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Chronic Stress Contributes to Osteosarcopenic Adiposity via Inflammation and Immune Modulation: The Case for More Precise Nutritional Investigation.
Ilich, JZ, Gilman, JC, Cvijetic, S, Boschiero, D
Nutrients. 2020;(4)
Abstract
Chronic stress and low-grade chronic inflammation (LGCI) are key underlying factors formany diseases, including bone and body composition impairments. Objectives of this narrativereview were to examine the mechanisms by which chronic stress and LGCI may influenceosteosarcopenic adiposity (OSA) syndrome, originally named as ostoesarcopenic obesity (OSO).We also examined the crucial nutrients presumed to be affected by or cause of stress andinflammation and compared/contrasted them to those of our prehistoric ancestors. The evidenceshows that stress (particularly chronic) and its related inflammatory processes, contribute toosteoporosis, sarcopenia, and adiposity ultimately leading to OSA as a final and most derangedstate of body composition, commencing at the mesenchymal cell lineage disturbance. Thefoods/nutrients consumed by modern humans, as well as their altered lifestyle, also contribute tostress, LGCI and subsequently to OSA. The processes can also go in opposite direction when stressand inflammation impact nutritional status, particularly some micronutrients' levels. Whilenutritional management of body composition and LGCI have been studied, the nutrients (and theirquantities) most affected by stressors and those which may act toward the alleviation of stressfulstate, ultimately leading to better body composition outcomes, need to be elucidated.
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The alteration of stress-related physiological parameters after probiotics administration in oral surgeons with different degrees of surgical experience.
Pacifici, A, Pacifici, L, Nuzzolese, M, Cascella, G, Ballini, A, Santacroce, L, Dipalma, G, Aiello, E, Amantea, M, Saini, R, et al
La Clinica terapeutica. 2020;(3):e197-e208
Abstract
PURPOSE Stress is a multifactorial and complex pathway, gaining growing attention from the healthcare community. Surgeons are subjected to higher levels of stress, due to surgical procedures that are demanding and repetitive; unfortunately, high-stress levels may also cause side-effects, as surgical mistakes. This study aimed to evaluate the efficacy of specific probiotics strains formula on stress levels in oral and maxillofacial surgeons, to improve their quality of life. METHODS We have investigated the hormonal (salivary Cortisol; sC), immune (salivary Immunoglobulin A; sIgA) and cardiovascular (Heart rate, HR, and systolic blood pressure, SBP) responses induced by stress conditions in 40 oral surgeons, randomly selected and allocated, according to their experience level, in three categories: senior, expert, and junior. RESULTS The results described how the number of heartbeats/ minute and SBP are slightly raised in all surgeons at different timepoints. Such data allow us to assess that work-related stress can induce an increase in cardiovascular parameters, even if they are not significantly modified by the use of probiotics. On the other hand, our data indicate that 10 weeks of probiotic integration may induce the improvement of other stress-related physiological parameters in oral surgeons with different degrees of surgical experience, such as the salivary cortisol levels, even under stress conditions. Moreover, in the test group (probiotics administration), the immunoglobulin levels were higher than the control (placebo administration) group: this happens as a consequence of the regular use of probiotics, which may induce an increased number of IgA producing cells. DISCUSSION Our data indicated that 10 weeks of probiotics-enriched diet modify some stress-related physiological parameters in oral surgeons with different degrees of surgical experience, but it does not impact on the overall cardiovascular risk.
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Sex Differences in Physiological Stress Induced by a Long-Lasting Adventure Race: A Prospective Observational Analytical Study.
Silva, RPM, Vilaça, A, Guerra, FD, Mundim, AV, de Agostini, GG, de Abreu, LC, Zhiguo, Z, Sorpreso, IC, Valenti, VE, Penha-Silva, N
Sportverletzung Sportschaden : Organ der Gesellschaft fur Orthopadisch-Traumatologische Sportmedizin. 2020;(2):84-95
Abstract
BACKGROUND In order to provide additional information on the behaviour of biochemical parameters related to stress responses to a specific long-term competition, we aimed to compare the stressful effects of a long-lasting competition on physiological variables in men and women. METHODS This is a prospective observational analytical study. Twenty-five professional athletes, 15 men and 10 women, travelled 460 km for 4 days in an international edition of the Ecomotion/Pro AR World. RESULTS After the competition, we detected an increase in α-amylase and cortisol levels and a decrease in salivary immunoglobulin A (lgA) levels. The relative percentage changes in α-amylase, IgA and cortisol levels were significantly higher in women than in men, whereas women had lower relative percentage changes in glucose and lactate levels compared with men. There was a decrease in lymphocyte, eosinophil and monocyte counts, with relative percentage decreases in lymphocytes and monocytes being significantly higher in female athletes than in males. There were increases in the serum activities of total creatine kinase (CK), the creatine kinase myocardial isoform (CKMB), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) at the end of the test, with significantly higher elevations of total CK, CKMB and LDH in men and ALT in women. CONCLUSION Long-lasting competition induced stress, muscle damage, anaemia and changes in the immune system. Women had more intense responses of cortisol and leukocytes.
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The impact of sport related stressors on immunity and illness risk in team-sport athletes.
Keaney, LC, Kilding, AE, Merien, F, Dulson, DK
Journal of science and medicine in sport. 2018;(12):1192-1199
Abstract
OBJECTIVES Elite team-sport athletes are frequently exposed to stressors that have the potential to depress immunity and increase infection risk. Therefore, the purpose of this review is to describe how team-sport stressors impact upon immune responses, along with exploring whether alterations in these markers have the potential to predict upper respiratory tract illness symptoms. DESIGN Narrative review. METHODS Salivary secretory immunoglobulin A (SIgA) and T-cell markers have been shown to predict infection risk in individual endurance athletes. Papers discussing the impact of team-sport stressors on SIgA and T-cells were discussed in the review, studies discussing other aspects of immunity were excluded. Journal articles were sourced from PubMed, Web of science and Scopus. Key search terms included team-sport athletes, stressors, immunity, T-cells, cytokines, SIgA and upper respiratory illness. RESULTS Most team-sport stressors appear to increase risk for illness. An association between reduced SIgA and increased illness incidence has been demonstrated. Intensive training and competition periods have been shown to reduce SIgA, however, it is less clear how additional stressors including extreme environmental conditions, travel, psychological stress, sleep disturbance and poor nutrition affect immune responses. CONCLUSIONS Monitoring SIgA may provide an assessment of a team-sport athletes risk status for developing upper respiratory tract symptoms, however there is currently not enough evidence to suggest SIgA alone can predict illness. Team-sport stressors challenge immunity and it is possible that the combination of stressors could have a compounding effect on immunodepression and infection risk. Given that illness can disrupt training and performance, further research is required to better elucidate how stressors individually and collectively influence immunity and illness.
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The Transcription Factor EB Links Cellular Stress to the Immune Response
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Nabar, NR, Kehrl, JH
The Yale journal of biology and medicine. 2017;(2):301-315
Abstract
The transcription factor EB (TFEB) is the master transcriptional regulator of autophagy and lysosome biogenesis. Recent advances have led to a paradigm shift in our understanding of lysosomes from a housekeeping cellular waste bin to a dynamically regulated pathway that is efficiently turned up or down based on cellular needs. TFEB coordinates the cellular response to nutrient deprivation and other forms of cell stress through the lysosome system, and regulates a myriad of cellular processes associated with this system including endocytosis, phagocytosis, autophagy, and lysosomal exocytosis. Autophagy and the endolysosomal system are critical to both the innate and adaptive arms of the immune system, with functions in effector cell priming and direct pathogen clearance. Recent studies have linked TFEB to the regulation of the immune response through the endolysosmal pathway and by direct transcriptional activation of immune related genes. In this review, we discuss the current understanding of TFEB's function and the molecular mechanisms behind TFEB activation. Finally, we discuss recent advances linking TFEB to the immune response that positions lysosomal signaling as a potential target for immune modulation.
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Fetal Metabolic Stress Disrupts Immune Homeostasis and Induces Proinflammatory Responses in Human Immunodeficiency Virus Type 1- and Combination Antiretroviral Therapy-Exposed Infants.
Schoeman, JC, Moutloatse, GP, Harms, AC, Vreeken, RJ, Scherpbier, HJ, Van Leeuwen, L, Kuijpers, TW, Reinecke, CJ, Berger, R, Hankemeier, T, et al
The Journal of infectious diseases. 2017;(4):436-446
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Abstract
Increased morbidity and fetal growth restriction are reported in uninfected children born to human immunodeficiency virus type 1 (HIV-1)-infected women treated with antiretroviral (ARV) therapy. Viruses and/or pharmacological interventions such as ARVs can induce metabolic stress, skewing the cell's immune response and restricting (cell) growth. Novel metabolomic techniques provided the opportunity to investigate the impact of fetal HIV-1 and combination ARV therapy (cART) exposure on the infants' immune metabolome. Peroxidized lipids, generated by reactive oxygen species, were increased in cART/HIV-1-exposed infants, indicating altered mitochondrial functioning. The lipid metabolism was further dysregulated with increased triglyceride species and a subsequent decrease in phospholipids in cART/HIV-1-exposed infants compared to control infants. Proinflammatory immune mediators, lysophospholipids as well as cytokines such as CXCL10 and CCL3, were increased whereas anti-inflammatory metabolites from the cytochrome P450 pathway were reduced in cART/HIV-1-exposed infants. Taken together, these data demonstrate that the fetal metabolism is impacted by maternal factors (cART and HIV-1) and skews physiological immune responses toward inflammation in the newborn infant.