BACKGROUND: Lipocalin-2 (LCN-2) is an osteokine that suppresses appetite, stimulates insulin secretion, regulates bone remodeling, and is induced by proinflammatory cytokines. The aim of this work was to investigate the participation of LCN-2 in periodontitis associated with type 2 diabetes (T2D) by evaluating alveolar bone loss, glycemic control, inflammation, and femur fragility.
METHODS: A murine model of periodontitis with T2D and elevated LCN-2 concentration was used. Functional LCN-2 inhibition was achieved using an anti-LCN-2 polyclonal antibody, and isotype immunoglobulin G was used as a control. The alveolar bone and femur were evaluated by micro-CT. Glucose metabolism was determined. Tumor necrosis factor (TNF-α) and receptor activator of nuclear factor kappa-B ligand (RANKL) levels in alveolar bone lysates were quantified using ELISA, and serum cytokines were quantified using flow cytometry. A three-point bending test was performed in the femur, and RANKL levels were measured in femur lysates using ELISA.
RESULTS: Functional inhibition of LCN-2 in T2D-periodontitis mice decreased alveolar bone loss in buccal and palatal surfaces and preserved the microarchitecture of the remaining bone, decreased TNF-α and RANKL in alveolar bone, reduced hyperglycemia, glucose intolerance, and insulin resistance, and increased insulin production through improving the functionality of pancreatic β cells. Furthermore, this inhibition increased serum free-glycerol levels, decreased serum interleukin (IL)-6, increased serum IL-4, and reduced femur fragility and RANKL expression in the femur.
CONCLUSIONS: LCN-2 participates in periodontitis associated with T2D. Inhibiting its function in mice with T2D and periodontitis improves pancreatic β-cell function, and glucose metabolism and decreases inflammatory cytokines and bone-RANKL levels, which results in the preservation of femoral and alveolar bone microarchitecture.
CONCLUSIONS: In this study, we explored the role of a bone protein known as lipocalin-2 (LCN-2) in the connection between periodontitis and type 2 diabetes (T2D). Periodontitis is a destructive gum and alveolar bone disease. LCN-2 levels are increased in both T2D and periodontitis. Using a mouse model of T2D with periodontitis, we examined how blocking LCN-2 function affected various aspects of these two diseases. We found that this inhibition led to significant improvements. First, it reduced alveolar bone loss and preserved bone structure by decreasing local inflammation and bone resorption. Second, it improved glucose and lipid metabolism, leading to better blood-sugar control and decreased insulin resistance. Blocking the functions of LCN-2 also decreased systemic inflammation throughout the body and strengthened bone integrity. Overall, our results suggest that LCN-2 plays a crucial role in the periodontitis associated with T2D. By inhibiting LCN-2 function, we were able to improve pancreatic function, improve glucose metabolism, reduce inflammation, and enhance bone health. Targeting LCN-2 could be a promising strategy for the harmful effects of T2D and periodontitis.

Sarcopenia and pelvic floor disorders (PFDs) are prevalent and often cooccurring conditions in the aging population. However, their bidirectional relationship and underlying mechanisms remain underexplored. This narrative review aims to elucidate this relationship by exploring potential causative interplays, shared pathophysiological mechanisms, and common risk factors. A comprehensive literature search was conducted to identify relevant studies focusing on epidemiological associations, interaction mechanisms, and implications for patient care. While epidemiological studies demonstrate associations between sarcopenia and PFDs, our findings reveal a cyclical relationship where sarcopenia may exacerbate PFDs through mechanisms such as decreased muscle strength and mobility. Conversely, the presence of PFDs often leads to reduced physical activity due to discomfort and mobility issues, which in turn exacerbate the muscle atrophy associated with sarcopenia. Additionally, shared risk factors such as physical inactivity, nutritional deficiencies, metabolic syndrome, and menopausal hormonal changes likely contribute to the onset and progression of both conditions. These interactions underscore the importance of concurrently integrated care approaches that address both conditions. Effective management requires comprehensive screening, the recognition of contributing factors, and tailored exercise regimens supported by a multidisciplinary approach. Future research should focus on longitudinal studies tracking disease progression and evaluating the efficacy of multidisciplinary care models in optimizing patient outcomes.

Sleep is crucial for wellness, and emerging research reveals a profound connection to gut microbiota. This review explores the bidirectional relationship between gut microbiota and sleep, exploring the mechanisms involved and the therapeutic opportunities it presents. The gut-brain axis serves as a conduit for the crosstalk between gut microbiota and the central nervous system, with dysbiosis in the microbiota impairing sleep quality and vice versa. Diet, circadian rhythms, and immune modulation all play a part. Specific gut bacteria, like Lactobacillus and Bifidobacterium, enhance sleep through serotonin and gamma-aminobutyric acid production, exemplifying direct microbiome influence. Conversely, sleep deprivation reduces beneficial bacteria, exacerbating dysbiosis. Probiotics, prebiotics, postbiotics, and fecal transplants show therapeutic potential, backed by animal and human research, yet require further study on safety and long-term effects. Unraveling this intricate link paves the way for tailored sleep therapies, utilizing microbiome manipulation to improve sleep and health. Accelerated research is essential to fully tap into this promising field for sleep disorder management.

BACKGROUND: The study aimed to examine the bidirectional relationship between sarcopenia and depressive symptoms in a national, community-based cohort study, despite the unclear temporal sequence demonstrated previously.
METHODS: Data were derived from four waves (2011 baseline and 2013, 2015, and 2018 follow-ups) of the China Health and Retirement Longitudinal Study (CHARLS). A total of 17,708 participants aged 45 years or older who had baseline data on both sarcopenia status and depressive symptoms in 2011 were included in the study. For the two cohort analyses, a total of 8092 adults without depressive symptoms and 11,292 participants without sarcopenia in 2011 were included. Sarcopenia status was defined according to the Asian Working Group for Sarcopenia 2019 (AWGS 2019) criteria. Depressive symptoms were defined as a score of 20 or higher on the 10-item Center for Epidemiologic Studies Depressive Scale (CES-D-10). Cox proportional hazard regression models were conducted to examine the risk of depressive symptoms and sarcopenia risk, while cross-lagged panel models were used to examine the temporal sequence between depressive symptoms and sarcopenia over time.
RESULTS: During a total of 48,305.1 person-years follow-up, 1262 cases of incident depressive symptoms were identified. Sarcopenia exhibited a dose-response relationship with a higher risk of depressive symptoms (HR = 1.7, 95%CI: 1.2-2.3 for sarcopenia, and HR = 1.5, 95%CI: 1.2-1.8 for possible sarcopenia, p trend < 0.001). In the second cohort analysis, 240 incident sarcopenia cases were identified over 39,621.1 person-years. Depressive symptoms (HR = 1.5, 95%CI: 1.2-2.0) are significantly associated with a higher risk of developing sarcopenia after multivariable adjustment (p < 0.001, Cross-lagged panel analyses demonstrated that depressive symptoms were associated with subsequent sarcopenia (β = 0.003, p < 0.001). Simultaneously, baseline sarcopenia was also associated with subsequent depressive symptoms (β = 0.428, p < 0.001).
CONCLUSIONS: This study identified a bidirectional relationship between depressive symptoms and sarcopenia. It seems more probable that baseline sarcopenia is associated with subsequent depressive symptoms in a stronger pattern than the reverse pathway. The interlinkage indicated that maintaining normal muscle mass and strength may serve as a crucial intervention strategy for alleviating mood disorders.

UNASSIGNED: Sarcopenia and disability represent significant concerns impacting the health of older people. This study aimed to explore the bidirectional relationship between sarcopenia and disability in Chinese older people.
UNASSIGNED: This study recruited older people ≥60 years old from the China Health and Retirement Longitudinal Study. In phase I, the study analyzed the relation between disability and subsequent sarcopenia using multinomial logistic regression models. Conversely, in phase II, the study assessed whether sarcopenia was associated with future disability using binary logistic regression models.
UNASSIGNED: In phase I, 65 (16.80%) new cases of possible sarcopenia, 18 (4.65%) cases of sarcopenia, and 9 (2.33%) cases of severe sarcopenia were observed in the disabled older people and 282 (10.96%) new cases of possible sarcopenia, 97 (3.77%) cases of sarcopenia, 35 (1.36%) cases of severe sarcopenia were observed in the older people without disability. The OR (95% CI) for sarcopenia in older disabled individuals compared to those without disability was 1.61 (1.25-2.07). Adjusting for all covariates in 2011, the OR (95% CI) value for disabled individuals vs. those without disability was 1.35 (1.02-1.79). Subgroup analyses showed that disabled participants aged < 80 years were more likely to have sarcopenia (OR = 1.42, 95% CI: 1.07-1.89), and the risk of sarcopenia did not differ significantly between sex subgroups. In phase II, 114 cases (33.83%) in the possible sarcopenia patients, 85 cases (28.91%) in the sarcopenia patients, 23 cases (35.94%) in the severe sarcopenia patients, and 501 cases (16.10%) in the individuals without sarcopenia showed symptoms of disability. The OR (95% CI) for disability was 2.66 (2.08-3.40) in the possible sarcopenia patients, 2.12 (1.62-2.77) in the sarcopenia patients, and 2.92 (1.74-4.91) in the severe sarcopenia patients compared with the no sarcopenia patients. After adjusting for all covariates in 2011, the OR (95% CI) values were 2.21 (1.70-2.85) in the possible sarcopenia patients, 1.58 (1.14-2.19) in the sarcopenia patients, and 1.99 (1.14-3.49) in the severe sarcopenia patients, as compared to the older people without sarcopenia. Subgroup analyses showed that compared with men, women with possible sarcopenia had a higher risk of disability (OR = 2.80, 95% CI: 1.98-3.97). In addition, participants aged < 80 years with sarcopenia or severe sarcopenia s were more likely to have disability (OR = 2.13, 95% CI: 1.52-2.98; OR = 2.98, 95% CI: 1.60-5.54).
UNASSIGNED: The occurrence of disability increase the risk of sarcopenia in the older people, and baseline sarcopenia predicts the future disability in older people.

OBJECTIVE: The objective of this study was to examine the relationship between sleep duration and prediabetes, as well as to evaluate the influence of inflammation in mediating this association.
METHODS: A total of 4632 participants from the China Health and Retirement Longitudinal Study (CHARLS) were included in this study, comprising both baseline and 4-year follow-up data. The prospective relationship between sleep duration and the risk of prediabetes was examined using logistic regression models. We used multinomial logistic regression to evaluate the impact of prediabetes on sleep duration changes over follow-up, assessing the role of C-reactive protein in the association using mediation analysis.
RESULTS: Participants with short sleep duration (<5 hours) had a higher risk of prediabetes (odds ratios=1.381 [95% CI: 1.028-1.857]) compared to those with normal sleep durations (7-8 hours). However, excessive sleep durations (≥9 hours) did not show a statistically significant association with prediabetes risk. Moreover, individuals at least 60years old who experienced short sleep durations exhibited a higher risk of prediabetes. Individuals with prediabetes were more likely to have shorter sleep duration than excessive sleep duration (relative risk ratios=1.280 [95% CI: 1.059-1.547]). The mediation analysis revealed a mediating effect of C-reactive protein on the association between prediabetes and reduced sleep duration.
CONCLUSIONS: Short sleep duration was identified as a risk factor for the incidence of prediabetes. Conversely, prediabetes was found to contribute to shorter sleep duration rather than excessive sleep duration. Moreover, elevated levels of C-reactive protein may serve as a potential underlying mechanism that links prediabetes with shorter sleep.

Frailty and activities of daily living (ADL) disability are common conditions among older population. Studies on the bidirectional relationship between frailty and ADL are limited. The current study examined the cross-sectional and longitudinal associations between frailty and ADL in middle-aged and older Chinese individuals.
The data was collected through the China Health and Retirement Longitudinal Study (CHARLS), conducted in 2011, 2013, and 2015, encompassing 17,284 individuals aged ≥45 years. We excluded individuals without follow-up data. 2,631 participants finished the baseline survey. The definition of ADL disability encompasses difficulty in engaging in either basic activities of daily living (BADL) or instrumental activities of daily living (IADL). Frailty was assessed according to the Fried criteria. Logistic regression was utilized to examine odds ratios (ORs) and 95% confidence intervals (CIs) for assessing the cross-sectional relationships between ADL with frailty at baseline. The prediction effects were explored using Cox proportional hazards analysis, testing hazard ratios (HRs) and 95%CIs.
In cross-sectional analysis, BADL [OR = 6.660 (4.519-9.815)], IADL [OR = 5.950 (4.490-7.866)], and ADL [OR = 5.658 (4.278-7.483)] exhibited significant associations with frailty; frailty demonstrated significant associations with BADL [OR = 6.741 (4.574-9.933)], IADL [OR = 6.042 (4.555-8.016)] and ADL [OR = 5.735 (4.333-7.591)]. In longitudinal analysis, IADL and ADL were significantly associated with frailty in participants without baseline frailty in the short-term period [IADL: HR = 1.971 (1.150-3.379), ADL: HR = 1.920 (1.146-3.215)], IADL exhibited a significant association with frailty in the long-term period [HR = 2.056 (1.085-3.895)]. There was no significant link observed between frailty and an elevated risk of disability onset in BADL, IADL and ADL during the short-term period. When considering the long-term perspective, frailty exhibited a significant association with an elevated risk of disability onset in BADL [HR= 1.820 (1.126-2.939)] and IADL [HR = 1.724 (1.103-2.694)].
In middle-aged and older adults, ADL and IADL disability predicted frailty after 2-year follow-up, IADL disability predicted frailty after 4-year follow-up. Moreover, frailty did not predict BADL, IADL and ADL disability after 2-year follow-up. However, frailty predicted BADL and IADL disability after 4-year follow-up.

UNASSIGNED: Previous research has shown that testosterone deficiency (TD) increases the risk of anemia, but it is unclear whether anemia affects testosterone levels. This study investigated the influence of anemia on testosterone levels.
UNASSIGNED: Utilizing data from six NHANES cycles, including demographic, testosterone levels, and hemoglobin concentrations, we employed multivariable-adjusted logistic regression to investigate the relationship between anemia and testosterone levels. Moreover, a two-sample Mendelian randomization (MR) study employing genome-wide association study (GWAS) data examined the causal relationship. Kaplan-Meier survival estimation was used to compared the overall survival (OS) of anemic and nonanemic patients with low testosterone and normal testosterone levels.
UNASSIGNED: The inclusion of 21,786 participants (2318 with anemia and19,468 without anemia) revealed that nonanemic patients exhibited higher testosterone levels than did anemic patients (β = 22.616, 95% CI: 3.873-41.359, p = 0.01807). MR analysis confirmed anemia as a cause of TD (OR = 1.045, 95% CI: 1.020-1.071, p < 0.001). Anemic males with low testosterone had reduced OS compared to those with normal levels (p < 0.001).
UNASSIGNED: Anemia emerged as a potential risk factor for TD, highlighting a bidirectional relationship between these conditions. Additional prospective investigations are essential for the validation and reinforcement of our findings.

Glaucoma, a prevalent and debilitating eye disease, has long been associated with vision impairment and blindness. However, recent research has shed light on the often-underestimated psychological dimensions of this condition. Anxiety and depression, two pervasive psychiatric comorbidities, have been increasingly recognized among glaucoma patients. This comprehensive review aims to explore the intricate relationship between psychiatry and ophthalmology, in the context of managing depression and anxiety in glaucoma patients. By meticulously examining peer-reviewed literature, we synthesize current knowledge on the prevalence, risk factors, and underlying mechanisms of anxiety and depression in glaucoma. The evidence reveals that glaucoma patients face an elevated risk of experiencing these mood disorders. Factors such as progressive vision loss, complex medication regimens, and the fear of further visual deterioration contribute to their vulnerability. Moreover, we delve into the bidirectional relationship between glaucoma and mood disorders, shedding light on the complex interplay between ocular and emotional health. Our review investigates the implications of anxiety and depression on glaucoma management, including their potential impact on treatment adherence, disease progression, and overall quality of life. We also explore the neurobiological pathways linking glaucoma and mood disorders, providing a foundation for future research and potential therapeutic interventions. In conclusion, recognizing the psychological burden carried by glaucoma patients is essential for holistic and patient-centered care. This review underscores the pressing need for integrated approaches that bring together ophthalmological and psychiatric expertise to optimize the well-being of individuals facing the challenges of glaucoma. By addressing anxiety and depression in glaucoma care, healthcare providers can enhance the overall quality of life for these patients, ultimately leading to improved outcomes and a brighter future for those affected by this condition. This review offers valuable insight for healthcare practitioners and researchers, providing a concise overview of key topics and research in the field of managing depression and anxiety in glaucoma patients.

This comprehensive review examines the intricate interplay between personality factors and alcohol use, shedding light on the dynamic relationship that shapes the initiation, progression, and outcomes of alcohol-related behaviors. The exploration encompasses vital personality traits such as sensation seeking, impulsivity, neuroticism, extroversion, agreeableness, conscientiousness, and openness to experience. The bidirectional nature of this association is underscored, emphasizing how personality influences and is influenced by alcohol consumption patterns. Protective personality factors, including resilience, emotional regulation, and social support, are identified as crucial elements in mitigating the risk of alcohol use disorders (AUDs). The implications for clinical practice advocate for tailored interventions that address individual personality profiles, while policy considerations highlight the need for targeted prevention efforts that acknowledge the diverse ways individuals respond to alcohol use. Furthermore, a call for future research emphasizes emerging perspectives, improved methodologies, and ongoing exploration of intervention strategies to advance our understanding of this complex relationship and refine approaches for prevention and treatment. As we navigate this evolving field, the insights gleaned hold promise for shaping more compelling and nuanced interventions to address the diverse needs of individuals affected by AUDs.