Depressive disorders pose significant challenges to global public health, necessitating effective prevention and management strategies. Notably, the occurrence of suicide frequently coincides with depressive episodes. Suicide is as a paramount global health concern that demands efficacious preventive strategies. Current psychiatric approaches heavily rely on pharmacological interventions but have had limited success in addressing the global burden of mental health issues. Suboptimal nutrition, with its impact on the neuroendocrine system, has been implicated in the underlying pathology of depressive disorders. Folate, a group of water-soluble compounds, plays a crucial role in various central nervous system functions. Depressed individuals often exhibit low levels of serum and red blood cell folate. Multiple studies and systematic reviews have investigated the efficacy of folic acid and its derivative, L-methylfolate, which can cross the blood-brain barrier, as stand-alone or adjunct therapies for depression. Although findings have been mixed, the available evidence generally supports the use of these compounds in depressed individuals. Recent studies have established links between the one-carbon cycle, folate-homocysteine balance, immune system function, glutamate excitation via NMDA (N-methyl-D-aspartate) receptors, and gut microbiome eubiosis in mood regulation. These findings provide insights into the complex neurobiological mechanisms underlying the effects of folate and related compounds in depression. Through a comprehensive review of the existing literature, this study aims to advance our understanding of the therapeutic potential of folic acid and related compounds in depression treatment. It also seeks to explore their role in addressing suicidal tendencies and shed light on the neurobiological mechanisms involved, leveraging the latest discoveries in depression research.

Folate and Its Significance in Depressive Disorders and Suicidality: A Comprehensive Narrative Review.

Background Both obesity (OB) and periodontitis (PD) are chronic non-communicable diseases, and numerous epidemiological studies have demonstrated the association between these two diseases. However, the molecular mechanisms that could explain the association between OB and PD are largely unclear. This study aims to investigate the common gene signatures and biological pathways in OB and PD through bioinformatics analysis of publicly available transcriptome datasets. Methods The RNA expression profile datasets of OB (GSE104815) and PD (GSE106090) were used as training data, and GSE152991 and GSE16134 as validation data. After screening for differentially expressed genes (DEGs) shared by OB and PD, gene enrichment analysis, protein-protein interaction (PPI) network construction, GeneMANIA analysis, immune infiltration analysis and gene set enrichment analysis (GSEA) were performed. In addition, receiver operating characteristic (ROC) curves were used to assess the predictive accuracy of the hub gene. Finally, we constructed the hub gene-associated TF-miRNA-mRNA regulatory network. Results We identified a total of 147 DEGs shared by OB and PD (38 down-regulated and 109 up-regulated). Functional analysis showed that these genes were mainly enriched in immune-related pathways such as B cell receptor signalling, leukocyte migration and cellular defence responses. 14 hub genes (FGR, MNDA, NCF2, FYB1, EVI2B, LY86, IGSF6, CTSS, CXCR4, LCK, FCN1, CXCL2, P2RY13, MMP7) showed high sensitivity and specificity in the ROC curve analysis. The results of immune infiltration analysis showed that immune cells such as macrophages, activated CD4 T cells and immune B cells were present at high infiltration levels in both OB and PD samples.The results of GeneMANIA analysis and GSEA analysis suggested that five key genes (FGR, LCK, FYB1, LY86 and P2RY13) may be strongly associated with macrophages. Finally, we constructed a TF-miRNA-mRNA regulatory network consisting of 233 transcription factors (TFs), 8 miRNAs and 14 mRNAs based on the validated information obtained from the database. Conclusions Five key genes (FGR, LCK, FYB1, LY86, P2RY13) may be important biomarkers of OB and PD. These genes may play an important role in the pathogenesis of OB and PD by affecting macrophage activity and participating in immune regulation and inflammatory responses.

/pdf/transcriptomic-analysis-reveals-shared-gene-signatures-and-1mnzjl4b.pdf

Transcriptomic analysis reveals shared gene signatures and molecular mechanisms between obesity and periodontitis

Periodontal disease is a complex and progressive chronic inflammatory condition that leads to the loss of alveolar bone and teeth. It has been associated with various systemic diseases, including diabetes mellitus and obesity, among others. Some of these conditions are part of the metabolic syndrome cluster, a group of interconnected systemic diseases that significantly raise the risk of cardiovascular diseases, diabetes mellitus, and stroke. The metabolic syndrome cluster encompasses central obesity, dyslipidemia, insulin resistance, and hypertension. In this review, our objective is to investigate the correlation between periodontal disease and the components and outcomes of the metabolic syndrome cluster. By doing so, we aim to gain insights into the fundamental mechanisms that link each systemic condition with the metabolic syndrome. This deeper understanding of the interplay between these conditions and periodontal disease can pave the way for more effective treatments that take into account the broader impact of managing periodontal disease on the comprehensive treatment of systemic diseases, and vice versa.

Periodontal Disease and Its Association with Metabolic Syndrome—A Comprehensive Review

Periodontitis is a chronic infectious disorder damaging periodontal tissues, including the gingiva, periodontal ligament, cementum, and alveolar bone. It arises from the complex interplay between pathogenic oral bacteria and host immune response. Contrary to the previous view of “energy factories”, mitochondria have recently been recognized as semi-autonomous organelles that fine-tune cell survival, death, metabolism, and other functions. Under physiological conditions, periodontal tissue cells participate in dynamic processes, including differentiation, mineralization, and regeneration. These fundamental activities depend on properly functioning mitochondria, which play a crucial role through bioenergetics, dynamics, mitophagy, and quality control. However, during the initiation and progression of periodontitis, mitochondrial quality control is compromised due to a range of challenges, such as bacterial–host interactions, inflammation, and oxidative stress. Currently, mounting evidence suggests that mitochondria dysfunction serves as a common pathological mechanism linking periodontitis with systemic conditions like type II diabetes, obesity, and cardiovascular diseases. Therefore, targeting mitochondria to intervene in periodontitis and multiple associated systemic diseases holds great therapeutic potential. This review provides advanced insights into the interplay between mitochondria, periodontitis, and associated systemic diseases. Moreover, we emphasize the significance of diverse therapeutic modulators and signaling pathways that regulate mitochondrial function in periodontal and systemic cells.

Mitochondrial Dysfunction in Periodontitis and Associated Systemic Diseases: Implications for Pathomechanisms and Therapeutic Strategies

Modulatory influence of melatonin on apical periodontitis in Wistar rats fed a high-fat diet.

Background A previous 2014 meta-analysis reported a positive association between obesity and periodontitis. It was considered necessary to update the recently published papers and to analyse subgroups on important clinical variables that could affect the association between obesity and periodontitis. Therefore, we updated the latest studies and attempted to derive more refined results. Methods All observational studies were eligible for inclusion. The Newcastle–Ottawa scale was used to qualitatively evaluate the risk of bias. Subgroup analyses were conducted for patients aged 18–34, 35–54, and 55+ years and the countries (European countries, USA, Brazil, Japan, Korea, and other Asian countries). Results Thirty-seven full-text articles were included. Obesity conferred increased odds of periodontal disease with an odds ratio (1.35, 95% CI: 1.05–1.75). In the subgroup analysis by age, the odds ratio was the highest in the 18–34 years group (2.21, 95% CI: 1.26–3.89). In the subgroup analysis by country, European countries had the highest odds ratio (2.46, 95% CI: 1.11–5.46). Conclusion Despite the differences in degree, a positive association between obesity and periodontitis was found regardless of country or age. Therefore, medical professionals should try to prevent periodontitis by controlling patient weights, and more studies should be conducted to determine the association between obesity and oral health. Systematic Review Registration https://www.crd.york.ac.uk/prospero/, identifier CRD42022301343.

/pdf/obesity-and-periodontitis-a-systematic-review-and-updated-1wj7kln7.pdf

Obesity and periodontitis: A systematic review and updated meta-analysis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9822839

Global prevalence of suicide by latitude: A systematic review and meta-analysis

White blood cells (WBCs) act as mediators of inflammatory responses and are commonly measured in hospitals. Although several studies have reported a relation between WBC count and mortality, no systematic review or meta-analysis has been conducted. This study aimed to identify an association between WBC count and mortality. We conducted a systematic search on Embase using keywords such as “white blood cell” and “mortality.” We analyzed the hazard ratios (HRs) for WBC count of 1.0 × 109 cells/L regarding 2 criteria: the cause of mortality and the follow-up period. A total of 13 of 222 articles comprising a total of 62,904 participants were included in this study, meeting the criteria set. A positive association was observed between WBC count and mortality, as indicated by an HR of 1.10 (95% confidence interval [CI] 1.08 to 1.13). In additionally, WBC count emerged as a significant predictor of mortality in both groups, with an HR of 1.10 (95% CI 1.07 to 1.12) for patients with cardiovascular disease and an HR of 1.12 (95% CI 1.07 to 1.17) for the general population or patients with COVID-19. Furthermore, a higher WBC count demonstrated a significant association with long-term all-cause mortality (HR 1.09, 95% CI 1.07 to 1.12) and long-term cardiovascular mortality (HR 1.05, 95% CI 1.02 to 1.07). Similarly, a significant association was found between higher WBC count and short-term all-cause mortality (HR 1.12, 95% CI 1.09 to 1.16) and cardiovascular mortality (HR 1.12, 95% CI 1.07 to 1.17). Further research is necessary to explore the relation between WBC count and disease progression or death and to establish causality between elevated WBC count and disease progression. White blood cells (WBCs) act as mediators of inflammatory responses and are commonly measured in hospitals. Although several studies have reported a relation between WBC count and mortality, no systematic review or meta-analysis has been conducted. This study aimed to identify an association between WBC count and mortality. We conducted a systematic search on Embase using keywords such as “white blood cell” and “mortality.” We analyzed the hazard ratios (HRs) for WBC count of 1.0 × 109 cells/L regarding 2 criteria: the cause of mortality and the follow-up period. A total of 13 of 222 articles comprising a total of 62,904 participants were included in this study, meeting the criteria set. A positive association was observed between WBC count and mortality, as indicated by an HR of 1.10 (95% confidence interval [CI] 1.08 to 1.13). In additionally, WBC count emerged as a significant predictor of mortality in both groups, with an HR of 1.10 (95% CI 1.07 to 1.12) for patients with cardiovascular disease and an HR of 1.12 (95% CI 1.07 to 1.17) for the general population or patients with COVID-19. Furthermore, a higher WBC count demonstrated a significant association with long-term all-cause mortality (HR 1.09, 95% CI 1.07 to 1.12) and long-term cardiovascular mortality (HR 1.05, 95% CI 1.02 to 1.07). Similarly, a significant association was found between higher WBC count and short-term all-cause mortality (HR 1.12, 95% CI 1.09 to 1.16) and cardiovascular mortality (HR 1.12, 95% CI 1.07 to 1.17). Further research is necessary to explore the relation between WBC count and disease progression or death and to establish causality between elevated WBC count and disease progression. 

The Prognostic Significance of Leukocyte Count on All-Cause and Cardiovascular Disease Mortality: A Systematic Review and Meta-Analysis.

Introduction: Debate on the association between the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) and the risk of developing cancer has been ongoing for decades. This study aimed to generate reliable results by analysing observational studies published in the decade after our last meta-analysis was conducted. Methods: We searched Embase and Medline databases on 21 January 2021 for cohort and case-control studies. Two researchers independently reviewed the literature and assessed the title and abstract of each publication. The I2 statistic used to evaluate the heterogeneity of the effect measures. Risk of bias was qualitatively assessed using the Newcastle–Ottawa scale. Results and discussion: We included an additional 16 cohort, 6 nested case-control, and 9 conventional case-control studies in the updated analysis. Overall HRs decreased, while overall relative risks increased. Conclusion: Our results show some protective effects through the hazard ratio and some detrimental effects through the relative risk. Large-scale investigations of cohorts followed up for decades are needed to clarify association. Plain Language Summary Introduction: Two types of drug, angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), have been linked to the risk of developing cancer. We performed a meta-analysis by aggregating individual studies looking into the cancer risk of ACEIs and ARBs. Methods: We searched for articles on Embase and Medline databases until 21 January, 2021. Two researchers independently reviewed the literature and assessed the title and abstract of each publication. Results: Overall, the hazard ratio showed less than 1, while the relative risks showed higher than 1. Conclusion: Our results show some protective effects through the hazard ratio and some detrimental effects through the relative risk. Evidence supporting the risk of developing cancer is insufficient to prevent prescribing ACEIs or ARBs for patients with high blood pressure.

https://doi.org/10.1177/20420986221129335

Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and cancer risk: an updated meta-analysis of observational studies

INTRODUCTION Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder primarily affecting the voluntary motor nervous system. Several observational studies have provided conflicting results regarding the association between smoking and ALS. Therefore, our objective was to investigate this association through a systematic review, meta-analysis, and dose-response analysis. METHODS On 16 January 2023, we initially extracted records from medical databases, which included Medline, Embase, Web of Science, Scopus, and ScienceDirect. We included case-control and cohort studies as eligible studies. Subgroup analyses were performed based on sex, study design, and current smoking. Restricted cubic-spline analysis was utilized to assess the dose-response relationship between smoking (pack-years) and ALS. RESULTS Twenty-eight case-control and four cohort studies met the inclusion criteria. The unadjusted OR for the overall association between smoking and ALS was 1.14 (95% CI: 1.06–1.22, I2=44%, p<0.001), and the adjusted OR (AOR) was 1.12 (95% CI: 1.03–1.21, I2=49%, p=0.009). Subgroup analysis revealed a more pronounced association among current smokers, with an AOR of 1.28 (95% CI: 1.10–1.49, I2=66%, p<0.001) and AOR of 1.28 (95% CI: 1.10–1.48, I2=58%, p=0.001). In the dose-response analysis, the non-linear model revealed an inverted U-shaped curve. CONCLUSIONS Our study provides evidence of a positive relationship between smoking and the risk of ALS. To mitigate the risk of developing ALS, discontinuing smoking, which is a modifiable risk factor, may be crucial. TRIAL REGISTRATION: The study was registered in PROSPERO. IDENTIFIER: CRD42023388822

Association of smoking with amyotrophic lateral sclerosis: A systematic review, meta-analysis, and dose-response analysis

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