had a lifetime history of attempted suicide. Attempters versus nonattempters as well as attempters who used a violent versus a nonviolent suicide method were compared. RESULTS: Patients who had attempted suicide at least once in their life differed significantly from those who had no history of suicide attempts. Univariate analyses showed that they were younger (41.7 years vs 46.8 years; p = 0.003), were more often smokers (97% vs 77%; p = 0.011), had more frequently coabused benzodiazepines (54% vs 17%; p = 0.002), and scored currently higher on the Montgomery and Asberg Depression Rating Scale (MADRS) global scale (26.3 vs 20.2; p = 0.005) as well as the "suicidal thoughts" item (1.8 vs 0.6; p = 0.001). Additionally, they had higher serum triglyceride levels (178.9 vs 127.5; p = 0.039). A logistic regression analysis left coabuse of benzodiazepines [odds ratio (OR), 5.26; p = 0.001], younger age (OR per year increase of age, 0.91; p = 0.006), and current MADRS item 10 ("suicidal thoughts") score (OR per point increase in MADRS item 10 score, 1.43; p = 0.019) as significant factors. Suicide attempters who had used a violent method were significantly more often male (82% vs 44%; p = 0.035), were younger (38.2% vs 45.1 years; p = 0.008), and had less frequently coabused tranquilizers (35% vs 78%; p = 0.018) than nonviolent attempters. CONCLUSIONS: These findings contribute to the development of a more specific profile of alcohol-dependent individuals at risk for suicidal behavior. Further research is required to determine the role of serum triglycerides for suicidal behavior in patients with alcohol dependence.

Olfactory functions and volumetric measures of orbitofrontal and limbic regions in schizophrenia.

OBJECTIVE: Olfactory deficits in schizophrenia patients have been suggested to reflect medial temporal and/or prefrontal brain abnormalities. In this study, we examined the relationship between different olfactory functions and volumes of the hippocampus-amygdala complex (HAC) and the orbitofrontal brain region using magnetic resonance imaging (MRI). METHODS: Thirty-three young men with schizophrenia (DSM-IV) and 40 healthy controls performed unirhinal olfactory assessment including the main olfactory functions (threshold, discrimination, and identification), and odor judgements (intensity, edibility, familiarity, and pleasantness). Volumes of regions in the medial temporal lobe (hippocampus and amygdala) and the prefrontal region (orbitofrontal gray and white matter) were measured on MRI scans. RESULTS: Compared with controls, patients showed bilaterally impaired thresholds, quality discrimination and identification, as well as edibility judgements. Olfactory deficits were not attributable to smoking, premorbid intelligence, or impaired thresholds. Relative to controls, patients had bilateral reduced hippocampus and amygdala volumes. In patients, smaller hippocampus volumes were associated with poorer olfactory discrimination ability. CONCLUSIONS: Olfactory deficits in schizophrenia appear to be associated with morphometric abnormalities in the medial temporal rather than the orbitofrontal region (OFR). These results indicate that olfactory quality discrimination deficits are related to structural hippocampus abnormalities. Future studies of genetic and behavioral high-risk samples seem warranted.

No deterioration of cognitive performance in an aggressive unilateral and bilateral antidepressant rTMS add-on trial.

BACKGROUND: Cognitive functions were assessed before and following a course of repetitive transcranial magnetic stimulation (rTMS) in patients with depression participating in a sham-controlled, randomized trial of rTMS as adjunct to antidepressant treatment. METHOD: Forty-one medicated inpatients with a DSM-IV diagnosis of a depressive episode were consecutively randomly assigned to 1 of 3 groups comparing 2 active rTMS conditions with sham stimulation. The rTMS was applied either at high frequency over the left dorsolateral-prefrontal cortex (DLPFC) (10 sessions x 10 trains x 10 seconds 20 Hz at 100% motor threshold [MT], 90-second intertrain interval) or in a combined high- and low-frequency manner to the left and right DLPFC, respectively (10 sessions x 1 train x 10 minutes at 120% MT). Thirty-eight patients completed a neuropsychological test battery at baseline and following day 14. The cognitive assessment focused on motor skills, attention, executive functions, learning, and memory. Data were collected from November 1999 to August 2002. RESULTS: Active treatment groups did not differ with respect to assessed cognitive measures and thus were pooled. A comparison of short-term changes (baseline-day 14) in neuropsychological performance revealed a more favorable time course of the actively treated patients for encoding in the verbal memory test compared with the sham-stimulated patients. CONCLUSIONS: Unilateral rTMS as well as bilateral combined rTMS revealed no detrimental effects on cognition, as compared with the sham group. Moreover, neither the add-on design nor the used aggressive parameters had a negative impact on cognitive measures in comparison with sham. Repetitive transcranial magnetic stimulation might have mild beneficial cognitive effects partly independent of its antidepressant efficacy.