610 Medizin und Gesundheit
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Introduction Vagally mediated heart rate variability is an index of autonomic nervous system activity that is associated with a large variety of outcome variables including psychopathology and self-regulation. While practicing heart rate variability biofeedback over several weeks has been reliably associated with a number of positive outcomes, its acute effects are not well known. As the strongest association with vagally mediated heart rate variability has been found particularly within the attention-related subdomain of self-regulation, we investigated the acute effect of heart rate variability biofeedback on attentional control using the revised Attention Network Test.
Methods Fifty-six participants were tested in two sessions. In one session each participant received a heart rate variability biofeedback intervention, and in the other session a control intervention of paced breathing at a normal ventilation rate. After the biofeedback or control intervention, participants completed the Attention Network Test using the Orienting Score as a measure of attentional control.
Results Mixed models revealed that higher resting baseline vagally mediated heart rate variability was associated with better performance in attentional control, which suggests more efficient direction of attention to target stimuli. There was no significant main effect of the intervention on attentional control. However, an interaction effect indicated better performance in attentional control after biofeedback in individuals who reported higher current stress levels.
Discussion The results point to acute beneficial effects of heart rate variability biofeedback on cognitive performance in highly stressed individuals. Although promising, the results need to be replicated in larger or more targeted samples in order to reach stronger conclusions about the effects.
External temperature change has been shown to modify epigenetic patterns, such as DNA methylation, which regulates gene expression. DNA methylation is heritable, and as such provides a mechanism to convey environmental information to subsequent generations. Studies on epigenetic response to temperature increase are still scarce in wild mammals, even more so studies that compare tissue-specific epigenetic responses. Here, we aim to address differential epigenetic responses on a gene and gene pathway level in two organs, liver and testis. We chose these organs, because the liver is the main metabolic and thermoregulation organ, and epigenetic modifications in testis are potentially transmitted to the F2 generation. We focused on the transmission of DNA methylation changes to naive male offspring after paternal exposure to an ambient temperature increase of 10 degrees C, and investigated differential methylated regions of sons sired before and after the paternal exposure using Reduced Representation Bisulfite Sequencing. We detected both a highly tissue-specific epigenetic response, reflected in genes involved in organ-specific metabolic pathways, and a more general regulation of single genes epigenetically modified in both organs. We conclude that genomes are context-specifically differentially epigenetically regulated in response to temperature increase. These findings emphasize the epigenetic relevance in cell differentiation, which is essential for the specific function(s) of complex organs, and is represented in a diverse molecular regulation of genes and gene pathways. The results also emphasize the paternal contribution to adaptive processes.
External temperature change has been shown to modify epigenetic patterns, such as DNA methylation, which regulates gene expression. DNA methylation is heritable, and as such provides a mechanism to convey environmental information to subsequent generations. Studies on epigenetic response to temperature increase are still scarce in wild mammals, even more so studies that compare tissue-specific epigenetic responses. Here, we aim to address differential epigenetic responses on a gene and gene pathway level in two organs, liver and testis. We chose these organs, because the liver is the main metabolic and thermoregulation organ, and epigenetic modifications in testis are potentially transmitted to the F2 generation. We focused on the transmission of DNA methylation changes to naive male offspring after paternal exposure to an ambient temperature increase of 10 degrees C, and investigated differential methylated regions of sons sired before and after the paternal exposure using Reduced Representation Bisulfite Sequencing. We detected both a highly tissue-specific epigenetic response, reflected in genes involved in organ-specific metabolic pathways, and a more general regulation of single genes epigenetically modified in both organs. We conclude that genomes are context-specifically differentially epigenetically regulated in response to temperature increase. These findings emphasize the epigenetic relevance in cell differentiation, which is essential for the specific function(s) of complex organs, and is represented in a diverse molecular regulation of genes and gene pathways. The results also emphasize the paternal contribution to adaptive processes.
Objective: The aim of the present study was to examine the effect of Cold Water Immersion (CWI) on the recovery of physical performance, hematological stress markers and perceived wellness (i.e., Hooper scores) following a simulated Mixed Martial Arts (MMA) competition.
Methods: Participants completed two experimental sessions in a counter-balanced order (CWI or passive recovery for control condition: CON), after a simulated MMAs competition (3 x 5-min MMA rounds separated by 1-min of passive rest). During CWI, athletes were required to submerge their bodies, except the trunk, neck and head, in the seated position in a temperature-controlled bath (similar to 10 degrees C) for 15-min. During CON, athletes were required to be in a seated position for 15-min in same room ambient temperature. Venous blood samples (creatine kinase, cortisol, and testosterone concentrations) were collected at rest (PRE-EX, i.e., before MMAs), immediately following MMAs (POST-EX), immediately following recovery (POST-R) and 24 h post MMAs (POST-24), whilst physical fitness (squat jump, countermovement-jump and 5- and 10-m sprints) and perceptual measures (well-being Hooper index: fatigue, stress, delayed onset muscle soreness (DOMS), and sleep) were collected at PRE-EX, POST-R and POST-24, and at PRE-EX and POST-24, respectively.
Results: The main results indicate that POST-R sprint (5- and 10-m) performances were 'likely to very likely' (d = 0.64 and 0.65) impaired by prior CWI. However, moderate improvements were in 10-m sprint performance were 'likely' evident at POST-24 after CWI compared with CON (d = 0.53). Additionally, the use of CWI 'almost certainly' resulted in a large overall improvement in Hooper scores (d = 1.93). Specifically, CWI 'almost certainly' resulted in improved sleep quality (d = 1.36), stress (d = 1.56) and perceived fatigue (d = 1.51), and 'likely' resulted in a moderate decrease in DOMS (d = 0.60).
Conclusion: The use of CWI resulted in an enhanced recovery of 10-m sprint performance, as well as improved perceived wellness 24-h following simulated MMA competition.
Genetic and environmental factors both contribute to cognitive test performance. A substantial increase in average intelligence test results in the second half of the previous century within one generation is unlikely to be explained by genetic changes. One possible explanation for the strong malleability of cognitive performance measure is that environmental factors modify gene expression via epigenetic mechanisms. Epigenetic factors may help to understand the recent observations of an association between dopamine-dependent encoding of reward prediction errors and cognitive capacity, which was modulated by adverse life events. The possible manifestation of malleable biomarkers contributing to variance in cognitive test performance, and thus possibly contributing to the "missing heritability" between estimates from twin studies and variance explained by genetic markers, is still unclear. Here we show in 1475 healthy adolescents from the IMaging and GENetics (IMAGEN) sample that general IQ (gIQ) is associated with (1) polygenic scores for intelligence, (2) epigenetic modification of DRD2 gene, (3) gray matter density in striatum, and (4) functional striatal activation elicited by temporarily surprising reward-predicting cues. Comparing the relative importance for the prediction of gIQ in an overlapping subsample, our results demonstrate neurobiological correlates of the malleability of gIQ and point to equal importance of genetic variance, epigenetic modification of DRD2 receptor gene, as well as functional striatal activation, known to influence dopamine neurotransmission. Peripheral epigenetic markers are in need of confirmation in the central nervous system and should be tested in longitudinal settings specifically assessing individual and environmental factors that modify epigenetic structure.
Fluid intelligence (fluid IQ), defined as the capacity for rapid problem solving and behavioral adaptation, is known to be modulated by learning and experience. Both stressful life events (SLES) and neural correlates of learning [specifically, a key mediator of adaptive learning in the brain, namely the ventral striatal representation of prediction errors (PE)] have been shown to be associated with individual differences in fluid IQ. Here, we examine the interaction between adaptive learning signals (using a well-characterized probabilistic reversal learning task in combination with fMRI) and SLES on fluid IQ measures. We find that the correlation between ventral striatal BOLD PE and fluid IQ, which we have previously reported, is quantitatively modulated by the amount of reported SLES. Thus, after experiencing adversity, basic neuronal learning signatures appear to align more closely with a general measure of flexible learning (fluid IQ), a finding complementing studies on the effects of acute stress on learning. The results suggest that an understanding of the neurobiological correlates of trait variables like fluid IQ needs to take socioemotional influences such as chronic stress into account.
Purpose: Psychosocial variables are known risk factors for the development and chronification of low back pain (LBP). Psychosocial stress is one of these risk factors. Therefore, this study aims to identify the most important types of stress predicting LBP. Self-efficacy was included as a potential protective factor related to both, stress and pain.
Participants and Methods: This prospective observational study assessed n = 1071 subjects with low back pain over 2 years. Psychosocial stress was evaluated in a broad manner using instruments assessing perceived stress, stress experiences in work and social contexts, vital exhaustion and life-event stress. Further, self-efficacy and pain (characteristic pain intensity and disability) were assessed. Using least absolute shrinkage selection operator regression, important predictors of characteristic pain intensity and pain-related disability at 1-year and 2-years follow-up were analyzed.
Results: The final sample for the statistic procedure consisted of 588 subjects (age: 39.2 (± 13.4) years; baseline pain intensity: 27.8 (± 18.4); disability: 14.3 (± 17.9)). In the 1-year follow-up, the stress types “tendency to worry”, “social isolation”, “work discontent” as well as vital exhaustion and negative life events were identified as risk factors for both pain intensity and pain-related disability. Within the 2-years follow-up, Lasso models identified the stress types “tendency to worry”, “social isolation”, “social conflicts”, and “perceived long-term stress” as potential risk factors for both pain intensity and disability. Furthermore, “self-efficacy” (“internality”, “self-concept”) and “social externality” play a role in reducing pain-related disability.
Conclusion: Stress experiences in social and work-related contexts were identified as important risk factors for LBP 1 or 2 years in the future, even in subjects with low initial pain levels. Self-efficacy turned out to be a protective factor for pain development, especially in the long-term follow-up. Results suggest a differentiation of stress types in addressing psychosocial factors in research, prevention and therapy approaches.
Purpose: Psychosocial variables are known risk factors for the development and chronification of low back pain (LBP). Psychosocial stress is one of these risk factors. Therefore, this study aims to identify the most important types of stress predicting LBP. Self-efficacy was included as a potential protective factor related to both, stress and pain.
Participants and Methods: This prospective observational study assessed n = 1071 subjects with low back pain over 2 years. Psychosocial stress was evaluated in a broad manner using instruments assessing perceived stress, stress experiences in work and social contexts, vital exhaustion and life-event stress. Further, self-efficacy and pain (characteristic pain intensity and disability) were assessed. Using least absolute shrinkage selection operator regression, important predictors of characteristic pain intensity and pain-related disability at 1-year and 2-years follow-up were analyzed.
Results: The final sample for the statistic procedure consisted of 588 subjects (age: 39.2 (± 13.4) years; baseline pain intensity: 27.8 (± 18.4); disability: 14.3 (± 17.9)). In the 1-year follow-up, the stress types “tendency to worry”, “social isolation”, “work discontent” as well as vital exhaustion and negative life events were identified as risk factors for both pain intensity and pain-related disability. Within the 2-years follow-up, Lasso models identified the stress types “tendency to worry”, “social isolation”, “social conflicts”, and “perceived long-term stress” as potential risk factors for both pain intensity and disability. Furthermore, “self-efficacy” (“internality”, “self-concept”) and “social externality” play a role in reducing pain-related disability.
Conclusion: Stress experiences in social and work-related contexts were identified as important risk factors for LBP 1 or 2 years in the future, even in subjects with low initial pain levels. Self-efficacy turned out to be a protective factor for pain development, especially in the long-term follow-up. Results suggest a differentiation of stress types in addressing psychosocial factors in research, prevention and therapy approaches.
The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts
The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts