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Background Ankle sprain is the most common injury in basketball. Chronic ankle instability develops from an acute ankle sprain may cause negative effects on quality of life, ankle functionality or on increasing risk for recurrent ankle sprains and post-traumatic osteoarthritis. To facilitate a preventative strategy of chronic ankle instability (CAI) in the basketball population, gathering epidemiological data is essential. However, the epidemiological data of CAI in basketball is limited. Therefore, this study aims to investigate the prevalence of CAI in basketball athletes and to determine whether gender, competitive level, and basketball playing position influence this prevalence. Methods In a cross-sectional study, in total 391 Taiwanese basketball athletes from universities and sports clubs participated. Besides non-standardized questions about demographics and their history of ankle sprains, participants further filled out the standard Cumberland Ankle Instability Tool applied to determine the presence of ankle instability. Questionnaires from 255 collegiate and 133 semi-professional basketball athletes (male = 243, female = 145, 22.3 +/- 3.8 years, 23.3 +/- 2.2 kg/m(2)) were analyzed. Differences in prevalence between gender, competitive level and playing position were determined using the Chi-square test. Results In the surveyed cohort, 26% had unilateral CAI while 50% of them had bilateral CAI. Women had a higher prevalence than men in the whole surveyed cohort (X-2(1) = 0.515, p = 0.003). This gender disparity also showed from sub-analyses, that the collegiate female athletes had a higher prevalence than collegiate men athletes (X-2(1) = 0.203, p = 0.001). Prevalence showed no difference between competitive levels (p > 0.05) and among playing positions (p > 0.05). Conclusions CAI is highly prevalent in the basketball population. Gender affects the prevalence of CAI. Regardless of the competitive level and playing position the prevalence of CAI is similar. The characteristic of basketball contributes to the high prevalence. Prevention of CAI should be a focus in basketball. When applying the CAI prevention measures, gender should be taken into consideration.
Background:
Osteoporosis is a growing public health problem. It is known that stress-related diseases such as depression may impair bone quality and lead to osteoporosis. The association between psychosocial stress and bone health may be triggered by alterations of mitochondrial function and cell signaling and intercellular communication. In this context, extracellular vesicles (EVs) may be relevant due to their crucial role in intercellular communicators through the transfer of cargo.
Aim:
This narrative review aims to summarize if the cargo of extracellular vesicles can constitute a biological link between psychosocial stress and osteoporosis.
Methods:
To evaluate this research question, a thorough literature search was conducted using PubMed, Google Scholar, and Science Direct. The research keywords are allostatic load, bone remodeling, microRNA, osteoblast, and osteoclast. A total of 21 articles were included in the narrative review.
Results:
We found that certain miRNAs in EVs, including miR-126a-3p, miR-128-3p, and miR-187-5p, have been described as crucial players in both psychosocial stress and osteoporosis.
Discussion:
This review describes EVs and their cargo as a potential mediator linking psychosocial stress and osteoporosis for the first time by highlighting common crucial miRNAs. However, based on the included studies, it is unclear whether EV-mediated transport of biological cargoes can alter the function of target cells in a real physiological environment.
Stress and pain
(2022)
Introduction: Low back pain (LBP) leads to considerable impairment of quality of life worldwide and is often accompanied by psychosomatic symptoms.
Objectives: First, to assess the association between stress and chronic low back pain (CLBP) and its simultaneous appearance with fatigue and depression as a symptom triad. Second, to identify the most predictive stress-related pattern set for CLBP for a 1-year diagnosis.
Methods: In a 1-year observational study with four measurement points, a total of 140 volunteers (aged 18–45 years with intermittent pain) were recruited. The primary outcomes were pain [characteristic pain intensity (CPI), subjective pain disability (DISS)], fatigue, and depressive mood. Stress was assessed as chronic stress, perceived stress, effort reward imbalance, life events, and physiological markers [allostatic load index (ALI), hair cortisol concentration (HCC)]. Multiple linear regression models and selection procedures for model shrinkage and variable selection (least absolute shrinkage and selection operator) were applied. Prediction accuracy was calculated by root mean squared error (RMSE) and receiver-operating characteristic curves.
Results: There were 110 participants completed the baseline assessments (28.2 7.5 years, 38.1% female), including HCC, and a further of 46 participants agreed to ALI laboratory measurements. Different stress types were associated with LBP, CLBP, fatigue, and depressive mood and its joint occurrence as a symptom triad at baseline; mainly social-related stress types were of relevance. Work-related stress, such as “excessive demands at work”[b = 0.51 (95%CI -0.23, 1.25), p = 0.18] played a role for upcoming chronic pain disability. “Social overload” [b = 0.45 (95%CI -0.06, 0.96), p = 0.080] and “over-commitment at work” [b = 0.28 (95%CI -0.39, 0.95), p = 0.42] were associated with an upcoming depressive mood within 1-year. Finally, seven psychometric (CPI: RMSE = 12.63; DISS: RMSE = 9.81) and five biomarkers (CPI: RMSE = 12.21; DISS: RMSE = 8.94) could be derived as the most predictive pattern set for a 1-year prediction of CLBP. The biomarker set showed an apparent area under the curve of 0.88 for CPI and 0.99 for DISS.
Conclusion: Stress disrupts allostasis and favors the development of chronic pain, fatigue, and depression and the emergence of a “hypocortisolemic symptom triad,” whereby the social-related stressors play a significant role. For translational medicine, a predictive pattern set could be derived which enables to diagnose the individuals at higher risk for the upcoming pain disorders and can be used in practice.
Stress and pain
(2022)
Introduction: Low back pain (LBP) leads to considerable impairment of quality of life worldwide and is often accompanied by psychosomatic symptoms.
Objectives: First, to assess the association between stress and chronic low back pain (CLBP) and its simultaneous appearance with fatigue and depression as a symptom triad. Second, to identify the most predictive stress-related pattern set for CLBP for a 1-year diagnosis.
Methods: In a 1-year observational study with four measurement points, a total of 140 volunteers (aged 18–45 years with intermittent pain) were recruited. The primary outcomes were pain [characteristic pain intensity (CPI), subjective pain disability (DISS)], fatigue, and depressive mood. Stress was assessed as chronic stress, perceived stress, effort reward imbalance, life events, and physiological markers [allostatic load index (ALI), hair cortisol concentration (HCC)]. Multiple linear regression models and selection procedures for model shrinkage and variable selection (least absolute shrinkage and selection operator) were applied. Prediction accuracy was calculated by root mean squared error (RMSE) and receiver-operating characteristic curves.
Results: There were 110 participants completed the baseline assessments (28.2 7.5 years, 38.1% female), including HCC, and a further of 46 participants agreed to ALI laboratory measurements. Different stress types were associated with LBP, CLBP, fatigue, and depressive mood and its joint occurrence as a symptom triad at baseline; mainly social-related stress types were of relevance. Work-related stress, such as “excessive demands at work”[b = 0.51 (95%CI -0.23, 1.25), p = 0.18] played a role for upcoming chronic pain disability. “Social overload” [b = 0.45 (95%CI -0.06, 0.96), p = 0.080] and “over-commitment at work” [b = 0.28 (95%CI -0.39, 0.95), p = 0.42] were associated with an upcoming depressive mood within 1-year. Finally, seven psychometric (CPI: RMSE = 12.63; DISS: RMSE = 9.81) and five biomarkers (CPI: RMSE = 12.21; DISS: RMSE = 8.94) could be derived as the most predictive pattern set for a 1-year prediction of CLBP. The biomarker set showed an apparent area under the curve of 0.88 for CPI and 0.99 for DISS.
Conclusion: Stress disrupts allostasis and favors the development of chronic pain, fatigue, and depression and the emergence of a “hypocortisolemic symptom triad,” whereby the social-related stressors play a significant role. For translational medicine, a predictive pattern set could be derived which enables to diagnose the individuals at higher risk for the upcoming pain disorders and can be used in practice.
Association of primary allostatic load mediators and metabolic syndrome (MetS): A systematic review
(2022)
Allostatic load (AL) exposure may cause detrimental effects on the neuroendocrine system, leading to metabolic syndrome (MetS). The primary mediators of AL involve serum dehydroepiandrosterone sulfate (DHEAS; a functional HPA axis antagonist); further, cortisol, urinary norepinephrine (NE), and epinephrine (EPI) excretion levels (assessed within 12-h urine as a golden standard for the evaluation of the HPA axis activity and sympathetic nervous system activity). However, the evidence of an association between the primary mediators of AL and MetS is limited. This systematic review aimed to critically examine the association between the primary mediators of AL and MetS. PubMed and Web of Science were searched for articles from January 2010 to December 2021, published in English. The search strategy focused on cross-sectional and case–control studies comprising adult participants with MetS, obesity, overweight, and without chronic diseases. The STROBE checklist was used to assess study quality control. Of 770 studies, twenty-one studies with a total sample size (n = 10,666) met the eligibility criteria. Eighteen studies were cross-sectional, and three were case–control studies. The included studies had a completeness of reporting score of COR % = 87.0 ± 6.4%. It is to be noted, that cortisol as a primary mediator of AL showed an association with MetS in 50% (urinary cortisol), 40% (serum cortisol), 60% (salivary cortisol), and 100% (hair cortisol) of the studies. For DHEAS, it is to conclude that 60% of the studies showed an association with MetS. In contrast, urinary EPI and urinary NE had 100% no association with MetS. In summary, there is a tendency for the association between higher serum cortisol, salivary cortisol, urinary cortisol, hair cortisol, and lower levels of DHEAS with MetS. Future studies focusing on longitudinal data are warranted for clarification and understanding of the association between the primary mediators of AL and MetS.
Association of primary allostatic load mediators and metabolic syndrome (MetS): A systematic review
(2022)
Allostatic load (AL) exposure may cause detrimental effects on the neuroendocrine system, leading to metabolic syndrome (MetS). The primary mediators of AL involve serum dehydroepiandrosterone sulfate (DHEAS; a functional HPA axis antagonist); further, cortisol, urinary norepinephrine (NE), and epinephrine (EPI) excretion levels (assessed within 12-h urine as a golden standard for the evaluation of the HPA axis activity and sympathetic nervous system activity). However, the evidence of an association between the primary mediators of AL and MetS is limited. This systematic review aimed to critically examine the association between the primary mediators of AL and MetS. PubMed and Web of Science were searched for articles from January 2010 to December 2021, published in English. The search strategy focused on cross-sectional and case–control studies comprising adult participants with MetS, obesity, overweight, and without chronic diseases. The STROBE checklist was used to assess study quality control. Of 770 studies, twenty-one studies with a total sample size (n = 10,666) met the eligibility criteria. Eighteen studies were cross-sectional, and three were case–control studies. The included studies had a completeness of reporting score of COR % = 87.0 ± 6.4%. It is to be noted, that cortisol as a primary mediator of AL showed an association with MetS in 50% (urinary cortisol), 40% (serum cortisol), 60% (salivary cortisol), and 100% (hair cortisol) of the studies. For DHEAS, it is to conclude that 60% of the studies showed an association with MetS. In contrast, urinary EPI and urinary NE had 100% no association with MetS. In summary, there is a tendency for the association between higher serum cortisol, salivary cortisol, urinary cortisol, hair cortisol, and lower levels of DHEAS with MetS. Future studies focusing on longitudinal data are warranted for clarification and understanding of the association between the primary mediators of AL and MetS.
Training intervention effects on cognitive performance and neuronal plasticity — A pilot study
(2022)
Studies suggest that people suffering from chronic pain may have altered brain plasticity, along with altered functional connectivity between pain-processing brain regions. These may be related to decreased mood and cognitive performance. There is some debate as to whether physical activity combined with behavioral therapy (e.g. cognitive distraction, body scan) may counteract these changes. However, underlying neuronal mechanisms are unclear. The aim of the current pilot study with a 3-armed randomized controlled trial design was to examine the effects of sensorimotor training for nonspecific chronic low back pain on (1) cognitive performance; (2) fMRI activity co-fluctuations (functional connectivity) between pain-related brain regions; and (3) the relationship between functional connectivity and subjective variables (pain and depression). Six hundred and sixty two volunteers with non-specific chronic low back pain were randomly allocated to a unimodal (sensorimotor training), multidisciplinary (sensorimotor training and behavioral therapy) intervention, or to a control group within a multicenter study. A subsample of patients (n = 21) from one study center participated in the pilot study presented here. Measurements were at baseline, during (3 weeks, M2) and after intervention (12 weeks, M4 and 24 weeks, M5). Cognitive performance was measured by the Trail Making Test and functional connectivity by MRI. Pain perception and depression were assessed by the Von Korff questionnaire and the Hospital and Anxiety. Group differences were calculated by univariate and repeated ANOVA measures and Bayesian statistics; correlations by Pearson's r. Change and correlation of functional connection were analyzed within a pooled intervention group (uni-, multidisciplinary group). Results revealed that participants with increased pain intensity at baseline showed higher functional connectivity between pain-related brain areas used as ROIs in this study. Though small sample sizes limit generalization, cognitive performance increased in the multimodal group. Increased functional connectivity was observed in participants with increased pain ratings. Pain ratings and connectivity in pain-related brain regions decreased after the intervention. The results provide preliminary indication that intervention effects can potentially be achieved on the cognitive and neuronal level. The intervention may be suitable for therapy and prevention of non-specific chronic low back pain.
Training intervention effects on cognitive performance and neuronal plasticity — A pilot study
(2022)
Studies suggest that people suffering from chronic pain may have altered brain plasticity, along with altered functional connectivity between pain-processing brain regions. These may be related to decreased mood and cognitive performance. There is some debate as to whether physical activity combined with behavioral therapy (e.g. cognitive distraction, body scan) may counteract these changes. However, underlying neuronal mechanisms are unclear. The aim of the current pilot study with a 3-armed randomized controlled trial design was to examine the effects of sensorimotor training for nonspecific chronic low back pain on (1) cognitive performance; (2) fMRI activity co-fluctuations (functional connectivity) between pain-related brain regions; and (3) the relationship between functional connectivity and subjective variables (pain and depression). Six hundred and sixty two volunteers with non-specific chronic low back pain were randomly allocated to a unimodal (sensorimotor training), multidisciplinary (sensorimotor training and behavioral therapy) intervention, or to a control group within a multicenter study. A subsample of patients (n = 21) from one study center participated in the pilot study presented here. Measurements were at baseline, during (3 weeks, M2) and after intervention (12 weeks, M4 and 24 weeks, M5). Cognitive performance was measured by the Trail Making Test and functional connectivity by MRI. Pain perception and depression were assessed by the Von Korff questionnaire and the Hospital and Anxiety. Group differences were calculated by univariate and repeated ANOVA measures and Bayesian statistics; correlations by Pearson's r. Change and correlation of functional connection were analyzed within a pooled intervention group (uni-, multidisciplinary group). Results revealed that participants with increased pain intensity at baseline showed higher functional connectivity between pain-related brain areas used as ROIs in this study. Though small sample sizes limit generalization, cognitive performance increased in the multimodal group. Increased functional connectivity was observed in participants with increased pain ratings. Pain ratings and connectivity in pain-related brain regions decreased after the intervention. The results provide preliminary indication that intervention effects can potentially be achieved on the cognitive and neuronal level. The intervention may be suitable for therapy and prevention of non-specific chronic low back pain.
Background
Recent research emphasized the role of inflammatory processes in the pathophysiology of depression. Theories hypothesizes that life events (LE) can affect the immune system and trigger depressive symptoms. LE are also considered as one of the best predictors for the onset and course of depressive disorders.
Methods
Observational study across three treatment settings: n=208 depressive patients (75.5%f, M 46.6 y) were examined on depression (BDI-II), life events (ILE) and inflammatory markers (IL-6, CRP, fibrinogen, ICAM-1, TNF-alpha, E-selectin) at baseline (t0), 5-week(t1) and 5-month(t2) follow-up. Effects and interactions were analyzed with regression models.
Results
LE were associated with depressive symptoms at t0 (beta=.209; p=.002) and both follow-ups. Except for CRP, which was linked to depression symptoms at t2 (betai=-.190; p=.032), there were no effects of inflammatory markers on depressive symptoms. At t1, an interaction between CRP and LE in total (beta=-.249; p=.041) was found as well as for LE in the past five years (beta=-.122; p=.027). Similar interactions were found between cumulative LE and ICAM-1 (beta=-.197; p=.003) and IL-6 (beta=-.425; p=.001).
Conclusion
The cumulative burden of LE effects symptoms and treatment outcome in depressive patients. There is some evidence that inflammatory marker may have long-term effects on treatment outcome as they seem to weaken the determining relation between LE and depression.