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Background Methods Results Conclusions Stressors induce depression together with parenting experienced in childhood, personality traits, and sleep. In this study, we investigated factors associated with the development of depression in a long‐term stressful environment, namely, the Antarctic Research Expedition wintering party, by comparing 2 groups, the depression and nondepression groups.A self‐administered questionnaire was used to survey 91 members of the Japanese Antarctic Research Expedition who spent winters in the Antarctic base. Psychological evaluations of depression, anxiety, and sleep were performed using a questionnaire every 3 months during the participants’ stay in Antarctica. The primary endpoint was the occurrence of minor or major depression, as evaluated by the PHQ‐9 score.Participants with a PHQ‐9 score of 5 or more during their stay in Antarctica were defined as the depression group (25 subjects), and participants with a PHQ score of 4 or less were defined as the nondepression group (43 subjects). Compared with the nondepression group, the depression group had significantly higher scores for predeparture PHQ‐9, state and trait anxiety, sleep disturbance, and neuroticism. Multivariable logistic regression analyses showed that higher predeparture scores of subthreshold depressive symptoms and neuroticism were found to be significant predictors of the occurrence of depression during their stay in Antarctica.This study prospectively showed that subthreshold depressive symptoms and neuroticism, which were suggested as risk factors in previous studies, were confirmed to be risk factors for depression. The results of our study are expected to contribute to the understanding of depression in harsh environments. [ABSTRACT FROM AUTHOR]

Background: Prior research has shown that inappropriate childhood nurturing experiences (low care and high overprotection), trait anxiety, and depressive rumination are risk factors for depression. However, no studies to date have analyzed the overall association between these factors and depressive symptoms. In the present study, we hypothesized that depressive rumination mediates the impacts of inappropriate childhood nurturing experiences on depressive symptoms, and that these mediating effects are moderated by trait anxiety, and tested these hypotheses in adult volunteers. Methods: The subjects were adult volunteers who were investigated between April 2017 and April 2018. A self-report questionnaire on demographic data, childhood nurturing experiences, trait anxiety, depressive rumination, and depressive symptoms was distributed to conduct the survey, and written informed consent and valid responses were obtained from 585 subjects. Mediation and moderated-mediation analyses were performed by SPSS 28 and macro PROCESS 4.0 software. This study was approved by the Ethics Committee of Tokyo Medical University. Results: Parental care showed a significant negative indirect effect on depressive symptoms via its effect on depressive rumination (p < 0.01), whereas parental overprotection showed the opposite effect (p < 0.01). Furthermore, the mediation effect of depressive rumination on depressive symptoms was increased by trait anxiety (p < 0.05). Conclusion: Our present study demonstrated that the main factor affecting depressive symptoms is inappropriate childhood nurturing experiences, which indirectly enhance depression by intensifying depressive rumination, and that depressive rumination and trait anxiety mutually reinforce each other to enhance depressive symptoms. These findings may be useful for the prevention of depressive symptoms. Large-scale prospective studies are needed to confirm the causal associations among these factors in the future. [ABSTRACT FROM AUTHOR]

Background: Previously, we demonstrated that childhood maltreatment could worsen depressive symptoms through neuroticism. On the one hand, some studies report that sleep disturbances are related to childhood maltreatment and neuroticism and worsens depressive symptoms. But, to our knowledge, no reports to date have shown the interrelatedness between childhood maltreatment, neuroticism, and depressive symptoms, and sleep disturbance in the one model. We hypothesized that sleep disturbance enhances the influence of maltreatment victimization in childhood or neuroticism on adulthood depressive symptoms and the mediation influence of neuroticism between maltreatment victimization in childhood and adulthood depressive symptoms. Subjects and methods: Total 584 Japanese volunteer adults recruited through convenience sampling from 4/2017 to 4/2018 were assessed regarding their characteristics of demographics, history of childhood maltreatment, sleep disturbance, neuroticism, and depressive symptoms with questionnaires self-administered. Survey data were analyzed using simple moderation models and a moderating mediation model. Results: The interaction of sleep disturbance with childhood maltreatment or neuroticism on depressive symptoms was significantly positive. Furthermore, the moderating effect of sleep disturbance on the indirect effect of childhood maltreatment to depressive symptoms through neuroticism was significantly positive. Limitations: Because this was a cross-sectional study, a causal relationship could not be confirmed. Conclusions: Our findings indicate that individuals with milder sleep disturbance experience fewer depressive symptoms attributable to neuroticism and childhood maltreatment. Additionally, people with less sleep disturbance have fewer depressive symptoms arising from neuroticism owing to childhood maltreatment. Therefore, improvement of sleep disturbance will buffer the aggravating effect of childhood maltreatment, neuroticism caused by various factors, and neuroticism resulting from childhood maltreatment on depressive symptoms. [ABSTRACT FROM AUTHOR]

The regulation of cue-induced craving for cigarettes is a key factor in smoking cessation. Outcomes of smoking cessation have been linked to self-efficacy, faith in one's own ability, in smokers. However, no study has examined the neural basis of self-efficacy during the control of craving. We examined whether self-efficacy can affect the neural response to smoking cues in smokers and ex-smokers using functional magnetic resonance imaging. During scanning, participants were instructed (1) to view smoking-related images passively, (2) to view the smoking-related images with a strategy focused on self-efficacy to control cue-induced craving or (3) to view neutral images. In smokers, the self-efficacy strategy significantly reduced self-reported craving. This strategy was related to increased activation in the rostral medial prefrontal cortex (rmPFC) and the pregenual anterior cingulate cortex in smokers compared with ex-smokers. Furthermore, smokers showed increased effective connectivity between rmPFC and hippocampus and between pregenual anterior cingulate cortex and parahippocampus gyrus when employing the self-efficacy strategy compared with ex-smokers. The magnitude of the rmPFC-hippocampus connectivity was positively correlated with self-reported self-efficacy. Our findings suggest that in smokers, self-efficacy is related to activation and connectivity in brain regions involved in regulating craving and self-assessment. The current study provides evidence for understanding the vunderlying cognitive and neurobiological mechanisms involved in the control of craving to smoke cigarettes. [ABSTRACT FROM AUTHOR]

Aim: The association of parenting experiences in childhood with anxiety symptoms in adulthood has yet to be clarified. We hypothesized that interpersonal sensitivity (IPS) mediates the impacts of parenting experiences in childhood on anxiety symptoms and negative assessment of life events in adulthood., Methods: An observational cross-sectional study was carried out from January 2014 to August 2014 on 853 adults. Participants provided their demographic information and answered the following four self-administered questionnaires: Parental Bonding Instrument (PBI), Interpersonal Sensitivity Measure (IPSM), Life Experiences Survey (LES), and State-Trait Anxiety Inventory Form Y (STAI-Y). The data of a total of 404 participants who agreed to take part in this study were analyzed., Results: Multiple regression analysis with the State Anxiety subscale of STAI-Y as the dependent variable identified the following five out of the 15 independent variables as being statistically significant: IPSM total, LES positive and negative, PBI paternal overprotection, and employment status. This model explains 17.8% of the State Anxiety subscale score. In the structural equation models, the Care subscale showed significant indirect negative effects on State Anxiety subscale and LES negative score through a decrease in IPSM total score ( β  = -0.061 and -0.042, respectively). The former indirect effect accounted for 31.6%, and the latter accounted for 56.8% of the total effects. In contrast, Overprotection subscale had opposite effects to Care subscale., Conclusion: These results suggest that parenting experiences in childhood are related to adult anxiety symptoms and the negative assessment of life events indirectly through IPS., Competing Interests: Jiro Masuya has received personal compensation from Otsuka Pharmaceutical, Eli Lilly, Astellas, and Meiji Yasuda Mental Health Foundation, and grants from Pfizer. Ichiro Kusumi has received personal compensation from Astellas, Chugai Pharmaceutical, Daiichi Sankyo, Dainippon Sumitomo Pharma, Eisai, Eli Lilly, Janssen Pharmaceutical, Kyowa Hakko Kirin, Meiji Seika Pharma, MSD, Nippon Chemiphar, Novartis Pharma, Ono Pharmaceutical, Otsuka Pharmaceutical, Pfizer, Tanabe Mitsubishi Pharma, Shionogi, and Yoshitomiyakuhin, and has received research grants from AbbVie GK, Asahi Kasei Pharma, Astellas, Boehringer Ingelheim, Chugai Pharmaceutical, Daiichi Sankyo, Dainippon Sumitomo Pharma, Eisai, Eli Lilly, GlaxoSmithKline, Kyowa Hakko Kirin, Meiji Seika Pharma, MSD, Novartis Pharma, Ono Pharmaceutical, Otsuka Pharmaceutical, Pfizer, Takeda Pharmaceutical, Tanabe Mitsubishi Pharma, Shionogi, and Yoshitomiyakuhin, and is a member of the advisory board of Dainippon Sumitomo Pharma and Tanabe Mitsubishi Pharma. Takeshi Inoue has received personal compensation from Mochida Pharmaceutical, Takeda Pharmaceutical, Eli Lilly, Janssen Pharmaceutical, MSD, Taisho Toyama Pharmaceutical, Yoshitomiyakuhin, and Daiichi Sankyo; grants from Shionogi, Astellas, Tsumura, and Eisai; and grants and personal compensation from Otsuka Pharmaceutical, Dainippon Sumitomo Pharma, Mitsubishi Tanabe Pharma, Kyowa Pharmaceutical Industry, Pfizer, Novartis Pharma, and Meiji Seika Pharma; and is a member of the advisory boards of Pfizer, Novartis Pharma, and Mitsubishi Tanabe Pharma. The other authors declare that they have no actual or potential conflicts of interest associated with this study., (© 2023 The Authors. Psychiatry and Clinical Neurosciences Reports published by John Wiley & Sons Australia, Ltd on behalf of Japanese Society of Psychiatry and Neurology.)

It is widely known that there is a high prevalence of cigarette smoking in schizophrenia. One of the explanations is the self-medication hypothesis. Based on this hypothesis, it has been suggested that nicotine has procognitive effect or even neuroprotective effect in schizophrenia. However, cigarettes contain numerous neurotoxic substances, making the net effect of cigarette smoking on brain function and structure complex. Indeed, recent studies have called into question the self-medication hypothesis. We aimed to test whether there is an interaction between diagnosis and smoking status in gray matter volume, ie, whether smoking has specific effects on gray matter or whether main effects of these 2 variables additively affect common brain regions. Magnetic resonance imaging (MRI) images were obtained from 4 groups: (1) normal controls with no smoking history, (2) normal controls currently smoking and/or with a past history of smoking, (3) schizophrenia patients with no smoking history, and (4) schizophrenia patients currently smoking and/or with a past history of smoking. We used voxel-based morphometry to compare gray matter volumes among the 4 groups. We did not find any interaction between diagnosis and smoking, but we did find negative additive effects of schizophrenia diagnosis and smoking status in the left prefrontal cortex. The decrease in left prefrontal volume was associated with greater numbers of cigarette pack years and severe positive and negative symptoms. The current findings do not support the neuroprotective effect of smoking on gross brain structure in schizophrenia, emphasizing the necessity of longitudinal studies to test causal relationships among these variables.