Background: The aim of this study was to examine the relationship between depressive symptoms and lifestyle related factors.

Methods: 2,220 employees (1,069 for males and 1,151 for females) in Japan completed the screening test of the Center for Epidemiologic Studies Depression Scale (CES-D). The cutoff point for the CES-D scores was 16 or above (high scorers).

Results: The identified factors that showed significant effect from the binomial multivariate logistic regression for high scorers were as follows: “habits of having breakfast” in all participants; “have good eating habits” in females and all participants; “satisfaction with sleep” in males, females, and all participants; “smoking habits” in females; “daily alcohol consumption” in males and all participants; “hypertension” in females; “periodontal disease” in all participants; “history of medication” in females and all participants.

Conclusion: Healthy lifestyle was found to be a factor related to the depressive symptoms of the Japanese employees.

Without either, the diagnosis of depression among children is rare, increased knowledge has shown through the study of its prevalence it is not uncommon and despite the problems presented between different researchers in the scientific community for it to be accepted, due to the different types of population studied, the lack of agreement to define depression (symptom, syndrome or disorder) and to establish the diagnostic criteria; the different methods of evaluation used; the influence of the level of development and age and the presence of comorbidity; they were given the task of finding their symptoms and characteristics.

Depression is a heterogeneous mental illness and one of the leading causes of disability worldwide. Poor understanding of neurobiology of depression and neural mechanisms of antidepressant drugs could be associated to their serendipitous discoveries. The first line of antidepressant medications (tricyclics, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, noradrenaline reuptake inhibitors, serotonin and noradrenaline reuptake inhibitors) are apparently ineffective in several patients. In principle, some of these antidepressant medications increase monoamine transmission directly (through serotoninergic or adrenergic receptors) or indirectly (by inhibiting the enzymatic breakdown and transport of serotonin and norepinephrine neurotransmitters). Meanwhile, other mechanistic hypotheses of antidepressant drugs have been linked to cholinergic transmission, γ-amino butyric acid, neuronal plasticity, hypothalamic pituitary adrenal axis, reward system, receptor activation or blockade (κ opioid receptor, cannabinoid receptor, cytokine-regulated pathways, Melatonin receptor), protein/enzyme inhibition (histone deacetylase, tissue plasminogen, vasopressin receptor, NK1 receptor antagonists, phosphor-diesterase inhibitors, circadian gene products. This review sought to highlight the neural structures, biomolecules and circuits that participate in the mechanisms of the first line antidepressant drugs. The contents of this review were retrieved from globally available database (Science Direct, PubMed, ACS, SciFinder, Scopus, Web of Science among others). Findings showed that, most of the first line antidepressant drugs are associated with different side effects and delayed therapeutic effects. The side effects are consequences of multiple interactions or mechanisms of antidepressant drug’s action. The delayed effect otherwise called therapeutic action lag has been worsened by low level of adherence to long term antidepressant treatment. Researchers are still groping in the dark in their attempts to understand mechanisms of antidepressant drugs, promote development of fast acting drugs, improve medical diagnosis, drug prescription and ensure effective treatment of depression with little or no side effects of drugs.