Illicit drugs are often used as aphrodisiacs to enhance sexual performance and/or pleasure; however, the available data suggest that most illicit drugs have adverse effects on erection, sexual desire and ejaculation latency in males and that these effects are not fully understood. This study aimed to determine the effect of illicit drug abuse on male sexual function, based on the International Index of Erectile Function (IIEF) score. This descriptive study was conducted at the Alcohol and Substance Research Treatment and Education Center, Ankara, Turkey. Males diagnosed as substance use disorder according to DSM-IV (n = 101) were included as the patient group, and age-matched healthy male volunteers (n = 43) were included as the control group. A 30-item sociodemographic interview form developed by researchers and the 15-item IIEF were administered to all the participants. Data were compared between the patient and control groups. Mean IIEF score was 46.7 ± 3.3 in the patients that used alcohol, 23.7 ± 3.3 in the opioid users, 34.1 ± 5.3 in the ecstasy users, 43.5 ± 4.2 in the cannabis users and 55.3 ± 1.6 in the control group. There was not a significant difference between the alcohol and cannabis users' mean IIEF scores and that in the control group (P > 0.05 and >0.05 respectively), whereas there was a significant difference between the opioid and ecstasy users' mean IIEF scores and that in the control group (P < 0.001 and <0.001 respectively). All IIEF subscale scores in the opioid users were significantly lower than in the control group (P < 0.001). IIEF erectile function, sexual desire and general satisfaction subscale scores were significantly lower in the ecstasy users than in the control group (P < 0.001, <0.005 and <0.001 respectively). In the alcohol users only, the IIEF general satisfaction subscale score was lower than in the control group (P < 0.005).
Olanzapine is a thienobenzodiazepine that blocks especially the serontonin (5-hydroxytryptamine [5-HT]) 5-HT2A and the dopamine D2 receptors as well as muscarinic (M1), histamine (H1), 5-HT2C, 5-HT3 to 5-HT6, adrenergic (α(l)), and D4 receptors. This case report presents an olanzapine abuse. A 48-year-old, primary school graduate, married woman applied to psychiatry clinic with tachycardia, insomnia, and anxiety complaints. In psychiatric evaluations, it was determined that these complaints have been continuing for 15 years at intervals and that she has been using citalopram 40 mg/day and olanzapine 50 mg/day for the last 3 years. As diabetes mellitus was diagnosed in follow-ups, interruption of olanzapine treatment was planned. The patient stated that she started taking the medicine again upon discomfort, increase in anxiety, dysphoria, insomnia, and nervousness, which started just after olanzapine was interrupted. She said that she was feeling dense stress when she did not take the medicine, and she thought that this situation would recover only by taking that medicine and hence she could not discontinue the medicine. In addition to medications with obvious abuse potential such as benzodiazepines and methylphenidate, and other stimulants, abuse of a number of commonly prescribed psychiatric medications has been reported. There are only 2 cases of olanzapine abuse in literature.
Although we did not observe a significant relationship between craving and any of the 3 biomarkers on day 0, craving was positively correlated with the levels of adiponectin and ghrelin and negatively correlated resistin levels on day 7. Our findings support the hypothesis that appetite hormones are trait markers for alcohol craving. Nevertheless, more conclusive results require future studies that evaluate the relationship between these hormones and withdrawal/detoxification period or long-term soberness.
Introduction Women suffer from depression more frequently than men, which indicates that sex hormones might be involved in the etiology of this disease. Aims The purpose of this study was to assess the relationship between testosterone and depression pathophysiology in depressive women along with sexual function. We also investigated whether antidepressant treatment causes any change in levels of this hormone or in sexual function. Methods Premenopausal female patients aged 25–46 years (n = 52) with diagnosed major depression were included in this study as the patient group, and 25- to 46-year-old premenopausal women without depression (n = 30) were included as the control group. Main Outcome Measures Serum testosterone and sex hormone-binding globulin (SHBG) levels were measured twice, before and after the antidepressant treatment. Bioavailable testosterone (cBT) levels were calculated using the assay results for total testosterone (TT), SHBG, and albumin according to the formulas of Vermeulen et al. Depression severity was measured using the 17-item Hamilton Depression Rating Scale, and sexual function was evaluated with the Arizona Sexual Experience Scale. Results The mean TT and cBT levels significantly increased in the patient group after the antidepressant treatment (P < 0.001). Pre-treatment TT and cBT levels were significantly lower in the patient group than in the control group (P < 0.001). Similar results were obtained for post-treatment serum TT and cBT levels in the patient and control groups (P > 0.05). There were no significant differences among the groups in terms of SHBG level. Conclusion The low testosterone levels in depressed women compared with women in the control group and the elevated levels post-pharmacotherapy suggest that testosterone may be involved in depression.
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