Background Sunlight has profound impacts on physical and mental health, beyond vision, including effects on circadian rhythms, alertness, mood, and sleep. A family history of any mood disorders is strongly associated with psychiatric disorders including bipolar disorder. The purpose of this study was to evaluate the association between a family history of any mood disorder in patients with bipolar I disorder and solar insolation at varied international onset locations.Methods Data for this analysis were available from 5842 patients with a diagnosis of bipolar I disorder obtained at 83 collection sites in both hemispheres. This included 4752 patients from 71 collection sites in the northern hemisphere and 1090 patients from 12 collection sites in the southern hemisphere. Patient data variables were obtained from records or interviews. Solar insolation data were obtained from The National Aeronautics and Space Administration (NASA) Power database for each onset location, and the ratio of the mean monthly minimum/mean monthly maximum solar insolation was calculated. Typically, the ratio is largest near the equator (little yearly change in solar insolation) and smallest near the poles (large yearly change in solar insolation).Results A significant relationship was found between a family history of any mood disorder, the ratio of the mean monthly minimum/mean monthly maximum solar insolation, and gender. The odds of a family history of mood disorder increased as patient location nears the poles and decreased near the equator. Female gender also increased the odds of having a family history of a mood disorder.Conclusions This study highlighted the association between family history, solar insolation, and gender in international patients with bipolar I disorder. Given the profound effects of sunlight on human health, the family of patients with bipolar disorder who live in the same location with the same solar insolation, and especially females, may be at increased risk for a mood disorder.
Background:Postictal psychosis (PIP) is a serious complication that can follow seizure clusters, including those provoked during long-term video-electroencephalographic monitoring (LTVEM). Early detection and appropriate treatment of PIP are crucial to implement LTVEM safely. However, managing PIP becomes challenging when patients conceal symptoms, and psychotic symptoms are ambiguous. Case Presentation:A female patient in her 30s with drug-resistant mesial temporal lobe epilepsy due to right hippocampal sclerosis underwent LTVEM at an epilepsy center. After seizure clusters occurred on hospital Days 2 and 3, she remained superficially stable apart from subtle psychotic symptoms beginning on hospital Day 4. Despite a thorough psychiatric assessment, she denied any psychotic experiences and was discharged as scheduled on hospital Day 7. Immediately after discharge, however, she displayed overt psychotic symptoms, necessitating emergency involuntary psychiatric admission. Her psychotic symptoms resolved within 16 days of psychiatric hospitalization. Upon recovery, she disclosed that she had concealed her symptoms during LTVEM because auditory command hallucinations had discouraged her from discussing the symptoms with her physicians, and her persecutory delusions, which were directed specifically toward the hospital and medical staff, had fostered a profound mistrust. Conclusion:The present case highlights a diagnostic pitfall caused by overlooking PIP occurring during LTVEM, particularly in patients in whom the psychotic content is directed against the hospital and medical staff. The absence of overt behavioral disturbances does not exclude PIP. Close multidisciplinary collaboration between epileptologists and psychiatrists is essential to ensure the patient's safety.
Abstract Background Individuals at ultra-high risk for psychosis (UHR) exhibit an elevated vulnerability to psychosis as a result of excessive stress, rendering resilience of critical importance. As a biological marker for UHR, blood levels of cytokines are gaining attention. Specifically, serum concentrations of transforming growth factor-β1 (TGF-β1), a neuroprotective cytokine, have been suggested to maintain social functioning in UHR individuals. Aims & Objectives The present study examined longitudinal changes in serum concentrations of several inflammatory and neuroprotective cytokines among UHR individuals before and after the first state of emergency declared in response to COVID-19 on April 7, 2020, in Japan, which imposed strong nationwide behavioral restrictions. Method A multicenter, longitudinal cohort study was conducted which included seven hospitals affiliated with academic institutions in Japan, i.e., the National Center of Neurology and Psychiatry, the University of Toyama, Toho University, Nara Medical University, Tohoku University, Kurume University, and Chiba University. This study was also a joint collaborative study with Janssen Pharmaceutical K.K. of Johnson and Johnson in Japan. Results Participants included 52 subjects with UHR and 28 healthy volunteers as a control group (HC). Serum concentrations of brain-derived neurotrophic factor, which has been demonstrated to decrease in response to psychological stressors, exhibited a decrease following the state of emergency declaration in comparison to levels prior to the declaration in both UHR (p < 0.001) and HC (p < 0.001). Especially in UHR, blood concentrations of TGF-β1 (p < 0.001) and TGF-β2 (p < 0.001), which possess neuroprotective effects, were increased, while levels of the inflammatory cytokines, e.g., interferon-γ (p < 0.001), interleukin-6 (p = 0.002), and interleukin-12p70 (p < 0.001), were decreased compared to pre-declaration levels. Mixed-effects models for repeated measures revealed a significant increase in TGF-β1 and TGF-β2 concentrations as well as a significant decrease in inflammatory cytokine levels only in the UHR, but not in the HC. Discussion & Conclusions Increased levels of neuroprotective cytokines in response to psychological stress for individuals with UHR may suggest compensatory mechanisms that could support resilience during the course of the pandemic which may avert the exacerbation of psychiatric symptoms due to neuroinflammation. The findings in this study provide potential insights for the development of strategies aimed at preventing the onset of psychosis and facilitating early intervention in individuals with UHR.
The association between body mass index (BMI) and pancreatic cancer remains elusive in Asian populations. Clarifying the causal relationship between type 2 diabetes (T2D) and pancreatic cancer warrants triangulation of evidence, with Mendelian Randomization (MR) providing a robust approach. A two-sample, multivariable MR analysis was performed to investigate the associations between BMI, T2D, and pancreatic cancer risk in the Japanese population. Single nucleotide polymorphisms (SNPs) associated with BMI and T2D were selected from the Genome-Wide Association Study (GWAS) Catalog, and summary statistics for pancreatic cancer were derived from our previous GWAS in the Japanese population. MR analyses were performed using a random-effects inverse variance-weighted (IVW) method as well as sensitivity analyses. Genetic predisposition to T2D, assessed using 891 SNPs, was associated with increased pancreatic cancer risk (IVW odds ratio [OR]: 1.16; 95% confidence interval [CI]: 1.08-1.25 per 1-unit increase in the ln odds of T2D). MR-Egger and weighted median MR analyses yielded similar results. By contrast, genetically indexed BMI showed no association with pancreatic cancer risk (IVW OR: 1.00; 95% CI: 0.95-1.04 per 1 kg/m2 increase). The association between T2D and pancreatic cancer remained significant after adjusting for BMI (OR: 1.15; 95% CI: 1.07-1.24), while BMI was not significant in univariable or multivariable analyses. Our MR study supports a modest causal association of T2D, independent of BMI, with pancreatic cancer risk.
