BACKGROUND: Depression among older adults is an important public health issue, and air and noise pollution have been found to contribute to exacerbation of depressive symptoms. This study examined the association of exposure to air and noise pollutants with clinically-newly-diagnosed depressive disorder. The mediating role of individual pro-inflammatory markers was explored. METHODS: We linked National Health Insurance claim data with 2998 healthy community-dwellers aged 55 and above who participated in the Healthy Aging Longitudinal Study between 2009 and 2013. Newly diagnosed depressive disorder was identified using diagnostic codes from the medical claim data. Pollutants were estimated using nationwide land use regression, including PM_2.5 and PM₁₀, carbon monoxide, ozone, nitrogen dioxide, sulfur dioxide, and road traffic noise. Cox proportional hazard models were employed to examine the association between pollutants and newly developed depressive disorders. The mediating effect of serum pro-inflammatory biomarkers on the relationship was examined. RESULTS: Among the 2998 participants, 209 had newly diagnosed depressive disorders. In adjusted Cox proportional hazard models, one interquartile range increase in PM_2.5 (8.53 µg/m³) was associated with a 17.5% increased hazard of developing depressive disorders. Other air pollutants and road traffic noise were not linearly associated with depressive disorder incidence. Levels of serum tumor necrosis factor receptor 1 mediated the relationship between PM_2.5 and survival time to newly onset depressive disorder. CONCLUSION PM_2.5 is related to an increased risk of newly developed depressive disorder among middle-aged and older adults, and the association is partially mediated by the pro-inflammatory marker TNF-R1.
Humans ; Particulate Matter/analysis* ; Male ; Female ; Middle Aged ; Longitudinal Studies ; Aged ; Incidence ; Air Pollutants/analysis* ; Environmental Exposure/adverse effects* ; Taiwan/epidemiology* ; Receptors, Tumor Necrosis Factor, Type I/blood* ; Proportional Hazards Models ; Biomarkers/blood* ; Depression/epidemiology* ; Aged, 80 and over ; Depressive Disorder/chemically induced* ; Risk Factors ; Air Pollution/adverse effects*

We report a case of severe hyponatremia related to duloxetine and ziprasidone. A 50-year-old woman on duloxetine and ziprasidone treatment for major depressive disorder developed polydipsia, polyuria, and two episodes of seizures, followed by admission to the emergency department on the 10th day of treatment. Laboratory investigations revealed elevated creatine kinase (CK) as well as hyponatremia, hypo-osmolality, and increased urine sodium. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) was considered, although urine osmolality was not measured. Duloxetine and ziprasidone were discontinued and the CK gradually normalized after correction of hyponatremia. Clinicians should be aware of the possibility of antipsychotic-induced hyponatremia, particularly in patients with symptoms of polydipsia.
Antidepressive Agents ; adverse effects ; Antipsychotic Agents ; adverse effects ; Creatine Kinase ; blood ; Depressive Disorder, Major ; drug therapy ; Duloxetine Hydrochloride ; Female ; Humans ; Hyponatremia ; chemically induced ; Middle Aged ; Piperazines ; adverse effects ; Thiazoles ; adverse effects ; Thiophenes ; adverse effects

This study is to explore a behavioral and pathological model for depression in mice, and evaluate the anti-depressant-like effect of agmatine. Neonatal Kunming mice were treated with fluoxetine (10 mg x kg(-1), ip, qd) for 17 d (between day 4 and 21 after birth), and then the mice were normally housed till being adult (about 10 weeks after birth). The behaviors of the mice were measured by using open-field test, novelty suppressed feeding test and tail-suspension test. Hippocampal adenylate cyclase (AC) activity was measured by radioimmunoassay. Neonatal exposure to fluoxetine induced a "depression-like" behaviors in the adult mice, shown as the decreased locomotor activity, increased feeding latency and immobility time in the open-field test, novelty suppressed feeding test, and tail-suspension test, respectively. Chronic agmatine treatment (10 mg x kg(-1), ig, bid) for 3 weeks significantly increased the locomotor activity, and decreased the feeding latency in the neonatal fluoxetine exposed mice. Furthermore, single treatment with agmatine (40 mg x kg(-1), ig) also decreased the immobility time in the tail-suspension test, and increased the hippocampal AC activity in the mice. These results indicate that neonatal exposure to fluoxetine induces depressive-like behaviors in the adult mice. Agmatine reverses these behaviors, which may be closely related to the enhancement of the hippocampal AC activity.
Agmatine ; pharmacology ; Animals ; Antidepressive Agents ; pharmacology ; Depressive Disorder ; chemically induced ; Disease Models, Animal ; Female ; Fluoxetine ; administration & dosage ; adverse effects ; Male ; Mice ; Mice, Inbred Strains

OBJECTIVETo compare the incidences of sexual dysfunction induced by mirtazapine and SSRI in the treatment of patients with depression.

METHODSUsing key-word retrieval from the compact disks of the Chinese biological medicine (CBM) data base, we analyzed the rates of sexual dysfunction from the published clinical control trials on depression treated with mirtazapine and SSRI by applying the fixed effects model (FEM) of evidence-based medicine (EBM).

RESULTSAmong 1108 cases in 14 studies, there were 5 cases of mirtazapine-induced and 106 cases of SSRI-induced sexual dysfunction, accounting for 0.90% and 19.2% respectively, OR = 0.07 (95% CI: 0.04-0.14), Z = 8.03, P < 0.01.

CONCLUSIONSSRI is far more likely to induce sexual dysfunction than mirtazapine in the treatment of depression.

Antidepressive Agents, Tricyclic ; adverse effects ; Depressive Disorder ; drug therapy ; Erectile Dysfunction ; chemically induced ; Humans ; Male ; Mianserin ; adverse effects ; analogs & derivatives ; Serotonin Uptake Inhibitors ; adverse effects