Shirodhara is a brain relaxation therapy. The treatment induces a relaxed state with awareness that results in treating neurological conditions like mental stress (depression/anxiety/hypertension) and some of its beneficial side effects are soothing the central nervous system.

In the present study, the investigation aimed to analyze the ratios of brain waves, particularly focusing on the frontal region.

In this study, Shirodhara with "Ksheerabala thailam" medicinal oil was conducted on 16 participants and pre-post treatment brain signals were collected using an EEG acquisition tool and it was found that treatment induced relaxation aspects were observed among participants.

Welch's Fast Fourier transform (FFT) was used to analyze the EEG signals in order to obtain power spectral density (PSD) features, which indicated a signal's power dispersed across a range of frequencies. The effectiveness of treatment has been evaluated by examining the spectral power ratios of alpha/beta, theta/beta in the frontal region of the brain and physiological and psychological parameters.

Background: This study aimed to assess the impact of Enhanced Recovery After Surgery (ERAS) compliance and to identify which components of this protocol are most likely to affect postoperative outcomes in patients undergoing colorectal cancer surgery. Methods: This is a retrospective cohort evaluating patients who underwent elective colon resection. ERAS compliance was assessed based on adherence to the protocol components. The study examined the following outcomes: postoperative complications, readmission rates, mortality, conversion to open surgery, stoma creation, and length of hospital stay. Results: Of the 410 patients studied, 59% achieved ≥75% compliance. Comparison between compliance groups (<75% versus ≥75%) showed significant differences in overall complications (P = .002), severe complications (P = .001), and length of hospital stay (P < .001). The area under the receiver operating characteristic curve for predicting the absence of severe complications based on ERAS compliance was 0.677 (95% confidence interval: 0.602-0.752). Logistic regression analyses demonstrated that ERAS compliance was significantly associated with a reduced risk of severe complications (P < .001), as well as that the following items: avoiding prophylactic drains (P < .001), minimal use of postoperative opioids (P = .045), avoidance of postoperative salt and water overload (P < .001), postoperative nutritional support (P = .048), and early mobilization (P = .025). Conclusion: High ERAS compliance is associated with improved postoperative outcomes in colorectal cancer surgery. Key protocol components for preventing severe complications include avoiding prophylactic drains, minimal postoperative opioid use, avoiding salt and water overload, nutritional support, and early mobilization.

The combination of tuberculosis and pregnancy always raises questions about therapy, the specialness of management of pregnancy, obstetrics, postpartum period, and lactation; the effect of therapy on fetal development and the peculiarities of the tuberculosis course. Until recently, tuberculosis and pregnancy were considered a rare combination, but with the growing problem of HIV infection and worsening tuberculosis screening among adults, this combination has become quite common. Moreover, cases of congenital tuberculosis in newborns have begun to emerge. In this review, we analyzed features of immunologic and immuno-neuroendocrine reactivity in pregnant women that influence for prevalence TB and TB/HIV coinfection. The immuno-neuroendocrine changes characteristic of pregnancy have a multifactorial effect on antituberculosis immunity and determine the specificity of the course of tuberculosis against the background of pregnancy. These changes contribute to a more severe course of TB than before pregnancy. The structure of TB clinical forms in women who became ill during pregnancy and in the first year after childbirth is characterized by greater severity, higher frequency of multi-organ lesions, and the percentage of bacterial isolates is significantly higher among women with TB that developed in the postpartum period compared to women who developed it during pregnancy. HIV infection poses a particular threat, exacerbating immune response disorders that affect the effectiveness of treatment and disease progression in general.

The word "cancer" evokes myriad emotions, ranging from fear and despair to hope and determination. Cancer is aptly defined as a complex and multifaceted group of diseases that has unapologetically led to the loss of countless lives and affected innumerable families across the globe. The battle with cancer is not only a physical battle, but also an emotional, as well as a psychological skirmish for patients and for their loved ones. Cancer has been a part of our history, stories, and lives for centuries and has challenged the ingenuity of health and medical science, and the resilience of the human spirit. From the early days of surgery and radiation therapy to cutting-edge developments in chemotherapeutic agents, immunotherapy, and targeted treatments, the medical field continues to make significant headway in the fight against cancer. However, even after all these advancements, cancer is still among the leading cause of death globally. This urges us to understand the central hallmarks of neoplastic cells to identify novel molecular targets for the development of promising therapeutic approaches. Growing research suggests that stress mediators, including epinephrine, play a critical role in the development and progression of cancer by inducing neoplastic features through activating adrenergic receptors, particularly β-adrenoreceptors. Further, our experimental data has also shown that epinephrine mediates the growth of T-cell lymphoma by inducing proliferation, glycolysis, and apoptosis evasion via altering the expression levels of key regulators of these vital cellular processes. The beauty of receptor-based therapy lies in its precision and higher therapeutic value. Interestingly, the enhanced expression of β-adrenergic receptors (ADRBs), namely ADRB2 (β2-adrenoreceptor) and ADRB3 (β3-adrenoreceptor) has been noted in many cancers, such as breast, colon, gastric, pancreatic, and prostate and has been reported to play a pivotal role in facilitating cancer growth mainly by promoting proliferation, evasion of apoptosis, angiogenesis, invasion and metastasis, and chemoresistance. The present review article is an attempt to summarize the available findings which indicate a distinct relationship between stress hormones and cancer, with a special emphasis on epinephrine, considered as a key stress regulatory molecule. This article also discusses the possibility of using beta-blockers for cancer therapy.

This state-of-the-art review explores the relationship between depression and diabetes, highlighting the two-way influences that make treatment challenging and worsen the outcomes of both conditions. Depression and diabetes often co-occur and share genetic, lifestyle, and psychosocial risk factors. Lifestyle elements such as diet, physical activity, and sleep patterns play a role on the development and management of both conditions, highlighting the need for integrated treatment strategies. The evidence suggests that traditional management strategies focusing on either condition in isolation fall short of addressing the intertwined nature of diabetes and depression. Instead, integrated care models encompassing psychological support and medical management are recommended to improve treatment efficacy and patient adherence. Such models require collaboration across multiple healthcare disciplines, including endocrinology, psychiatry, and primary care, to offer a holistic approach to patient care. This review also identifies significant patient-related barriers to effective management, such as stigma, psychological resistance, and health literacy, which need to be addressed through patient-centered education and support systems. Future directions for research include longitudinal studies in diverse populations to further elucidate causal relationships and the exploration of novel therapeutic targets, as well as the effectiveness of healthcare models aimed at preventing the onset of one condition in individuals diagnosed with the other.

Depression is a common psychological disorder, and traditional therapeutic drugs often result in side effects such as emesis, dry mouth, headache, dysentery and constipation. Probiotics and goat milk have garnered widespread attention for their ability to modulate immune function and regulate the endocrine system, and for their anti-inflammatory effects. In this work, the effects of Tibetan goat kefir on the behavior, immune status, neuroendocrine response and gut microbiological composition of chronic unpredictable mild stress (CUMS) mouse models were evaluated.

The results indicated that Tibetan kefir goat milk significantly alleviated behavioral despair in mice. Furthermore, the results demonstrated that Tibetan kefir goat milk mitigated the inflammatory response in the mice and moderated the hyperactivity of the hypothalamic-pituitary-adrenal axis and the expression of brain-derived neurotrophic factor. Meanwhile, chronic stress-induced gut microbial abnormalities were restored. In addition, the correlation between gut microbiota and nervous system was evaluated.

These results explained the potential mechanism of Tibetan kefir in the antidepressant effect on the CUMS model and enriched diets for depressed patients. © 2024 Society of Chemical Industry.

Sensitivity to environmental stress and adversity may influence lung cancer risk, highlighting a critical link between psychosocial factors and cancer etiology.

To evaluate whether genetically estimated sensitivity to environmental stress and adversity is associated with lung cancer risk.

Data were obtained from a genome-wide association study identifying 37 independent genetic variants strongly associated with sensitivity to environmental stress and adversity and a cross-ancestry genome-wide meta-analysis from the International Lung Cancer Consortium. Data were extracted between October 2023 and January 2024 and analyzed between February 2024 and June 2024.

Genetically estimated sensitivity to environmental stress and adversity.

The main outcome was lung cancer risk, and odds ratios and 95% CIs were used to assess the association between sensitivity to environmental stress and adversity with lung cancer risk. This genetic association study used a 2-sample Mendelian randomization (MR) to estimate the association between genetically estimated sensitivity to environmental stress and adversity and lung cancer risk across different histologic types.

Using data from 351 827 individuals from the UK Biobank and a cross-ancestry genome-wide analysis of 61 047 lung cancer cases and 947 237 controls from the International Lung Cancer Consortium, sensitivity to environmental stress and adversity was significantly associated with an increased risk of lung cancer among individuals of European ancestry (OR, 1.49; 95% CI, 1.13-1.98; P = .005) and in the cross-ancestry analysis (OR, 1.45; 95% CI, 1.13-1.85; P = .004). There were heterogeneities in the observed associations across histologic subtypes among different population ancestries. Among individuals of European ancestry, a significant association was noted among squamous cell carcinoma (OR, 1.69; 95% CI, 1.06-2.70; P = .03). Among individuals of East Asian ancestry, an increased risk was observed for adenocarcinoma (OR, 2.04; 95% CI, 1.00-4.18; P = .05). Associations were not observed across any of the 3 histologic subtypes among individuals of African ancestry.

In this genetic association study, sensitivity to environmental stress and adversity was associated with lung cancer risk. These results underscore the necessity for further research into the nuanced association between psychosocial stress and cancer risk, with a particular focus on diverse populations.

Aim: to evaluate the predictive ability of the Nutritional Risk Emergency - 2017 (NRE) to predict prolonged length of stay, ICU admission intra-mortality and readmission, severe postoperative complications. Methods: a prospective cohort was conducted with surgical patients admitted in a public tertiary hospital. The NRE-2017 tool was applied for detecting malnutrition risk in hospitalized patients. Surgical complications were assessed by Clavien-Dindo. Patients were followed during hospitalization to identify length of stay as well as stay after surgery in the Intensive Care Unit (ICU). Regression analysis was performed to assess the association between risk of malnutrition and clinical outcomes. Results: we included 162 elective surgery patients; 79 patients were identified with nutritional risk using the NRE-2017 (≥ 1.5) tool and 83 without nutritional risk. Patients with nutritional risk were at higher risk of prolonged hospitalization [18 (10-36) days vs. 13 (7-23 days); p: 0.006] and ICU hospitalization [6 (2-14 days vs. 3.5 (1-7 days; p: 0.020]. There was an association between surgical complications and nutritional risk independently, but the significance was lost when adjusting the analysis. There was no association with mortality and readmission in this sample of patients. Conclusion: the NRE-2017 tool was associated with hospital stay in those patients at nutritional risk, however there was no association with mortality and readmission.

The deleterious health impacts of polycyclic aromatic hydrocarbons (PAHs) on the population have been extensively substantiated and acknowledged. Mounting evidence underscores that PAH exposure is closely linked to an elevated risk of mental disorders, particularly in populations experiencing occupational and high-level exposure. In this study, we aimed to investigate the mechanisms underlying anxiety-like behaviors induced by different dosages of PAHs, with a concentrated focus on brain region-specific metabolic alterations in mice using various metabolomics approaches. Male C57BL/6 mice were exposed to benzo[a]pyrene (B[a]P), a typical PAH, through gavage at occupational exposure and EPA toxicologically relevant dosages (2.0 and 20.0 mg/kg/day) for 21 days, respectively. Behavioral assessments revealed that occupational exposure to B[a]P induced anxiety-like behaviors in C57BL/6 mice. Meanwhile, elevated serum norepinephrine and corticotropin-releasing hormone further confirmed the anxiety-inducing effects of B[a]P exposure. Metabolomics analysis uncovered dysregulation across various metabolic pathways following B[a]P exposure, encompassing brain neurotransmitter, organic acid, amino acid, lipid, fatty acid, and cholesterol. Anxiety levels and lipid metabolic abnormalities were notably exacerbated at the higher dosage, despite being only a 10-fold increase. Of particular significance, a decrease in lysophosphatidic acid (LPA) and lysophosphatidylserine (LPS) emerged as pivotal indicators of B[a]P neurotoxicity. Spatial-resolved metabolomics further demonstrated distinctive lipid and metabolite profiles across different brain subregions after exposure to B[a]P. Remarkably, alterations were specifically observed in the anxiety-related brain regions, such as the hippocampus, cortex, white matter, and thalamus, varying with exposure dosages. These findings underscore the significance of brain metabolic abnormalities in the development of mental disorders triggered by B[a]P exposure and highlight the need for establishing precise exposure limits of B[a]P to safeguard public mental health.

IL-2 regulates T cell differentiation: low-dose IL-2 induces immunoregulatory Treg differentiation, while high-dose IL-2 acts as a potent activator of cytotoxic T cells and NK cells. Therefore, high-dose IL-2 has been studied for use in cancer immunotherapy. We aimed to utilize low-dose IL-2 to treat inflammatory diseases such as obesity and insulin resistance, which involve low-grade chronic inflammation.

Systemic administration of low-dose IL-2 increased Treg cells and decreased inflammation in gonadal white adipose tissue (gWAT), leading to improved insulin sensitivity in high-fat diet-fed obese mice. Additionally, central administration of IL-2 significantly enhanced insulin sensitivity through the activation of the sympathetic nervous system. The sympathetic signaling induced by central IL-2 administration not only decreased interferon γ (IFNγ) + Th1 cells and the expression of pro-inflammatory cytokines, including Il-1β, Il-6, and Il-8, but also increased CD4 + CD25 + FoxP3 + Treg cells and Tgfβ expression in the gWAT of obese mice. These phenomena were accompanied by hypothalamic microgliosis and activation of pro-opiomelanocortin neurons. Furthermore, sympathetic denervation in gWAT reversed the enhanced insulin sensitivity and immune cell polarization induced by central IL-2 administration.

Overall, we demonstrated that IL-2 improves insulin sensitivity through two mechanisms: direct action on CD4 + T cells and via the neuro-immune axis triggered by hypothalamic microgliosis.

Type 1 diabetes (T1D) is an autoimmune disease characterized by the specific destruction of insulin-producing beta cells in the pancreas by the immune system, including CD4 cells which orchestrate the attack and CD8 cells which directly destroy the beta cells, resulting in the loss of glucose homeostasis.

This comprehensive document delves into the complex interplay between the immune system and beta cells, aiming to shed light on the mechanisms driving their destruction in T1D. Insights into the genetic predisposition, environmental triggers, and autoimmune responses provide a foundation for understanding the autoimmune attack on beta cells. From the role of viral infections as potential triggers to the inflammatory response of beta cells, an intricate puzzle starts to unfold. This exploration highlights the importance of beta cells in breaking immune tolerance and the factors contributing to their targeted destruction. Furthermore, it examines the potential role of autophagy and the impact of cytokine signaling on beta cell function and survival.

This review collectively represents current research findings on T1D which offers valuable perspectives on novel therapeutic approaches for preserving beta cell mass, restoring immune tolerance, and ultimately preventing or halting the progression of T1D. By unraveling the complex dynamics between the immune system and beta cells, we inch closer to a comprehensive understanding of T1D pathogenesis, paving the way for more effective treatments and ultimately a cure.

A glucose tolerance test (GTT) is routinely used to assess glucose homeostasis in clinical settings and in preclinical research studies using rodent models. The procedure assesses the ability of the body to clear glucose from the blood in a defined time after a bolus dose. In the human clinical setting, glucose is ingested via voluntary consumption of a glucose-sweetened drink. Typically, in the rodent GTT oral gavage (gavage-oGTT) or (more commonly) intraperitoneal injection (IPGTT) are used to administer the glucose bolus. Although used less frequently, likely due to investigator technical and experience barriers, the former is the more physiologically relevant as it integrates the gastrointestinal tract (GI), including release of key incretin hormones. However, orally gavaging glucose in the GTT is also not without its limitations: gavaging glucose straight into the stomach bypasses potentially critical early glucose-sensing via the mouth (cephalic phase) and associated physiological responses. Furthermore, gavaging is stressful on mice, and this by itself can increase blood glucose levels. We have developed and validated a refined protocol for mouse oral GTT which uses a voluntary oral glucose dosing method, micropipette-guided drug administration (MDA), without the need for water deprivation. This approach is simple and non-invasive. It is less stressful for the mice, as evidenced by lower circulating corticosterone levels 10 minutes after glucose-dosing compared to oral gavage. This is significant for animal and investigator welfare, and importantly minimising the confounding effect of stress on mouse glucose homeostasis. Using a randomised cross-over design, we have validated the MDA approach in the oGTT against oral gavage in male and female C57BL/6J and C57BL/6N mice. We show the ability of this method to detect changes in glucose tolerance in diet-induced obese animals. Compared to oral gavage there was lower inter-animal variation in the MDA-oGTT. In addition to being more representative of the human procedure, the MDA-oGTT is easy and has lower barriers to adoption than the gavage oGTT as it is non-invasive and requires no specialist equipment or operator training. The MDA-oGTT a more clinically representative, accessible, and refined replacement for the gavage-oGTT for mouse metabolic phenotyping, which is simple yet overcomes significant deficiencies in the current standard experimental approaches.

Background/Objectives: Rare diseases are a wide and heterogeneous group of multisystem life-threatening or chronically debilitating clinical conditions with reduced life expectancy and a relevant mortality rate in childhood. Some of these disorders have typical neurological symptoms, presenting from birth to adulthood. Dietary patterns and nutritional compounds play key roles in the onset and progression of neurological disorders, and the impact of alimentary needs must be enlightened especially in rare neurological diseases. This work aims to collect the in vitro, in vivo, and clinical evidence on the effects of diet and of nutrient intake on some rare neurological disorders, including some genetic diseases, and rare brain tumors. Herein, those aspects are critically linked to the genetic, biological, biochemical, and pathophysiological hallmarks typical of each disorder. Methods: By searching the major web-based databases (PubMed, Web of Science Core Collection, DynaMed, and Clinicaltrials.gov), we try to sum up and improve our understanding of the emerging role of nutrition as both first-line therapy and risk factors in rare neurological diseases. Results: In line with the increasing number of consensus opinions suggesting that nutrients should receive the same attention as pharmacological treatments, the results of this work pointed out that a standard dietary recommendation in a specific rare disease is often limited by the heterogeneity of occurrent genetic mutations and by the variability of pathophysiological manifestation. Conclusions: In conclusion, we hope that the knowledge gaps identified here may inspire further research for a better evaluation of molecular mechanisms and long-term effects.

Cardiometabolic multimorbidity (CMM) and depression are major health concerns, and the onset of either condition may heighten the risk of developing the other.

The goal of this study was to characterize the reciprocal associations between CMM and depression among middle-aged and older adults.

This multicohort study used harmonized data from 5 prospective cohorts from China, South Korea, the United States, the United Kingdom, and Europe. Cardiometabolic diseases (CMDs) (including diabetes, heart diseases, and stroke) and depression were assessed at baseline and at 7 to 8 years' follow-up. Lifestyle factors, including physical activity, alcohol consumption, and smoking status, were regarded as potential mediators. Two sets of analyses, CMM-depression analyses (n = 67,188) and depression-CMM analyses (n = 65,738), were conducted to explore the bidirectional associations between CMM and depression.

In the CMM-depression analyses, 16,596 (24.7%) individuals developed depression. Participants with a single CMD (HR: 1.24; 95% CI:1.19-1.29) and CMM (HR: 1.52; 95% CI: 1.42-1.63) at baseline had higher risks of depression occurring. Physical activity and alcohol consumption significantly mediated 7.5% and 6.9% of the CMM-depression association, respectively. In the depression-CMM analyses, 1,461 (2.2%) participants developed CMM. The HR for developing CMM was 1.31 (95% CI: 1.14-1.50) in patients with depression, with increased risk of developing more CMDs. Physical activity and alcohol consumption mediated 12.0% and 7.1% of the depression-CMM association. The bidirectional relationships were more pronounced in Western countries than in Asian countries.

CMM and depression were bidirectionally associated. The mediated effects of lifestyle factors were larger in the depression-lifestyle-CMM pathway than in the CMM-lifestyle-depression pathway.

Racial differences in breast cancer morbidity and mortality have been examined between Black/African American women and White women as part of efforts to characterize multilevel drivers of disease risk and outcomes. Current models of cancer disparities recognize the significance of physiological stress responses, yet data on stress hormones in Black/African American women with breast cancer and their social risk factors are limited. We examined cortisol levels in Black/African American breast cancer patients and tested their association with social and clinical factors to understand the relationship between stress responses and women's lived experiences. Seventy-two patients who completed primary surgical treatment were included in this cross-sectional study. Data on sociodemographic characteristics and chronic diseases were obtained by self-report. Breast cancer stage and diagnosis date were abstracted from electronic health records. Cortisol levels were determined from saliva samples. Compared to those without hypertension, patients with hypertension were 6.84 (95% CI 1.33, 35.0) times as likely to have high cortisol (p = 0.02). The odds of having high cortisol increased by 1.42 (95% CI 1.03, 1.95, p = 0.03) times for every point increase in negative life events. Hypertension and negative life events are associated with high cortisol levels in Black/African American patients. These findings illustrate the importance of understanding the lived experiences of these patients to enhance cancer health equity.

Depression is a prevalent psychiatric disease with the characteristic of persistently gloomy mood. The treatment of depression with traditional therapeutic medications suffers from low efficacy and adverse side effects due to the extremely unpredictable courses and uneven responses to treatment. The goal of this paper was to investigate the preparation of selenium-enriched fermented goat milk and the potential mechanism of its intervention on the chronic unpredictable stress-induced depression mice model. The results showed that Se-Lactobacillus paracasei 20241 (Se-20241) significantly alleviated depressive behavior, reversed the upregulation of inflammatory factors, and attenuated glucocorticoid resistance. Meanwhile, the results showed a modulatory function on oxidative stress dysfunction in the liver, hippocampus, and prefrontal cortex. The change in abundance of Ileibacterium, Muribaculaceae, Turicibacter, Dubosiella, and Bifidobacterium was also modified. These results provided the theoretical groundwork for the development of psychoactive probiotic supplements for depressed patients and clarified the probable mechanism of Se-20241 for antidepressant impact on the CUMS model.

Food insecurity is highly prevalent and linked to poorer diet and worse metabolic outcomes. Food insecurity can be stressful, and could elicit chronic psychological and physiological stress. In this study, we tested whether stress could be used to identify those at highest risk for worse diet and metabolic measures from food insecurity. Specifically, we hypothesized that cortisol (a physiological marker of stress) and perceived psychological stress would amplify the link between food insecurity and hyperpalatable food intake as well as metabolic measures. In a sample of 624 Black and White women aged 36-43 who participated in the NHLBI Growth and Health Study's midlife assessment, we assessed associations between food insecurity with hyperpalatable food intake (high fat + high sodium foods; high fat + high sugar foods; and high carbohydrate + high sodium foods), and metabolic measures (fasting glucose, insulin resistance, and waist circumference). We found that food insecurity was associated with higher levels of perceived stress (R2 = 0.09), and greater intake of high fat + high sugar (hyperpalatable) foods (R2 = 0.03). In those with higher cumulative cortisol (as indexed by hair cortisol), food insecurity was associated with higher levels of fasting glucose. Neither cortisol nor perceived stress moderated any other relationships, and neither variable functioned as a mediator in sensitivity analyses. Given these largely null findings, further research is needed to understand the role stress plays in the chronic health burdens of food insecurity.

Epidemiological results on the link between chronic stress and cancer initiation have been inconsistent. This study examined the relation between chronic biological stress, indicated as hair cortisol (HairF) and hair cortisone (HairE), and cancer incidence, adjusting for metabolic syndrome (MetS) components. We analyzed HairF and HairE samples from 6341 participants from the population-based cohort Lifelines in 2014. A linkage with the Dutch Nationwide Pathology Databank (Palga) provided the cancer incidence from 2015 to 2021. The association between dichotomized HairF and log-transformed HairE (LogHairE) and cancer incidence was estimated using Cox regression. MetS components were evaluated as confounders or moderators. Of the 2776 participants with known HairF levels and no cancer history, 238 developed cancer. The HairF level did not predict cancer incidence (HR: 0.993, 95%CI: 0.740-1.333). No confounders or moderators were identified. Among the 4699 participants with known HairE levels and no cancer history, 408 developed cancer. There was no association between LogHairE and cancer incidence (HR: 1.113, 95%CI: 0.738-1.678). When including age as a confounder and gender as a moderator, LogHairE was statistically significantly associated with cancer incidence (HR: 6.403, 95%CI: 1.110-36.92). In a population-based cohort, chronic biological stress, measured by HairE, was associated with cancer incidence, after controlling for age and gender.

Background: Diabetes mellitus (DM) is a chronic condition associated with multiple complications and comorbidities. Some of these comorbidities are anxiety and depression, with a negative impact on the quality of life, non-adherence to treatment, and poor prognosis. The main aim of this study was to evaluate depression and anxiety in a group of patients with DM and their impact on quality of life and identify factors that improve the prognosis and increase the life expectancy and quality of life of patients with DM. Methods: A total of 209 patients with type 2 DM (T2DM) were enrolled cross-sectionally. Patients were screened for psychiatric disorders, cognitive impairment, and metabolic parameters. Results: Included patients had a median age of 66.0 (58; 70) years, a median DM duration of 9 (6; 15) years, and a suboptimal glycemic control reflected by a median HbA1c of 7.8 (7; 9.2) mg/dL. Patients presented anxiety at different stages in 51.5% of cases, and similarly, depression in 37.5% of cases. Age, duration of DM, HbA1c, and postprandial hyperglycemia (PPG) were predictive factors for anxiety and depression in patients with T2DM. An age > 57 years (sensitivity 84.3, specificity 33.7, AUROC 0.621, p = 0.002) and an HbA1c > 8.5% (sensitivity 45.8, specificity 83.1, AUROC = 0.635, p < 0.0001) predict a higher rate of anxiety, respectively, of depression in these patients. Conclusions: Patients with T2DM have an increased rate of anxiety and depression due to persistent hyperglycemia and aging, which is expressed in a lower quality of life.

Psychological distress has been linked to diabetes risk. Few population-based, epidemiologic studies have investigated the potential molecular mechanisms (eg, metabolic dysregulation) underlying this association.

To evaluate the association between a metabolomic signature for psychological distress and diabetes risk.

We conducted a nested case-control study of plasma metabolomics and diabetes risk in the Nurses' Health Study, including 728 women (mean age: 55.2 years) with incident diabetes and 728 matched controls. Blood samples were collected between 1989 and 1990 and incident diabetes was diagnosed between 1992 and 2008. Based on our prior work, we calculated a weighted plasma metabolite-based distress score (MDS) comprised of 19 metabolites. We used conditional logistic regression accounting for matching factors and other diabetes risk factors to estimate odds ratios (OR) and 95% confidence intervals (CI) for diabetes risk according to MDS.

After adjusting for sociodemographic factors, family history of diabetes, and health behaviors, the OR (95% CI) for diabetes risk across quintiles of the MDS was 1.00 (reference) for Q1, 1.16 (0.77, 1.73) for Q2, 1.30 (0.88, 1.91) for Q3, 1.99 (1.36, 2.92) for Q4, and 2.47 (1.66, 3.67) for Q5. Each SD increase in MDS was associated with 36% higher diabetes risk (95% CI: 1.21, 1.54; P-trend <.0001). This association was moderately attenuated after additional adjustment for body mass index (comparable OR: 1.17; 95% CI: 1.02, 1.35; P-trend = .02). The MDS explained 17.6% of the association between self-reported psychological distress (defined as presence of depression or anxiety symptoms) and diabetes risk (P = .04).

MDS was significantly associated with diabetes risk in women. These results suggest that differences in multiple lipid and amino acid metabolites may underlie the observed association between psychological distress and diabetes risk.

Over- and undernutrition coexist in many African countries and pose a threat to metabolic health. This study assessed the associations between relationship satisfaction and Body Mass Index (BMI), waist circumference (WC), and glycated hemoglobin (HbA1c), in a rural population of older adults in Burkina Faso. It also explored potential gender differences and the mediating role of depressive symptoms.

Data from the "Centre de Recherche en Santé de Nouna (CRSN) Heidelberg Aging Study (CHAS)," a cross-sectional population-based study conducted in 2018 in Burkina Faso, were used in our study. Hierarchical linear regression models were applied for each of the three outcome variables. Among 2291 participants aged 40 years or older who provided data on relationship satisfaction, 2221, 2223, and 2145 participants had BMI, waist circumference (WC), and HbA1c values respectively.

Higher relationship satisfaction (CSI-4 score) was associated with increased BMI (β = 0.05, p = 0.031) and WC (β = 0.12, p = 0.039). However, the association of CSI-4 and BMI became non-significant after controlling for depressive symptoms (PHQ-9 score) and physical inactivity (BMI: β = 0.04, p = 0.073). Depressive symptoms fully mediated the relationship between relationship satisfaction and BMI (β = -0.07, p = 0.005). There was no significant association between relationship satisfaction and HbA1c. These results were consistent across genders and age groups.

Higher relationship satisfaction may lead to increased body weight among Burkinabe adults aged 40 years and older, and depressive symptoms may be a mediator in this association.

The current study aimed to investigate the health implications of negative work-to-family spillover on cardiovascular risk biomarkers.

In a large-scale cross-sectional dataset of working or self-employed midlife and older adults in the United States (N = 1179), we examined five biomarkers linked to cardiovascular risk, including high-density lipoprotein (HDL) cholesterol, low-density lipoprotein cholesterol, triglyceride, interleukin-6, and C-reactive protein. Negative work-to-family spillover, measured using a four-item self-reported questionnaire, was included into our model to study its association with these cardiovascular risk biomarkers.

Our findings indicate a significant association between negative work-to-family spillover and cardiovascular risk biomarkers - higher triglycerides (β = 0.108, p < .001), interleukin-6 (β = 0.065, p = .026), and C-reactive protein (β = 0.067, p = .022), and lower HDL cholesterol (β = -0.104, p < .001). The associations on triglycerides (β = 0.094, p = .001) and HDL cholesterol (β = -0.098, p < .001) remained significant even after controlling numerous control variables of demographics, medication, health-status, and health-related behaviors. The findings were also consistent against slight variations in the analytic method and adjustment for multiple comparisons.

The current study supports the premise that spillover of work-related tensions into family life is associated with objective physiological changes that contribute to cardiovascular risk.

Myocardial infarction is a major contributor to CVD-related mortality. T2DM is a risk factor for MI. Stress activates the HPA axis, SNS, and endogenous OPS. These POMC derivatives increase the blood glucose and cardiovascular response by inhibiting the PI3K/AkT insulin signaling pathway and increasing cardiac contraction. Opioids regulate the effect of the HPA axis and SNS and they are cardioprotective. The chronic activation of the stress response may lead to insulin resistance, cardiac dysfunction, and MI. Stress and T2DM, therefore, increase the risk of MI. T2DM is preceded by prediabetes. Studies have shown that prediabetes is associated with an increased risk of MI because of inflammation, hyperlipidemia, endothelial dysfunction, and hypertension. The HPA axis is reported to be dysregulated in prediabetes. However, the SNS and the OPS have not been explored during prediabetes. The effect of prediabetes on POMC derivatives has yet to be fully explored and understood. The impact of stress and prediabetes on the cardiovascular response needs to be investigated. This study sought to review the potential impact of prediabetes on the POMC derivatives and pathways that could lead to MI.

Hair cortisol concentration (HCC) has shown remarkable promise as a stable, non-invasive measure of systemic cortisol; however, despite methodological advances, the value that would typically be seen in healthy adults has not been established. Therefore, we sought to review the relevant literature to determine a reference value for HCC in healthy (i.e., non-clinical) adults. To this end, we conducted a systematic review of the PubMed, Scopus, and CINAHL databases for studies that measured healthy adult HCC using immunoassay methods, given that these are the most widely accessible analytical tools. To be eligible, studies were required to have been published in English, to have provided relevant descriptive statistics (i.e., means and standard deviations), and to have used a healthy adult human sample. We found 17 studies that met our inclusion criteria; the reports involved 1348 participants with a mean age of about 38 years. Since we identified a large amount of between-study heterogeneity, we completed a random-effect meta-regression analysis and found that test kit vendor was the only significant variable of the model. As a result, when using methodologies from traditional finite mixture distributions to determine reference values for mean and elevated HCC in individual healthy adults, we calculated these estimates for each of the major test kit vendors. Future work will need to determine whether our estimated reference values need to be modified, and these efforts will be greatly assisted by studies that account for potential moderating factors, such as age, sex, and ethnicity.

Studies have shown that adults with a history of incarceration have elevated cardiovascular (CVD) risk. Research on racial/ethnic group differences in the association between incarceration and CVD risk factors of hypertension and hyperglycemia is limited.

To assess racial/ethnic group differences in the association between incarceration and hypertension and hyperglycemia.

We performed a secondary data analysis using the National Longitudinal Survey of Adolescent to Adult Health (Add Health). Using modified Poisson regression, we estimated the associations between lifetime history of incarceration reported during early adulthood with hypertension and hyperglycemia outcomes measured in mid-adulthood, including incident diagnosis. We evaluated whether associations varied by self-reported race/ethnicity (non-Hispanic White, non-Hispanic Black, Hispanic, and Asian).

The analytic sample included 4,015 Add Health respondents who self-identified as non-Hispanic White, Non-Hispanic Black, Hispanic, and Asian, and provided incarceration history and outcome data.

Outcome measures included (1) hypertension (2) systolic blood pressure  ≥ 130 mmHg, and (3) hyperglycemia.

In non-Hispanic Black and non-Hispanic White participants, there was not evidence of an association between incarceration and measured health outcomes. Among Hispanic participants, incarceration was associated with hyperglycemia (Adjusted Risk Ratio (ARR): 2.1, 95% Confidence Interval (CI): 1.1-3.7), but not with hypertension risk. Incarceration was associated with elevated systolic blood pressure (ARR: 3.1, CI: 1.2-8.5) and hypertension (ARR: 1.7, CI: 1.0-2.8, p = 0.03) among Asian participants, but not with hyperglycemia risk. Incarceration was associated with incident hypertension (ARR 2.5, CI 1.2-5.3) among Asian subgroups.

Our findings add to a growing body of evidence suggesting that incarceration may be linked to chronic disease outcomes. Race/ethnic-specific results, while limited by small sample size, highlight the need for long-term studies on incarceration's influence among distinct US groups.

As mobile and wearable devices continue to grow in popularity, there is strong yet unrealized potential to harness people's mobile sensing data to improve our understanding of their cellular and biologically-based diseases. Breakthrough technical innovations in tumor modeling, such as the three dimensional tumor microenvironment system (TMES), allow researchers to study the behavior of tumor cells in a controlled environment that closely mimics the human body. Although patients' health behaviors are known to impact their tumor growth through circulating hormones (cortisol, melatonin), capturing this process is a challenge to rendering realistic tumor models in the TMES or similar tumor modeling systems. The goal of this paper is to propose a conceptual framework that unifies researchers from digital health, data science, oncology, and cellular signaling, in a common cause to improve cancer patients' treatment outcomes through mobile sensing. In support of our framework, existing studies indicate that it is feasible to use people's mobile sensing data to approximate their underlying hormone levels. Further, it was found that when cortisol is cycled through the TMES based on actual patients' cortisol levels, there is a significant increase in pancreatic tumor cell growth compared to when cortisol levels are at normal healthy levels. Taken together, findings from these studies indicate that continuous monitoring of people's hormone levels through mobile sensing may improve experimentation in the TMES, by informing how hormones should be introduced. We hope our framework inspires digital health researchers in the psychosocial sciences to consider how their expertise can be applied to advancing outcomes across levels of inquiry, from behavioral to cellular.

Prolonged exposure to stress has detrimental effects on health, and the consumption of caffeine, mostly contained in energy drinks, has become a widely adopted stress coping strategy. Currently, there is limited information regarding the effects of caffeine intake on chronic stress exposure. Thus, this study investigated the effects of caffeine administration on chronic stress-induced behavioral deficits, neurochemical alterations, and glial disruptions in experimental rats. Thirty male Wistar rats were randomly assigned to five groups (n = 6): non-stress control, stress control, and caffeine groups of doses 12.5, 25, and 50 mg/kg. The stress control and caffeine groups were subjected to an unpredictable chronic mild stress (UCMS) protocol daily for 14 days. The rats were evaluated for phenotypic and neurobehavioral assessments. Thereafter, the rat brains were processed for biochemical and immunohistochemical assays. Caffeine administration was found to ameliorate behavioral dysfunctions in rats exposed to UCMS. The UCMS-induced changes in brain levels of monoamines, cholinesterases, and some oxidative stress biomarkers were reversed by caffeine. Caffeine administration also produced mild protective effects against UCMS-induced changes in GFAP and Iba-1 expression in stress-specific brain regions. These results showed that low and moderate doses of caffeine reversed most of the stress-induced changes, suggesting its ameliorative potential against chronic stress-induced alterations.

Traditional Chinese medicine (TCM) is increasingly used to manage type 2 diabetes and its nonpharmacological interventions are showing potential for preventing type 2 diabetes. This study mainly reviews relevant research. The most mentioned non-drug treatments for preventing type 2 diabetes in TCM are healthy diet, physical activity, emotional therapy, and acupuncture. In most studies, blood glucose status in patients with prediabetes and type 2 diabetes was significantly improved after TCM non-drug interventions, and there was no significant difference between the adverse effect of TCM and control groups or other intervention groups, while the methodological quality of the clinical trials involving TCM generally kept a low level. The effectiveness of TCM in preventing type 2 diabetes has yet to be validated in large randomized controlled trials and the underlying mechanism also needs further exploration.

Many studies have clearly established that chronic psychosocial stress may sustainably worsen glycemic control in patients with type 1 diabetes mellitus (T1DMM), thus promoting diabetes complications. Chronic psychosocial stress may be due to: i) the long-term accumulation of stressful life events that require readjustment on the part of the individual (loosing friends, changing schools), and/or ii) exposure to severe chronic stressors (persistent difficulties and adversities of life). Whatever the reason, many studies have clearly established a positive correlation between chronic psychosocial stress and HbA1c levels. However, a small fraction of patients is minimally affected or not affected at all by chronic psychosocial stress. Conversely, positive life events can substantially improve glycemic control. Recent evidence suggests the existence of subpopulations that differ in personality traits, neurohormonal regulatory responses, and food intake behavior (increased or decreased). Better characterization of the clinical and neurohormonal differences between these subpopulations may help develop personalized treatment strategies in the future. In the near future, psychotherapeutic support and automated insulin delivery (AID) could alleviate chronic stress, prevent worsening glycemic control, and ease the burden of diabetes.

Mental and psychological disorders are serious health problems worldwide. Anxiety among high school students can affect school performance, relationships, and family life.

Our aim is to understand the anxiety levels and associated factors among high school students and compare the results of psychological tests measuring anxiety with the cortisol levels obtained from biological sampling.

In our longitudinal follow-up study, we involved 125 individuals in May 2019. Validated measurement tools were used during questionnaire data collection, including the State-Trait Anxiety Inventory, Clear Communication Scale, Multiple Social Perceived Support Scale, and related HBSC questions. As objective data, we collected hair samples for cortisol level measurement.

At the end of the school year, the anxiety levels measured by psychological tests were significantly higher (p = 0.001) compared to the anxiety levels at the beginning of the next school year. Anxiety levels were higher among girls and were influenced by the type of school and parental expectations. Both state anxiety and trait anxiety showed a strong correlation with psychosomatic symptoms (p < 0.001) and anxiety arising from school expectations (p < 0.05). The changes in cortisol levels did not follow the changes in psychological tests. Cortisol level increased (p = 0.01) in the second sample.

The dorsomedial hypothalamus nucleus (DMH) is an important component of the autonomic nervous system and plays a critical role in regulating the sympathetic outputs of the heart. Stress alters the neuronal activity of the DMH, affecting sympathetic outputs and triggering heart rate variability. However, the specific molecular mechanisms behind stress leading to abnormal DMH neuronal activity have still not been fully elucidated. Therefore, in the present study, we successfully constructed a stressed rat model and used it to investigate the potential molecular mechanisms by which IL-6 regulates GABAA receptors in the DMH through activation of the JAK/STAT pathway and thus affects heart rate variability in rats. By detecting the c-Fos expression of neurons in the DMH and electrocardiogram (ECG) changes in rats, we clarified the relationship between abnormal DMH neuronal activity and heart rate variability in stressed rats. Then, using ELISA, immunohistochemical staining, Western blotting, RT-qPCR, and RNAscope, we further explored the correlation between the IL-6/JAK/STAT signaling pathway and GABAA receptors. The data showed that an increase in IL-6 induced by stress inhibited GABAA receptors in DMH neurons by activating the JAK/STAT signaling pathway, while specific inhibition of the JAK/STAT signaling pathway using AG490 obviously reduced DMH neuronal activity and improved heart rate variability in rats. These findings suggest that IL-6 regulates the expression of GABAA receptors via the activation of the JAK/STAT pathway in the DMH, which may be an important cause of heart rate variability in stressed rats.

Traditional Chinese medicine (TCM) theories assert that body constitution and meridian energy lay the foundation for disease prevention. TCM-based health concepts have not yet been incorporated into mobile health (mHealth) apps for individuals with prediabetes.

The aim of this study was to examine the effectiveness of a TCM mHealth app for individuals with prediabetes.

This randomized controlled trial recruited 121 individuals with prediabetes at a teaching hospital in New Taipei City between February 2020 and May 2021. The participants were randomly assigned to the TCM mHealth app group (n=42), ordinary mHealth app group (n=41), or control group (n=38). All participants received the usual care that included 15-20 minutes of health education about the disease, along with healthy diet and exercise encouragement. The ordinary mHealth app included physical activity (PA), diet, and disease education, along with individual records. The TCM mHealth app additionally included qi and body constitution information, along with constitution-based PA and diet advice. The control group received the usual care alone and did not have access to any app. Data were collected at baseline, at the end of the 12-week intervention, and 1 month after the intervention. Body constitution, including yang-deficiency, yin-deficiency, and phlegm-stasis, was measured according to the Body Constitution Questionnaire, with higher scores indicating a greater deficiency. Body energy was examined using the Meridian Energy Analysis Device. The Short-Form 36 questionnaire was used to evaluate health-related quality of life (HRQOL), which yielded physical component scores and mental component scores, with higher scores indicating better physical and mental aspects of HRQOL, respectively.

Compared to the control group, the TCM mHealth app group showed greater improvement in hemoglobin A1c (HbA1c), yang-deficiency and phlegm-stasis body constitution, and BMI; however, no significant differences were found in these outcomes between the TCM mHealth app and ordinary mHealth app groups. The TCM mHealth app group showed better improvement in body energy and mental component scores than the ordinary mHealth app group. There were no significant differences in fasting plasma glucose, yin-deficiency body constitution, Dietary Approaches to Stop Hypertension dietary behavior, and total PA among the three groups after the intervention.

Use of either the ordinary or TCM mHealth app improved HRQOL among individuals with prediabetes. Compared to the outcomes of controls not using any app, use of the TCM mHealth app was effective at improving HbA1c, BMI, yang-deficiency and phlegm-stasis body constitution, and HRQOL. Moreover, using the TCM mHealth app seemed to improve the body energy and HRQOL more than when using the ordinary mHealth app. Further studies with a larger sample size and longer follow-up period may be necessary to determine whether the differences favoring the TCM app are clinically meaningful.

ClinicalTrials.gov NCT04096989; https://clinicaltrials.gov/ct2/show/NCT04096989.

Type 2 diabetes mellitus (T2DM) patients show brain tissue changes in mood and cognitive regulatory sites, but the nature and extent of tissue injury and their associations with symptoms are unclear. Our aim was to examine brain tissue damage in T2DM over controls using mean diffusivity (MD) computed from diffusion tensor imaging (DTI), and assess correlations with mood and cognitive symptoms in T2DM. We collected DTI series (MRI), mood, and cognitive data, from 169 subjects (68 T2DM and 101 controls). Whole-brain MD-maps were calculated, normalized, smoothed, and compared between groups, as well as correlated with mood and cognition scores in T2DM subjects. Type 2 diabetes patients showed altered cognitive and mood functions over control subjects. Multiple brain sites in T2DM patients showed elevated MD values, indicating chronic tissue changes, including the cerebellum, insula, and frontal and prefrontal cortices, cingulate, and lingual gyrus. Associations between MD values and mood and cognition scores appeared in brain sites mediating these functions. Type 2 diabetes patients show predominantly chronic brain tissue changes in areas mediating mood and cognition functions, and tissue changes from those regions correlate with mood and cognitive symptoms suggesting that the microstructural brain changes may account for the observed functional deficits.

Recent studies have highlighted a key role played by the sympathetic nervous system (SNS) and adrenergic stress in mediating immune suppression associated with chronic inflammation in cancer and other diseases. The connection between chronic SNS activation, adrenergic stress and immune suppression is linked in part to the ability of catecholamines to stimulate the bone marrow release and differentiation of myeloid-derived suppressor cells (MDSC). Rodent model studies have revealed an important role for β-adrenergic receptor signalling in suppression of cancer immunity in mice subjected to chronic stresses, including thermal stress. Importantly, therapeutic blockade of beta-adrenergic responses by drugs such as propranolol can partially reverse the generation and differentiation of MDSC, and partly restore tumour immunity. Clinical trials in both humans and dogs with cancer have demonstrated that propranolol blockade can improve responses to radiation therapy, cancer vaccines and immune checkpoint inhibitors. Thus, the SNS stress response has become an important new target to relieve immune suppression in cancer and other chronic inflammatory conditions.

To evaluate the association of comorbid depression and obesity with the risk of incident cardiometabolic multimorbidity among middle-aged and older Chinese adults.

This cohort study extracted data from the 2011 and 2015 waves of the China Health and Retirement Longitudinal Study (CHARLS). Depression was confirmed by the 10-item Center for Epidemiologic Studies Depression Scale (CESD-10) with a cut-off score ≥10. Obesity was defined as a body mass index ≥28 kg/m². Participants were categorized into four groups based on depression and obesity status at baseline, i.e., with neither condition, depression only, obesity only, and with both conditions. Cardiometabolic multimorbidity was defined as the coexistence of two or more of heart diseases, stroke, and diabetes mellitus. Logistic regression models were established to estimate the associations.

A total of 9,308 participants without cardiometabolic multimorbidity at baseline were included (mean [SD] age, 58.8 [9.0] years; 4,449 [47.8%] were males). During four-year of follow-up, 349 (3.8%) participants developed cardiometabolic multimorbidity. Compared to participants without depression or obesity, comorbid depression and obesity was associated with greater risk of cardiometabolic multimorbidity (adjusted OR: 4.79, 95% CI: 3.09-7.43) than that in participants with depression alone (adjusted OR: 1.84, 95% CI: 1.37-2.46) or obesity alone (adjusted OR: 2.26, 95% CI: 1.48-3.45). The findings were consistent in different gender and age groups.

Comorbid depression and obesity was associated with excessive risk of cardiometabolic multimorbidity. Intervention targeting at individuals with both depression and obesity might have substantial benefit in minimizing the risk of cardiometabolic multimorbidity.

No studies have assessed the association between sleep duration and obesity in Chinese ethnic minorities. Whether the relationship between sleep duration and obesity is different between Chinese Han people and Chinese ethnic minorities remains unclear. The study aimed to explore the relationship between sleep duration and obesity among Chinese Han people and Chinese ethnic minorities.

We applied data from the Guizhou Population Health Cohort Study (GPHCS), which 9,280 participants were recruited in the baseline survey from 2010 to 2012, and 8,163 completed the follow-up survey from 2016 to 2020. A total of 5,096 participants (3,188 Han Chinese and 1,908 ethnic minorities) were included in the ultimate analysis. Information on sleep duration (total 24-hour sleep time), body mass index (BMI), and waist circumference (WC) was collected at the baseline and follow-up survey, respectively. Cross-lagged panel analyses were conducted to explore the temporal relationship between sleep duration and obesity for Han people and ethnic minorities.

For Han people, the results from cross-lagged panel analyses indicated that baseline sleep duration was significantly associated with follow-up BMI (β_BMI = -0.041, 95% CI_BMI: -0.072 ~ -0.009) and follow-up WC (β_WC = -0.070, 95%CI_WC: -0.103 ~ -0.038), but baseline BMI (β_BMI = -0.016, 95% CI_BMI: -0.050 ~ 0.018) and baseline WC (β_WC = -0.019, 95% CI_WC: -0.053 ~ 0.016) were not associated with follow-up sleep duration. In addition, the relationship between baseline sleep duration and follow-up BMI was gender-specific and significant only in the Han people female (β_BMI = -0.047, 95% CI_BMI: -0.090 ~ -0.003) but not in the Han people male (β_BMI = -0.029, 95% CI_BMI: -0.075 ~ 0.016). For ethnic minorities, the results indicated that there was no relationship between sleep duration and obesity at all, either from sleep duration to obesity (β_BMI = 0.028, 95%CI_BMI: -0.012 ~ 0.068; β_WC = 0.020, 95%CI_WC: -0.022 ~ 0.062), or from obesity to sleep duration (β_BMI = -0.022, 95%CI_BMI: -0.067 ~ 0.022; β_WC = -0.042, 95%CI_WC: -0.087 ~ 0.003).

The relationship pattern between sleep duration and obesity across Han people and ethnic minorities is different. Future sleep-aimed overweight and obesity intervention should be conducted according to population characteristics.

Evidence suggests that psychological and physical stress are relevant triggering factors for the onset of type 1 diabetes (T1D) and type 2 diabetes (T2D). The underlying mechanisms involve a complex neuroendocrine structure, involving the central nervous system and the periphery. Psychological stress leads to an increase of serum glucocorticoid concentrations and catecholamines release increasing the insulin need and the insulin resistance. According to the β-cell stress hypothesis, also causes of increased insulin demand, such as rapid growth, overweight, puberty, low physical activity, trauma, infections, and glucose overload, are potentially relevant factors in development of T1D. It has also been demonstrated that chronic stress and obesity form a vicious circle which leads to a definitive metabolic failure, increasing the risk of developing T2D. In this review, we will provide the most recent data concerning the role of stress in the outcomes of T1D and T2D, with a focus on the role of physical and psychological stress on the onset of T1D.

Preoperative nutrition status is an important determinant of surgical outcomes, yet malnutrition assessment is not integrated into all surgical pathways. Given its importance and the high prevalence of malnutrition in patients undergoing surgical procedures, preoperative nutrition screening, assessment, and intervention are needed to improve postoperative outcomes. This narrative review discusses novel methods to assess malnutrition and frailty in the surgical patient. The Global Leadership Initiative for Malnutrition (GLIM) criteria are increasingly used in surgical settings although further spread and implementation are strongly encouraged to help standardize the diagnosis of malnutrition. The use of body composition (ie, reduced muscle mass) as a phenotypic criterion in GLIM may lead to a greater number of patients identified as having malnutrition, which may otherwise be undetected if screened by other diagnostic tools. Skeletal muscle loss is a defining criterion of malnutrition and frailty. Novel direct and indirect approaches to assess muscle mass in clinical settings may facilitate the identification of patients with or at risk for malnutrition. Selected imaging techniques have the additional advantage of identifying myosteatosis (an independent predictor of morbidity and mortality for surgical patients). Feasible pathways for screening and assessing frailty exist and may determine the cost/benefit of surgery, long-term independence and productivity, and the value of undertaking targeted interventions. Finally, the evaluation of nutrition risk and status is essential to predict and mitigate surgical outcomes. Nascent to novel approaches are the future of objectively identifying patients at perioperative nutrition risk and guiding therapy toward optimal perioperative standards of care.

Longitudinal records of temperament can be used for assessing behavioral plasticity, such as aptness to learn, memorize, or change behavioral responses based on affective state. In this study, we evaluated the phenotypic and genomic background of North American Angus cow temperament measured throughout their lifetime around the weaning season, including the development of a new indicator trait termed docility-based learning and behavioral plasticity. The analyses included 273,695 and 153,898 records for yearling (YT) and cow at weaning (CT) temperament, respectively, 723,248 animals in the pedigree, and 8784 genotyped animals. Both YT and CT were measured when the animal was loading into/exiting the chute. Moreover, CT was measured around the time in which the cow was separated from her calf. A random regression model fitting a first-order Legendre orthogonal polynomial was used to model the covariance structure of temperament and to assess the learning and behavioral plasticity (i.e., slope of the regression) of individual cows. This study provides, for the first time, a longitudinal perspective of the genetic and genomic mechanisms underlying temperament, learning, and behavioral plasticity in beef cattle.

CT measured across years is heritable (0.38-0.53). Positive and strong genetic correlations (0.91-1.00) were observed among all CT age-group pairs and between CT and YT (0.84). Over 90% of the candidate genes identified overlapped among CT age-groups and the estimated effect of genomic markers located within important candidate genes changed over time. A small but significant genetic component was observed for learning and behavioral plasticity (heritability = 0.02 ± 0.002). Various candidate genes were identified, revealing the polygenic nature of the traits evaluated. The pathways and candidate genes identified are associated with steroid and glucocorticoid hormones, development delay, cognitive development, and behavioral changes in cattle and other species.

Cow temperament is highly heritable and repeatable. The changes in temperament can be genetically improved by selecting animals with favorable learning and behavioral plasticity (i.e., habituation). Furthermore, the environment explains a large part of the variation in learning and behavioral plasticity, leading to opportunities to also improve the overall temperament by refining management practices. Moreover, behavioral plasticity offers opportunities to improve the long-term animal and handler welfare through habituation.

Alzheimer's disease (AD) is a neurodegenerative disorder, comprising 70% of dementia diagnoses worldwide and affecting 1 in 9 people over the age of 65. However, the majority of its treatments, which predominantly target the cholinergic system, remain insufficient at reversing pathology and act simply to slow the inevitable progression of the disease. The most recent neurotransmitter-targeting drug for AD was approved in 2003, strongly suggesting that targeting neurotransmitter systems alone is unlikely to be sufficient, and that research into alternate treatment avenues is urgently required. Neuromodulators are substances released by neurons which influence neurotransmitter release and signal transmission across synapses. Neuromodulators including neuropeptides, hormones, neurotrophins, ATP and metal ions display altered function in AD, which underlies aberrant neuronal activity and pathology. However, research into how the manipulation of neuromodulators may be useful in the treatment of AD is relatively understudied. Combining neuromodulator targeting with more novel methods of drug delivery, such as the use of multi-targeted directed ligands, combinatorial drugs and encapsulated nanoparticle delivery systems, may help to overcome limitations of conventional treatments. These include difficulty crossing the blood-brain-barrier and the exertion of effects on a single target only. This review aims to highlight the ways in which neuromodulator functions are altered in AD and investigate how future therapies targeting such substances, which act upstream to classical neurotransmitter systems, may be of potential therapeutic benefit in the sustained search for more effective treatments.

Shift work is known to be associated with cardiovascular disease (CVD). It has been found that inflammatory reactions are involved in the onset and progression of CVD. Therefore, the purpose of this study was to investigate the association between shift work and inflammatory markers.

Among workers at an electronics manufacturing company, 2,329 workers who had a health checkup from January 2019 to December 2019 were targeted. The general and biochemical characteristics of daytime workers and shift workers were compared through the Independent-test and the χ² test. Through multiple linear regression analysis, the association with shift work and inflammatory markers was investigated. Through multiple logistic regression analysis, the association with shift work and high inflammatory markers.

The mean total leukocytes, neutrophils, monocytes, lymphocytes of shift workers were significantly higher than those of daytime worker. The mean high-sensitivity C-reactive protein (hs-CRP) of shift workers was also higher than that of daytime workers but not significantly. In multiple linear regression, shift work was associated with increase of total leukocyte count (β = 0.367, p < 0.001) and hs-CRP (β = 0.140, p = 0.005) after adjusting for all variables. In multiple logistic regression analysis, shift work showed 2.27 times risk of high leukocyte count and 1.8 times risk of high hs-CRP level compared to daytime work after adjusting for all variables.

This study confirmed that shift work is associated with high inflammatory markers. Considering that high inflammatory markers is independent indicator of CVD, the association between shift work and high inflammatory markers may help to understand the CVD risk of shift workers.

The stress response to surgery is essential for maintaining homeostasis and exhibits anti-tumor effects; however, an ongoing and exaggerated stress response may have adverse clinical consequences and even promote cancer progression. This review will discuss the complex relationship between surgical stress and cancer progression.

Surgical stress exhibits both anti-tumor and cancer-promoting effects by causing changes in the neuroendocrine, circulatory, and immune systems. Many studies have found that many mechanisms are involved in the process, and the corresponding targets could be applied for cancer therapy. Although surgical stress may have anti-tumor effects, it is necessary to inhibit an excessive stress response, mostly showing cancer-promoting effects.