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To determine stress-related influences on obesity, the eating behaviour of 100 overweight and normal weight children was investigated in the laboratory and in everyday life. A controlled repeated measures design was used for the laboratory study with stress vs. non-stress as one repeated factor. The eating style was measured by recording cumulative eating curves with a universal eating monitor. Stress eating during everyday life was measured by questionnaire. In everyday life, the amount of protein, carbohydrate, and fat as well the total amount of energy in each meal were analysed. The eating style after stress-induction in the laboratory did not differ between weight groups. However, in everyday life, overweight children more often pretended to eat when feeling stressed, than did normal weight children. The "stress eating" was more pronounced for children, who have high restraint scores. Overweight children didn`t ingest neither more calories nor fat, carbohydrate or protein. Stress-related eating behaviour in everyday life may be part of the development and maintenance of overweight in children. However, if the availability of food is limited and the environment is structured, stress-protective ressources of overweight children may help them to control their eating behaviour.
In jüngerer Zeit wurde in der neuroendokrinologischen Forschung das Phänomen eines Hypocortisolismus bei verschiedenen Störungen, die mit Stress assoziiert sind, beschrieben. Insbesondere bei der Posttraumatischen Belastungsstörung (PTSD) wurde eine verringerte adrenale Aktivität berichtet. Aber auch bei Patienten mit verschiedenen körperlichen Beschwerden wurden ähnliche neuroendokrine Veränderungen gefunden. Dazu zählen unter anderem das Fibromyalgiesyndrom (FMS) und chronische Unterbauchbeschwerden (CUBB). Die Mechanismen, welche dem Hypocortisolismus zugrunde liegen, sind bislang sowohl für die PTSD als auch für stressabhängige körperliche Beschwerden nicht abschließend geklärt. Weiterhin besteht Unklarheit darüber, inwieweit eine Vergleichbarkeit dieser Mechanismen zwischen den verschiedenen Störungsbildern besteht. Die Entstehung und Aufrechterhaltung dieser Erkrankungen scheinen somit ein sehr komplexes Zusammenspiel verschiedener Faktoren darzustellen. Andererseits weisen die Überlappungen hinsichtlich symptomatologischer, psychologischer und endokrinologischer Variablen zwischen PTSD, FMS und CUBB auf die Existenz störungsübergreifender Subgruppen hin. In der vorliegenden Studie wurden psychologische und endokrinologische Auffälligkeiten bei PTSD, FMS und CUBB weiter untersucht. Vorrangiges Ziel war, zu überprüfen, inwieweit störungsübergreifende Subgruppen mit vergleichbaren psychoendokrinologischen Auffälligkeiten bestehen. Insgesamt wurden 59 Patientinnen mittels verschiedener endokrinologischer Tests untersucht und mit 30 gesunden Kontrollfrauen verglichen. Mit einer Clusteranalyse konnten drei unabhängige störungsübergreifende Subgruppen identifiziert werden, die sich hinsichtlich ihrer Reaktionen in den endokrinologischen Tests unterschieden. Es konnte somit gezeigt werden, dass es sich bei den untersuchten Störungsgruppen weder um eine Störungsfamilie mit identischen endokrinen Auffälligkeiten noch um isolierte, d.h. distinkte, von einander unabhängige Erkrankungen handelt. Vielmehr scheinen störungsübergreifende Subgruppen zu bestehen. Weitere Studien sollten die gefunden Muster replizieren und gegebenenfalls erweitern.
Memory consists of multiple anatomically and functionally distinct systems. Animal studies suggest that stress modulates multiple memory systems in a manner that favors nucleus caudatus-based stimulus-response learning at the expense of hippocampus-based spatial learning. The present work aimed (i) to translate these findings to humans, (ii) to determine the involvement of the stress hormone cortisol in this effect, and (iii) to assess whether the use of stimulus-response and spatial strategies is a long lasting person characteristic. To address these issues we developed a new paradigm that differentiates the use of spatial and stimulus-response learning in humans. Our findings indicate that (i) psychosocial stress (Trier Social Stress Test) modulates the use of spatial and stimulus-response learning in humans, (ii) cortisol plays a key role in this modulatory effect of stress, and (iii) the use of spatial and stimulus-response learning is affected by situational rather than long lasting person factors.
Das Stresshormon Cortisol zeigt einen starken zirkadianen Rhythmus mit hohen Cortisolwerten nach dem morgendlichen Erwachen und niedrigen Werten am Abend. Die vorliegende Arbeit legt die Grundlagen dafür, dass der Cortisolspiegel nach dem Erwachen (Cortisol Awakening Response) zukünftig Bestandteil einer multimodalen Diagnostik stressbezogener Erkrankungen werden kann. Zu diesem Zweck werden besonders messmethodische Aspekte des Cortisol Awakening Response (CAR) dargestellt und eingehend diskutiert. Der Einfluss verschiedener konfundierender Variablen wurde in einer quantitativen Metaanalyse untersucht. Ein gesonderter Abschnitt beschreibt verschiedene Möglichkeiten der statistischen Analyse des CAR. Zu diesem Zweck wurden verschiedene statistische Kennwerte generiert und deren Reliabilitäten und Interkorrelationen an einem empirischen Datensatz untersucht. In dieser Arbeit werden auch Normwerte für die einzelnen statistischen Kennwerte des CAR angegeben.
The glucocorticoid (GC) cortisol, main mediator of the hypothalamic-pituitary-adrenal axis, has many implications in metabolism, stress response and the immune system. GC function is mediated mainly via the glucocorticoid receptor (GR) which binds as a transcription factor to glucocorticoid response elements (GREs). GCs are strong immunosuppressants and used to treat inflammatory and autoimmune diseases. Long-term usage can lead to several irreversible side effects which make improved understanding indispensable and warrant the adaptation of current drugs. Several large scale gene expression studies have been performed to gain insight into GC signalling. Nevertheless, studies at the proteomic level have not yet been made. The effects of cortisol on monocytes and macrophages were studied in the THP-1 cell line using 2D fluorescence difference gel electrophoresis (2D DIGE) combined with MALDI-TOF mass spectrometry. More than 50 cortisol-modulated proteins were identified which belonged to five functional groups: cytoskeleton, chaperones, immune response, metabolism, and transcription/translation. Multiple GREs were found in the promoters of their corresponding genes (+10 kb/-0.2 kb promoter regions including all alternative promoters available within the Database for Transcription Start Sites (DBTSS)). High quality GREs were observed mainly in cortisol modulated genes, corroborating the proteomics results. Differential regulation of selected immune response related proteins were confirmed by qPCR and immuno-blotting. All immune response related proteins (MX1, IFIT3, SYWC, STAT3, PMSE2, PRS7) which were induced by LPS were suppressed by cortisol and belong mainly to classical interferon target genes. Mx1 has been selected for detailed expression analysis since new isoforms have been identified by proteomics. FKBP51, known to be induced by cortisol, was identified as the strongest differentially expressed protein and contained the highest number of strict GREs. Genomic analysis of five alternative FKBP5 promoter regions suggested GC inducibility of all transcripts. 2D DIGE combined with 2D immunoblotting revealed the existence of several previously unknown FKBP51 isoforms, possibly resulting from these transcripts. Additionally multiple post-translational modifications were found, which could lead to different subcellular localization in monocytes and macrophages as seen by confocal microscopy. Similar results were obtained for the different cellular subsets of human peripheral blood mononuclear cells (PBMCs). FKBP51 was found to be constitutively phosphorylated with up to 8 phosphosites in CD19+ B lymphocytes. Differential Co-immunoprecipitation for cytoplasm and nucleus allowed us to identify new potential interaction partners. Nuclear FKBP51 was found to interact with myosin 9, whereas cytosolic FKBP51 with TRIM21 (synonym: Ro52, Sjögren`s syndrome antigen). The GR has been found to interact with THOC4 and YB1, two proteins implicated in mRNA processing and transcriptional regulation. We also applied proteomics to study rapid non-genomic effects of acute stress in a rat model. The nuclear proteome of the thymus was investigated after 15 min restraint stress and compared to the non-stressed control. Most of the identified proteins were transcriptional regulators found to be enriched in the nucleus probably to assist gene expression in an appropriate manner. The proteomic approach allowed us to further understand the cortisol mediated response in monocytes/macrophages. We identified several new target proteins, but we also found new protein variants and post-translational modifications which need further investigation. Detailed study of FKBP51 and GR indicated a complex regulation network which opened a new field of research. We identified new variants of the anti-viral response protein MX1, displaying differential expression and phosphorylation in the cellular compartments. Further, proteomics allowed us to follow the very early effects of acute stress, which happen prior to gene expression. The nuclear thymocyte proteome of restraint stressed rats revealed an active preparation for subsequent gene expression. Proteomics was successfully applied to study differential protein expression, to identify new protein variants and phosphorylation events as well as to follow translocation. New aspects for future research in the field of cortisol-mediated immune modulation have been added.
In this psycho-neuro-endocrine study the molecular basis of different variants of steroid receptors as well as highly conserved non steroidal receptors was investigated. These nuclear receptors (NRs) are important key regulators of a wide variety of different physiological and pathophysiological challenges ranging from inflammation and stress to complex behaviour and disease. NRs control gene transcription in a ligand dependent manner and are embedded in the huge interaction network of the neuroendocrine and immune system. Two receptors, the glucocorticoid receptor (GR) and the chicken ovalbumin upstream promoter-transcription factorII (Coup-TFII), both expressed in the immune and nervous system, were investigated regarding possible splice variants and their implication in the control of gene transcription. Both NRs are known to interact and modulate each other- target gene regulation. This study could be shown that both NRs have different splice variants that are expressed in a tissue specific manner. The different 5-´alternative transcript variants of the human GR were in silico identified in other species and evidence for a highly conserved and tightly controlled function was provided. Investigations of the N-terminal transactivation domain of the GR showed a deletion suggesting an altered glucocorticoid-dependent transactivation profile. The newly identified alternative transcript variant of Coup-TFII leads to a DNA binding deficient Coup-TFII isoform that is highly expressed in the brain. This Coup-TFII isoform alters Coup-TFII target gene expression and is suggested to interact with GR via its ligand binding domain resulting in an impaired GR target gene regulation in the nervous system. In this thesis it was demonstrated that NR variants are important for the understanding of the enormous regulatory potential of this receptor family and have to be taken into account for the development of therapeutic strategies for complex diseases such as stress related and neurodegenerative disorders.
In der vorliegenden Arbeit wurden die regulatorischen Regionen der Gene für den Kaliumchloridtransporter 3 (KCC3, SLC12A6) und den Glukokortikoidrezeptor (NR3C1) untersucht. Hierbei handelt es sich um Gene, die bereits mit psychiatrischen Erkrankungen assoziiert worden sind. Die Promotorregionen beider Gene wurden in Abhängigkeit von bereits in der Literatur beschriebenen DNA-Polymorphismen und unter besonderer Berücksichtigung epigenetischer DNA-Modifikationen mittels bisulfitspezifischer Sequenzierung und Luciferase-Assay funktionell charakterisiert. Es konnte gezeigt werden, dass DNA-Polymorphismen und epigenetische Veränderungen der Erbinformation - letztere können in Abhängigkeit unterschiedlicher Lebenserfahrungen entstehen - funktionelle Relevanz für die Promotoraktivität der untersuchten Gene haben. Strukturelle und modifikatorische DNA-Variationen sowie Gen-Umwelt Wechselwirkungen beeinflussen somit die Genregulation und können unter bestimmten Bedingungen krankheitsrelevant werden.
Zurzeit werden gesundheitliche Auswirkungen von Mobilfunkstrahlung auf den Menschen kontroversiell diskutiert. Die vorliegende Arbeit untersuchte mögliche Auswirkungen auf Befindlichkeit und psychische Variablen in zwei Studien. Es zeigte sich ein Trend bei einer Variable, es gab jedoch keine signifikanten Effekte. Bei den nicht-experimentellen Befunden wiesen Anrainer von Mobilfunksendeanlagen (self-rater) höhere psychische Belastung auf.
Stress and pain are common experiences in human lives. Both, the stress and the pain system have adaptive functions and try to protect the organism in case of harm and danger. However, stress and pain are two of the most challenging problems for the society and the health system. Chronic stress, as often seen in modern societies, has much impact on health and can lead to chronic stress disorders. These disorders also include a number of chronic pain syndromes. However, pain can also be regarded as a stressor itself, especially when we consider how much patients suffer from long-lasting pain and the impact of pain on life quality. In this way, the effects of stress on pain can be fostered. For the generation and manifestation of chronic pain symptoms also learning processes such as classical conditioning play an important role. Processes of classical conditioning can also be influenced by stress. These facts illustrate the complex and various interactions between the pain and the stress systems. Both systems communicate permanently with each other and help to protect the organism and to keep a homeostatic state. They have various ways of communication, for example mechanisms related to endogenous opioids, immune parameters, glucocorticoids and baroreflexes. But an overactivation of the systems, for example caused by ongoing stress, can lead to severe health problems. Therefore, it is of great importance to understand these interactions and their underlying mechanisms. The present work deals with the relationship of stress and pain. A special focus is put on stress related hypocortisolism and pain processing, stress induced hypoalgesia via baroreceptor related mechanisms and stress related cortisol effects on aversive conditioning (as a model of pain learning). This work is a contribution to the wide field of research that tries to understand the complex interactions of stress and pain. To demonstrate the variety, the selected studies highlight different aspects of these interactions. In the first chapter I will give a short introduction on the pain and the stress systems and their ways of interaction. Furthermore, I will give a short summary of the studies presented in Chapter II to V and their background. The results and their meaning for future research will be discussed in the last part of the first chapter. Chronic pain syndromes have been associated with chronic stress and alterations of the HPA axis resulting in chronic hypocortisolism. But if these alterations may play a causal role in the pathophysiology of chronic pain remains unclear. Thus, the study described in Chapter II investigated the effects of pharmacological induced hypocortisolism on pain perception. Both, the stress and the pain system are related to the cardiovascular system. Increase of blood pressure is part of the stress reaction and leads to reduced pain perception. Therefore, it is important for the usage of pain tests to keep in mind potential interferences from activation of the cardiovascular system, especially when pain inhibitory processes are investigated. For this reason we compared two commonly and interchangeably used pain tests with regard to the triggered autonomic reactions. This study is described in chapter III. Chapter IV and V deal with the role of learning processes in pain and related influences of stress. Processes of classical conditioning play an important role for symptom generation and manifestation. In both studies aversive eyeblink conditioning was used as a model for pain learning. In the study described in Chapter IV we compared classical eyeblink conditioning in healthy volunteers to patients suffering from fibromyalgia, a chronic pain disorder. Also, differences of the HPA axis, as part of the stress system, were taken in account. The study of Chapter V investigated effects of the very first stress reaction, particularly rapid non-genomic cortisol effects. Healthy volunteers received an intravenous cortisol administration immediately before the eyeblink conditioning. Rapid effects have only been demonstrated on a cellular level and on animal behavior so far. In general, the studies presented in this work may give an impression of the broad variety of possible interactions between the pain and the stress system. Furthermore, they contribute to our knowledge about theses interactions. However, more research is needed to complete the picture.
Stress is a common phenomenon for animals living in the wild, but also for humans in modern societies. Originally, the body's stress response is an adaptive reaction to a possibly life-threatening situation, and it has been shown to impact on energy distribution and metabolism, thereby increasing the chance of survival. However, stress has also been shown to impact on mating behaviour and reproductive strategies in animals and humans. This work deals with the effect of stress on reproductive behavior. Up to now, research has only focused on the effects of stress on reproduction in general. The effects of stress on reproduction may be looked at from two points of view. First, stress affects reproductive functioning by endocrine (e.g. glucocorticoid) actions on the reproductive system. However, stress can also influence reproductive behavior, i.e. mate choice and mating preferences. Animals and humans do not mate randomly, but exhibit preferences towards mating partners. One factor by which animals and humans choose their mating partners is similarity vs. dissimilarity: Similar mates usually carry more of one's own genes and the cooperation between similar mates is, at least theoretically, less hampered by expressing diverse behaviors. By mating with dissimilar mates on the other hand one may acquire new qualities for oneself, but also for one's offspring, useful to cope with environmental challenge. In humans we usually find a preference for similar mates. Due to the high costs of breeding, variables like cooperation and life-long partnerships may play a greater role than the acquaintance of new qualities.The present work focuses on stress effects on mating preferences of humans and will give a first answer to the question whether stress may affect our preference for similar mates. Stress and mating preferences are at the centre of this work. Thus, in the first Chapter I will give an introduction on stress and mating preferences and link these topics to each other. Furthermore, I will give a short summary of the studies described in Chapter II - Chapter IV and close the chapter with a general discussion of the findings and directions for further research on stress and mating preferences. Human mating behavior is complex, and many aspects of it may not relate to biology but social conventions and education. This work will not focus on those aspects but rather on cognitive and affective processing of erotic and sexually-relevant stimuli, since we assume that these aspects of mating behaviour are likely related to psychobiological stress mechanisms. Therefore, a paradigm is needed that measures such aspects of mating preferences in humans. The studies presented in Chapter II and Chapter III were performed in order to develop such a paradigm. In these studies we show that affective startle modulation may be used to indicate differences in sexual approach motivation to potential mating partners with different similarity levels to the participant. In Chapter IV, I will describe a study that aimed to investigate the effects of stress on human mating preferences. We showed that stress reverses human mating preferences: While unstressed individuals show a preference for similar mates, stressed individuals seem to prefer dissimilar mates. Overall, the studies presented in this work showed that affective startle modulation can be employed to measure mating preferences in humans and that these mating preferences are influenced by stress.
Aggression is one of the most researched topics in psychology. This is understandable, since aggression behavior does a lot of harm to individuals and groups. A lot is known already about the biology of aggression, but one system that seems to be of vital importance in animals has largely been overlooked: the hypothalamic-pituitary-adrenal (HPA) axis. Menno Kruk and Jószef Haller and their research teams developed rodent models of adaptive, normal, and abnormal aggressive behavior. They found the acute HPA axis (re)activity, but also chronic basal levels to be causally relevant in the elicitation and escalation of aggressive behavior. As a mediating variable, changes in the processing of relevant social information is proposed, although this could not be tested in animals. In humans, not a lot of research has been done, but there is evidence for both the association between acute and basal cortisol levels in (abnormal) aggression. However, not many of these studies have been experimental of nature. rnrnOur aim was to add to the understanding of both basal chronic levels of HPA axis activity, as well as acute levels in the formation of aggressive behavior. Therefore, we did two experiments, both with healthy student samples. In both studies we induced aggression with a well validated paradigm from social psychology: the Taylor Aggression Paradigm. Half of the subjects, however, only went through a non-provoking control condition. We measured trait basal levels of HPA axis activity on three days prior. We took several cortisol samples before, during, and after the task. After the induction of aggression, we measured the behavioral and electrophysiological brain response to relevant social stimuli, i.e., emotional facial expressions embedded in an emotional Stroop task. In the second study, we pharmacologically manipulated cortisol levels 60min before the beginning of the experiment. To do that, half of the subjects were administered 20mg of hydrocortisone, which elevates circulating cortisol levels (cortisol group), the other half was administered a placebo (placebo group). Results showed that acute HPA axis activity is indeed relevant for aggressive behavior. We found in Study 1 a difference in cortisol levels after the aggression induction in the provoked group compared to the non-provoked group (i.e., a heightened reactivity of the HPA axis). However, this could not be replicated in Study 2. Furthermore, the pharmacological elevation of cortisol levels led to an increase in aggressive behavior in women compared to the placebo group. There were no effects in men, so that while men were significantly more aggressive than women in the placebo group, they were equally aggressive in the cortisol group. Furthermore, there was an interaction of cortisol treatment with block of the Taylor Aggression Paradigm, in that the cortisol group was significantly more aggressive in the third block of the task. Concerning basal HPA axis activity, we found an effect on aggressive behavior in both studies, albeit more consistently in women and in the provoked and non-provoked groups. However, the effect was not apparent in the cortisol group. After the aggressive encounter, information processing patterns were changed in the provoked compared to the non-provoked group for all facial expressions, especially anger. These results indicate that the HPA axis plays an important role in the formation of aggressive behavior in humans, as well. Importantly, different changes within the system, be it basal or acute, are associated with the same outcome in this task. More studies are needed, however, to better understand the role that each plays in different kinds of aggressive behavior, and the role information processing plays as a possible mediating variable. This extensive knowledge is necessary for better behavioral interventions.
In this thesis, three studies investigating the impact of stress on the protective startle eye blink reflex are reported. In the first study a decrease in prepulse inhibition of the startle reflex was observed after intravenous low dose cortisol application. In the second study a decrease in reflex magnitude of the startle reflex was observed after pharmacological suppression of endogenous cortisol production. In the third study, a higher reflex magnitude of the startle reflex was observed at reduced arterial and central venous blood pressure. These results can be interpreted in terms of an adaption to hostile environments.
Stress represents a significant problem for Western societies inducing costs as high as 3-4 % of the European gross national products, a burden that is continually increasing (WHO Briefing, EUR/04/5047810/B6). The classical stress response system is the hypothalamic-pituitary-adrenal (HPA) axis which acts to restore homeostasis after disturbances. Two major components within the HPA axis system are the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). Cortisol, released from the adrenal glands at the end of the HPA axis, binds to MRs and with a 10 fold lower affinity to GRs. Both, impairment of the HPA axis and an imbalance in the MR/GR ratio enhances the risk for infection, inflammation and stress related psychiatric disorders. Major depressive disorder (MDD) is characterised by a variety of symptoms, however, one of the most consistent findings is the hyperactivity of the HPA axis. This may be the result of lower numbers or reduced activity of GRs and MRs. The GR gene consists of multiple alternative first exons resulting in different GR mRNA transcripts whereas for the MR only two first exons are known to date. Both, the human GR promoter 1F and the homologue rat Gr promoter 1.7 seem to be susceptible to methylation during stressful early life events resulting in lower 1F/1.7 transcript levels. It was proposed that this is due to methylation of a NGFI-A binding site in both, the rat promoter 1.7 and the human promoter 1F. The research presented in this thesis was undertaken to determine the differential expression and methylation patterns of GR and MR variants in multiple areas of the limbic brain system in the healthy and depressed human brain. Furthermore, the transcriptional control of the GR transcript 1F was investigated as expression changes of this transcript were associated with MDD, childhood abuse and early life stress. The role of NGFI-A and several other transcription factors on 1F regulation was studied in vitro and the effect of Ngfi-a overexpression on the rat Gr promoter 1.7 in vivo. The susceptibility to epigenetic programming of several GR promoters was investigated in MDD. In addition, changes in methylation levels have been determined in response to a single acute stressor in rodents. Our results showed that GR and MR first exon transcripts are differentially expressed in the human brain, but this is not due to epigenetic programming. We showed that NGFI-A has no effect on endogenous 1F/1.7 expression in vitro and in vivo. We provide evidence that the transcription factor E2F1 is a major element in the transcriptional complex necessary to drive the expression of GR 1F transcripts. In rats, highly individual methylation patterns in the paraventricular nucleus of the hypothalamus (PVN) suggest that this is not related to the stressor but can rather be interpreted as pre-existing differences. In contrast, the hippocampus showed a much more uniform epigenetic status, but still is susceptible to epigenetic modification even after a single acute stress suggesting a differential "state‟ versus "trait‟ regulation of the GR gene in different brain regions. The results of this thesis have given further insight in the complex transcriptional regulation of GR and MR first exons in health and disease. Epigenetic programming of GR promoters seems to be involved in early life stress and acute stress in adult rats; however, the susceptibility to methylation in response to stress seems to vary between brain regions.
The brain is the central coordinator of the human stress reaction. At the same time, peripheral endocrine and neural stress signals act on the brain modulating brain function. Here, three experimental studies are presented demonstrating this dual role of the brain in stress. Study I shows that centrally acting insulin, an important regulator of energy homeostasis, attenuates the stress related cortisol secretion. Studies II and III show that specific components of the stress reaction modulate learning and memory retrieval, two important aspects of higher-order brain function.
Cortisol is a stress hormone that acts on the central nervous system in order to support adaptation and time-adjusted coping processes. Whereas previous research has focused on slow emerging, genomic effects of cortisol likely mediated by protein synthesis, there is only limited knowledge about rapid, non-genomic cortisol effects on in vivo neuronal cell activity in humans. Three independent placebo-controlled studies in healthy men were conducted to test effects of 4 mg cortisol on central nervous system activity, occurring within 15 minutes after intravenous administration. Two of the studies (N = 26; N = 9) used continuous arterial spin labeling as a magnetic resonance imaging sequence, and found rapid bilateral thalamic perfusion decrements. The third study (N = 14) revealed rapid cortisol-induced changes in global signal strength and map complexity of the electroencephalogram. The observed changes in neuronal functioning suggest that cortisol may act on the thalamic relay of non-relevant background as well as on task specific sensory information in order to facilitate the adaptation to stress challenges. In conclusion, these results are the first to coherently suggest that a physiologically plausible amount of cortisol profoundly affects functioning and perfusion of the human CNS in vivo by a rapid, non-genomic mechanism.
There is a lot of evidence for the impact of acute glucocorticoid treatment on hippocampus-dependent explicit learning and memory (memory for facts and events). But there have been few studies, investigating the effect of glucocorticoids on implicit learning and memory. We conducted three studies with different methodology to investigate the effect of glucocorticoids on different forms of implicit learning. In Study 1, we investigated the effect of cortisol depletion on short-term habituation in 49 healthy subjects. 25 participants received oral metyrapone (1500 mg) to suppress endogenous cortisol production, while 24 controls received oral placebo. Eye blink electromyogram (EMG) responses to 105 dB acoustic startle stimuli were assessed. Effective endogenous cortisol suppression had no effect on short-term habituation of the startle reflex, but startle eye blink responses were significantly increased in the metyrapone group. The latter findings are in line with previous human studies, which have shown that excess cortisol, sufficient to fully occupy central nervous system (CNS) corticosteroid receptors, may reduce startle eye blink. This effect may be mediated by CNS mechanisms controlling cortisol feedback. In Study 2, we investigated delay or trace eyeblink conditioning in a patient group with a relative hypocortisolism (30 patients with fibromyaligia syndrome/FMS) compared to 20 healthy control subjects. Conditioned eyeblink response probability was assessed by EMG. Morning cortisol levels, ratings of depression, anxiety and psychosomatic complaints as well as general symptomatology and psychological distress were assessed. As compared to healthy controls FMS patients showed lower morning cortisol levels, and trace eyeblink conditioning was facilitated whereas delay eyeblink conditioning was reduced. Cortisol measures correlate significantly only with trace eyeblink conditioning. Our results are in line with studies of pharmacologically induced hyper- and hypocortisolism, which affected trace eyeblink conditioning. We suggest that endocrine mechanisms affecting hippocampus-mediated forms of associative learning may play a role in the generation of symptoms in these patients.rnIn Study 3, we investigated the effect of excess cortisol on implicit sequence learning in healthy subjects. Oral cortisol (30 mg) was given to 29 participants, whereas 31 control subjects received placebo. All volunteers performed a 5-choice serial reaction time task (SRTT). The reaction speed of every button-press was determined and difference-scores were calculated as a proof of learning. Compared to the control group, we found a delayed learning in the cortisol group at the very beginning of the task. This study is the first human investigation, indicating impaired implicit memory function after exogenous administration of the stress hormone cortisol. Our findings support a previous neuroimaging study, which suggested that the medial temporal lobe (including the hippocampus) is also active in implicit sequence learning, but our results may also depend on the engagement of other brain structures.
The stress hormone cortisol as the end-product of the hypothalamic-pituitary-adrenal (HPA) axis has been found to play a crucial role in the release of aggressive behavior (Kruk et al., 2004; Böhnke et al., 2010). In order to further explore potential mechanisms underlying the relationship between stress and aggression, such as changes in (social) information processing, we conducted two experimental studies that are presented in this thesis. In both studies, acute stress was induced by means of the Socially Evaluated Cold Pressor Test (SECP) designed by Schwabe et al. (2008). Stressed participants were classified as either cortisol responders or nonresponders depending on their rise in cortisol following the stressor. Moreover, basal HPA axis activity was measured prior to the experimental sessions and EEG was recorded throughout the experiments. The first study dealt with the influence of acute stress on cognitive control processes. 41 healthy male participants were assigned to either the stress condition or the non-stressful control procedure of the SECP. Before as well as after the stress induction, all participants performed a cued task-switching paradigm in order to measure cognitive control processes. Results revealed a significant influence of acute and basal cortisol levels, respectively, on the motor preparation of the upcoming behavioral response, that was reflected in changes in the magnitude of the terminal Contingent Negative Variation (CNV). In the second study, the effect of acute stress and subsequent social provocation on approach-avoidance motivation was examined. 72 healthy students (36 males, 36 females) took part in the study. They performed an approach-avoidance task, using emotional facial expressions as stimuli, before as well as after the experimental manipulation of acute stress (again via the SECP) and social provocation realized by means of the Taylor Aggression Paradigm (Taylor, 1967). Additionally to salivary cortisol, testosterone samples were collected at several points in time during the experimental session. Results indicated a positive relationship between acute testosterone levels and the motivation to approach social threat stimuli in highly provoked cortisol responders. Similar results were found when the testosterone-to-cortisol ratio at baseline was taken into account instead of acute testosterone levels. Moreover, brain activity during the approach-avoidance task was significantly influenced by acute stress and social provocation, as reflected in reductions of early (P2) as well as of later (P3) ERP components in highly provoked cortisol responders. This may indicate a less accurate, rapid processing of socially relevant stimuli due to an acute increase in cortisol and subsequent social provocation. In conclusion, the two studies presented in this thesis provide evidence for significant changes in information processing due to acute stress, basal cortisol levels and social provocation, suggesting an enhanced preparation for a rapid behavioral response in the sense of a fight-or-flight reaction. These results confirm the model of Kruk et al. (2004) proposing a mediating role of changed information processes in the stress-aggression-link.
Cortisol exhibits typical ultradian and circadian rhythm and disturbances in its secretory pattern have been described in stress-related pathology. The aim of this thesis was to dissect the underlying structure of cortisol pulsatility and to develop tools to investigate the effects of this pulsatility on immune cell trafficking and the responsiveness of the neuroendocrine system and GR target genes to stress. Deconvolution modeling was set up as a tool for investigation of the pulsatile secretion underlying the ultradian cortisol rhythm. This further allowed us to investigate the role of the single cortisol pulses on the immune cell trafficking and the role of induced cortisol pulses on the kinetics of expression of GR target genes. The development of these three tools, would allow to induce and investigate in future the significance of single cortisol pulses for health and disease.
The startle response in psychophysiological research: modulating effects of contextual parameters
(2013)
Startle reactions are fast, reflexive, and defensive responses which protect the body from injury in the face of imminent danger. The underlying reflex is basic and can be found in many species. Even though it consists of only a few synapses located in the brain stem, the startle reflex offers a valuable research method for human affective, cognitive, and psychological research. This is because of moderating effects of higher mental processes such as attention and emotion on the response magnitude: affective foreground stimulation and directed attention are validated paradigms in startle-related research. This work presents findings from three independent research studies that deal with (1) the application of the established "affective modulation of startle"-paradigm to the novel setting of attractiveness and human mating preferences, (2) the question of how different components of the startle response are affected by a physiological stressor and (3) how startle stimuli affect visual attention towards emotional stimuli. While the first two studies treat the startle response as a dependent variable by measuring its response magnitude, the third study uses startle stimuli as an experimental manipulation and investigates its potential effects on a behavioural measure. The first chapter of this thesis describes the basic mechanisms of the startle response as well as the body of research that sets the foundation of startle research in psychophysiology. It provides the rationale for the presented studies, and offers a short summary of the obtained results. Chapter two to four represent primary research articles that are published or in press. At the beginning of each chapter the contribution of all authors is explained. The references for all chapters are listed at the end of this thesis. The overall scope of this thesis is to show how the human startle response is modulated by a variety of factors, such as the attractiveness of a potential mating partner or the exposure to a stressor. In conclusion, the magnitude of the startle response can serve as a measure for such psychological states and processes. Beyond the involuntary, physiological startle reflex, startle stimuli also affect intentional behavioural responses, which we could demonstrate for eye movements in a visual attention paradigm.
Im querschnittlichen Vergleich zwischen 10- bis 18-jährigen Mädchen mit Major Depression und gleichaltrigen gesunden Probandinnen wiesen die depressiven Mädchen mehr Probleme, mehr körperliche und psychische Stresssymptome, erhöhte Cortisolsekretion sowie eine ungünstigere Stressverarbeitung auf. Im Längsschnitt zeigte sich die Bedeutsamkeit von psychischer Stressbelastung und der Einfluss von Bewältigungsstrategien auf den Verlauf der Depression.
The present thesis addresses the validity of Binge Eating Disorder (BED) as well as underlying mechanisms of BED from three different angles. Three studies provide data discriminating obesity with BED from obesity without BED. Study 1 demonstrates differences between obese individuals with and without BED regarding eating in the natural environment, psychiatric comorbidity, negative affect as well as self reported tendencies in eating behavior. Evidence for possible psychological mechanisms explaining increased intake of BED individuals in the natural environment was given by analyzing associations of negative affect, emotional eating, restrained eating and caloric intake in obese BED compared to NBED controls. Study 2 demonstrated stress-induced changes in the eating behavior of obese individuals with BED. The impact of a psychosocial stressor, the Trier Social Stress Test (TSST, Kirschbaum, Pirke, & Hellhammer, 1993), on behavioral patterns of eating behavior in laboratory was investigated. Special attention was given to stress-induced changes in variables that reflect mechanisms of appetite regulation in obese BED individuals compared to controls. To further explore by which mechanisms stress might trigger binge eating, study 3 investigated differences in stress-induced cortisol secretion after a socially evaluated cold pressure test (SECPT, Schwabe, Haddad, & Schachinger, 2008) in obese BED as compared to obese NBED individuals.
Stress has been considered one of the most relevant factors promoting aggressive behavior. Animal and human pharmacological studies revealed the stress hormones corticosterone in rodents and cortisol in humans to constitute a particularly important neuroendocrine determinate in facilitating aggression and beyond that, assumedly in its continuation and escalation. Moreover, cortisol-induced alterations of social information processing, as well as of cognitive control processes, have been hypothesized as possible influencing factors in the stress-aggression link. So far, the immediate impact of a preceding stressor and thereby stress-induced rise of cortisol on aggressive behavior as well as higher-order cognitive control processes and social information processing in this context have gone mostly unheeded. The present thesis aimed to extend the hitherto findings of stress and aggression in this regard. For this purpose two psychophysiological studies with healthy adults were carried out, both using the socially evaluated-cold pressor test as an acute stress induction. Additionally to behavioral data and subjective reports, event related potentials were measured and acute levels of salivary cortisol were collected on the basis of which stressed participants were divided into cortisol-responders and "nonresponders. Study 1 examined the impact of acute stress-induced cortisol increase on inhibitory control and its neural correlates. 41 male participants were randomly assigned to the stress procedure or to a non-stressful control condition. Beforehand and afterwards, participants performed a Go Nogo task with visual letters to measure response inhibition. The effect of acute stress-induced cortisol increase on covert and overt aggressive behavior and on the processing of provoking stimuli within the aggressive encounter was investigated in study 2. Moreover, this experiment examined the combined impact of stress and aggression on ensuing affective information processing. 71 male and female participants were either exposed to the stress or to the control condition. Following this, half of each group received high or low levels of provocation during the Taylor Aggression Paradigm. At the end of the experiment, a passive viewing paradigm with affective pictures depicting positive, negative, or aggressive scenes with either humans or objects was realized. The results revealed that men were not affected by a stress-induced rise in cortisol on a behavioral level, showing neither impaired response inhibition nor enhanced aggressive behavior. In contrast, women showed enhanced overt and covert aggressive behavior under a surge of endogenous cortisol, confirming previous results, albeit only in case of high provocation and only up to the level of the control group. Unlike this rather moderate impact on behavior, cortisol showed a distinct impact on neural correlates of information processing throughout inhibitory control, aggression-eliciting stimuli, and emotional pictures for both men and women. At this, stress-induced increase of cortisol resulted in enhanced N2 amplitudes to Go stimuli, whereas P2 amplitudes to both and N2 to Nogo amplitudes retained unchanged, indicating an overcorrection and caution of the response activation in favor of successful inhibitory control. The processing of aggression-eliciting stimuli during the aggressive encounter was complexly altered by stress differently for women and men. Under increased cortisol levels, the frontal or parietal P3 amplitude patterns were either diminished or reversed in the case of high provocation compared to the control group and to cortisol-nonresponders, indicating a desensitization towards aggression-eliciting stimuli in males, but a more elaborate processing of those in women. Moreover, stress-induced cortisol and provocation jointly altered subsequent affective information processing at early as well as later stages of the information processing stream. Again, increased levels of cortisol led opposite directed amplitudes in the case of high provocation relative to the control group and cortisol-nonresponders, with enhanced N2 amplitudes in men and reduced P3 and LPP amplitudes in men and women for all affective pictures, suggesting initially enhanced emotional reactivity in men, but ensuing reduced motivational attention and enhanced emotion regulation in both, men and women. As a result, these present findings confirm the relevance of HPA activity in the elicitation and persistence of human aggressive behavior. Moreover, they reveal the significance of compensatory and emotion regulatory strategies and mechanisms in response to stress and provocation, indorsing the relevance of social information and cognitive control processes. Still, more research is needed to clarify the conditions which lead to the facilitation of aggression and by which compensatory mechanisms this is prevented.
Fast and Slow Effects of Cortisol on Several Functions of the Central Nervous System in Humans
(2014)
Cortisol is one of the key substances released during stress to restore homeostasis. Our knowledge of the impact of this glucocorticoid on cognition and behavior in humans is, however, still limited. Two modes of action of cortisol are known, a rapid, nongenomic and a slow, genomic mode. Both mechanisms appear to be involved in mediating the various effects of stress on cognition. Here, three experiments are presented that investigated fast and slow effects of cortisol on several functions of the human brain. The first experiment investigated the interaction between insulin and slow, genomic cortisol effects on resting regional cerebral blood flow (rCBF) in 48 young men. A bilateral, locally distinct increase in rCBF in the insular cortex was observed 37 to 58 minutes after intranasal insulin admission. Cortisol did not influence rCBF, neither alone nor in interaction with insulin. This finding suggests that cortisol does not influence resting cerebral blood flow within a genomic timeframe. The second experiment examined fast cortisol effects on memory retrieval. 40 participants (20 of them female) learned associations between neutral male faces and social descriptions and were tested for recall one week later. Cortisol administered intravenously 8 minutes before retrieval influenced recall performance in an inverted U-shaped dose-response relationship. This study demonstrates a rapid, presumably nongenomic cortisol effect on memory retrieval in humans. The third experiment studied rapid cortisol effects on early multisensory integration. 24 male participants were tested twice in a focused cross-modal choice reaction time paradigm, once after cortisol and once after placebo infusion. Cortisol acutely enhanced the integration of visual targets and startling auditory distractors, when both stimuli appeared in the same sensory hemi-field. The rapidity of effect onset strongly suggests that cortisol changes multisensory integration by a nongenomic mechanism. The work presented in this thesis highlights the essential role of cortisol as a fast acting agent during the stress response. Both the second and the third experiment provide new evidence of nongenomic cortisol effects on human cognition and behavior. Future studies should continue to investigate the impact of rapid cortisol effects on the functioning of the human brain.
Stressinduzierte Veränderungen gastrointestinaler Peptidhormone könnten eine biologische Grundlage für Überessen und einen Faktor bei der Entstehung von Adipositas darstellen. Darum wurden die Veränderungen der Plasmakonzentrationen von Ghrelin und Peptid YY (PYY) durch akuten Stress bei 85 adipösen und normalgewichtigen Frauen untersucht. Im Vergleich zu normalgewichtigen Frauen hatten adipöse Frauen eine geringere pre- als auch postprandiale Ghrelin-Sekretion. Darüber hinaus fiel auch der postprandiale Ghrelin-Abfall bei den adipösen Frauen geringer aus als bei der normalgewichtigen Vergleichsgruppe. Akuter Stress inhibierte die PYY-Sekretion in beiden Gruppen. Außerdem wurde der Effekt von akutem Stress auf das Essverhalten erfasst. Stress inhibierte die Nahrungsaufnahme in beiden Gruppen.
The last decades of stress research have yielded substantial advancements highlighting the importance of the phenomenon for basic psychological functions as well as physical health and well-being. Progress in stress research heavily relies on the availability of suitable and well validated laboratory stressors. Appropriate laboratory stressors need to be able to reliably provoke a response in the relevant parameters and be applicable in different research settings or experimental designs. This thesis focuses on the Cold Pressor Test (CPT) as a stress induction technique. Three published experiments are presented that show how the advantages of the CPT can be used to test stress effects on memory processes and how some of its disadvantages can be met by a simple modification that retains its feasibility and validity. The first experiment applies the CPT in a substantial sample to investigate the consolidation effects of post-learning sympathetic arousal. Stressed participants with high increases in heart rate during the CPT showed enhanced memory performance one day after learning compared to both the warm water control group and low heart rate responders. This finding suggests that beta-adrenergic activation elicited shortly after learning enhances memory consolidation and that the CPT induced heart rate response is a predictor for this effect. Moreover, the CPT proved to be an appropriate stressor to test hypothesis about endogenous adrenergic effects on memory processes. The second experiment addresses known practical limitations of the standard dominant hand CPT protocol. A bilateral feet CPT modification is presented, the elicited neuroendocrine stress response assessed and validated against the standard CPT in a within-subjects design. The bilateral feet CPT elicited a substantial neuroendocrine stress response. Moreover, with the exception of blood pressure responses, all stress parameters were enhanced compared to the standard CPT. This shows that the bilateral feet CPT is a valid alternative to the standard CPT. The third experiment further validates the bilateral feet CPT and its corresponding control procedure by employing it in a typical application scenario. Specifically, the bilateral feet CPT was used to modulate retrieval of event files in a distractor-response binding paradigm that required lateralized bimanual responses. Again, the bilateral feet CPT induced significant increases in heart rate, blood pressure and cortisol, no such increases could be observed in the warm water control condition. Moreover, stressed participants showed diminished retrieval compared to controls. These results provide further evidence for the feasibility and validity of the bilateral feet CPT and its warm water control procedure. Together the experiments presented here highlight the usefulness of the CPT as a tool in psychophysiological stress research. It is especially well suited to test hypothesis concerning stress effects on memory processes and its applicability can be further increased by the bilateral feet modification.
Ausgehend von einem multifaktoriellen biopsychosozialen Modell zur Entstehung und Aufrechterhaltung primärer Kopfschmerzen bei Kindern und Jugendlichen wurden n= 170 Mädchen im Alter von 12-17 Jahren hinsichtlich verschiedener stressbezogener Determinanten untersucht. Es wurde davon ausgegangen, dass sich Mädchen mit wiederkehrenden Kopfschmerzen sowohl in einem kontrollierten, messwiederholten Laborexperiment hinsichtlich ihrer physiologischen Reaktionen (Muskelspannung, Cortisolausschüttung) auf akuten Stress hin wie auch in der Cortisolaufwachreaktion im häuslichen Setting von einer gesunden Kontrollgruppe unterscheiden. Diese Annahmen konnten nach statistischer Auswertung der Studienergebnisse unter Kontrolle der familiären Schmerzbelastung und psychischen Stressbelastung jedoch nicht bestätigt werden. Somit kann nicht von einer dysregulierten Aktivität der Hypothalamus-Hypophysen-Nebennierenrinden-Achse ausgegangen werden, die eine zentrale Rolle in der biologischen Stressantwort spielt und auch die Schmerzverarbeitung mit beeinflusst. Ebenso wenig liegt bei Mädchen mit Kopfschmerzen eine erhöhte basale oder stressbedingte Muskelspannung im Kopf- und Schulterbereich vor. Lediglich auf subjektiver Ebene deutete sich ein tendenziell höheres Empfinden von Anspannung in Ruhephasen an. Auf psychologischer Ebene hingegen zeigte sich erwartungskonform eine höhere Stress-vulnerabilität bei den Mädchen mit Kopfschmerzen. Außerdem wurde bei ihnen der vermehrte Einsatz emotionsregulierender Stressbewältigungsstrategien, wie Ruhe und Entspannung, aber auch destruktiv-ärgerbezogenes Verhalten und Denken, bezogen auf soziale und leistungsbezogene Stresssituationen beobachtet. Auch unterschieden sie sich hinsichtlich der familiären Schmerzbelastung, körperlichen und psychischen Stress-symptomatik und Depressivität sowie Ängstlichkeit von der Kontrollgruppe. Sie zeigten durchweg höhere Ausprägungen auf diesen Variablen, die sich als signifikante Prädiktoren für Kopfschmerzen herausstellten. Die Verknüpfung von physiologischen Reaktionsmaßen mit der Stressverarbeitung zeigte, dass die Nutzung von konstruktiv-palliativer Emotionsregulation umso stärker ist, je höher der stressbedingte Anstieg der Cortisolausschüttung und der Muskelaktivität in der Frontalisregion ausfällt. Je stärker also die körperliche Reaktion auf Stress, umso mehr versuchen jugendliche Mädchen sich zu entspannen und auszuruhen.
Studien zeigen, dass sowohl die genetische Prädisposition als auch Umweltfaktoren zu häufigen Erkrankungen - wie Schmerzerkrankungen oder psychiatrischen Störungen - beitragen. Molekulargenetische Studien legen nahe, dass ein Teil der Erblichkeit in häufigen genetischen Varianten zu finden ist. Die Untersuchung des Zusammenwirkens dieser Faktoren kann das Verständnis der Ätiologie dieser Erkrankungen erweitern, und neue Präventions- und Behandlungsansätze hervorbringen. In der vorliegenden Arbeit werden vier Studien präsentiert, in denen Umwelt- und genetische Risikofaktoren für psychische Erkrankungen und Schmerz untersucht wurden: In der ersten Studie (Kapitel II) wurden mögliche Wirkmechanismen von etablierten Risikofaktoren für psychiatrische Störungen " das Aufwachsen und Leben in städtischer Umgebung " mit bildgebenden Verfahren untersucht. Einen möglichen Mechanismus stellt der erhöhte soziale Stress in städtischer Umgebung dar. In dieser Studie unterliefen zwei Stichproben von gesunden Probanden zwei verschiedene soziale Stressparadigmen für die Anwendung im fMRT, wovon eines im Rahmen dieser Doktorarbeit entwickelt wurde (ScanSTRESS). Hierbei zeigte sich eine erhöhte Amygdalaaktivität bei Probanden, welche aktuell in der Stadt lebten, während die Aktivität des perigenualen anterioren Cingulums mit dem Aufwachsen in der Stadt assoziiert war. Diese Befunde legen nahe, dass die akute Stressverarbeitung durch Umweltfaktoren in sensiblen Phasen der Entwicklung des Nervensystems beeinflusst wird. In der zweiten Studie (Kapitel III), wurde die Modulierung des Einflusses der städtischen Umwelt auf die Stressverarbeitung durch eine Einzelnukleotid-Polymorphismus (SNP; rs324981) im Gen, welches für den Neuropeptid S (NPS) Rezeptor kodiert (NPSR1), untersucht. In einer Stichprobe, welche das ScanSTRESS-Paradigma absolvierte, konnte gezeigt werden, dass rs324981 " in Interaktion mit städtischem Aufwachsen " die Aktivität der rechten Amygdala beeinflusste. Diese Resultate legen nahe, dass das NPS-System in der menschlichen Stressreaktion involviert ist, und diese in Interaktion mit Umweltfaktoren beeinflusst. In der dritten Studie (Kapitel IV), wurde der Effekt der genetischen Variation von NPSR1 auf die zentralnervöse und endokrine Stressverarbeitung weitergehend untersucht. Da sowohl die Stressregulation, als auch psychiatrische Störungen stark geschlechtsspezifische Ausprägungen aufweisen, wurde die Interaktion von genetischer Variation in NPSR1 mit dem Geschlecht berücksichtigt. Hierfür wurde eine Stichprobe von 277 Probanden mit dem Trierer Sozialen Stresstest (TSST) und eine Stichprobe von 65 Probanden mit dem ScanSTRESS-Paradigma untersucht. Die Analyse zeigte die geschlechtsspezifische Assoziation einer Allel-Kombination (Haplotyp) von drei funktionalen SNPs (rs2530547, rs324981 und rs727162) mit der Cortisolantwort auf den TSST, und einen geschlechtsspezifischen Effekt von rs324981 auf die zentralnervösen Aktivierungsmuster. Diese Ergebnisse legen nahe, dass das Geschlecht die Effekte von genetischer Variation im NPS-System auf die Stressregulation moduliert. In der vierten Studie (Kapitel V), wurde der Einfluss der genetischen Prädisposition und Umweltfaktoren auf chronischen Schmerz nach einer Amputation untersucht. Hierfür wurde eine Studie an 122 Individuen durchgeführt, bei welchen zwei Gliedmaßen amputiert wurden. Das Auftreten und die Intensität von sowohl Phantom- als auch Stumpfschmerzen zeigten einen starken Zusammenhang mit der Ausprägung des selben Schmerztyps zwischen den beiden amputierten Körpergliedern, es waren aber nur moderate Zusammenhänge zwischen den beiden Schmerzarten zu beobachten. Dieses Ergebnis legt den Einfluss von sowohl spezifischen, als auch gemeinsamen (potentiell genetischen) Risikofaktoren für beide Schmerztypen nahe.
Phase-amplitude cross-frequency coupling is a mechanism thought to facilitate communication between neuronal ensembles. The mechanism could underlie the implementation of complex cognitive processes, like executive functions, in the brain. This thesis contributes to answering the question, whether phase-amplitude cross-frequency coupling - assessed via electroencephalography (EEG) - is a mechanism by which executive functioning is implemented in the brain and whether an assumed performance effect of stress on executive functioning is reflected in phase-amplitude coupling strength. A huge body of studies shows that stress can influence executive functioning, in essence having detrimental effects. In two independent studies, each being comprised of two core executive function tasks (flexibility and behavioural inhibition as well as cognitive inhibition and working memory), beta-gamma phase-amplitude coupling was robustly detected in the left and right prefrontal hemispheres. No systematic pattern of coupling strength modulation by either task demands or acute stress was detected. Beta-gamma coupling might also be present in more basic attention processes. This is the first investigation of the relationship between stress, executive functions and phase-amplitude coupling. Therefore, many aspects have not been explored yet. For example, studying phase precision instead of coupling strength as an indicator for phase-amplitude coupling modulations. Furthermore, data was analysed in source space (independent component analysis); comparability to sensor space has still to be determined. These as well as other aspects should be investigated, due to the promising finding of very robust and strong beta-gamma coupling for all executive functions. Additionally, this thesis tested the performance of two widely used phase-amplitude coupling measures (mean vector length and modulation index). Both measures are specific and sensitive to coupling strength and coupling width. The simulation study also drew attention to several confounding factors, which influence phase-amplitude coupling measures (e. g. data length, multimodality).
Erschöpfung ist ein prominentes, unspezifisches Symptom mit vielfältigen Begleitsymptomen (z. B. Schmerzen, Schlafstörungen, Reizbarkeit, Niedergeschlagenheit). Gängige Konzepte erschöpfungsbezogener Erkrankungen und Syndrome werden häufig in Bezug auf ihre Differenzierungskraft oder Struktur kritisiert. Die Ursachen für die Entstehung von Erschöpfung sind vielfältig und die Behandlung kann nur mit gründlicher Differentialdiagnostik erfolgen. Anhand adaptionsbezogener Stressmodelle kann die Entstehung von Erschöpfung beschrieben und in drei Formen eingeteilt werden (I: reversibel, II: prädispositioniert und III: emotional-dysregulativ). Poststress-Symptome (z. B. "Wochenend-Migräne", "UrlaubsInfekte") stellen möglicherweise eine Erschöpfungsform dar, welche durch eine zentrale Entleerung der Noradrenalin-Spiegel bedingt ist. In der vorliegenden Arbeit wurden die Verlässlichkeit der Neuropattern-Erschöpfungsskala, sowie der Zusammenhang von Erschöpfung, Stress, dem Langzeit-Gesundheitsstatus und Poststress-Symptomen geprüft. Hierzu wurden Daten ambulanter und stationärer Patienten und Mitarbeitern verwendet, die an einer randomisierten klinischen Studie zur Neuropattern-Diagnostik teilnahmen. Zusätzlich wurden Daten von gesunden Personen zur Erhebung einer Normstichprobe verwendet. Die Neuropattern-Erschöpfungsskala zeigte sich als reliables und valides Maß. Sie war Indikator für direkte, indirekte und intangible Gesundheitskosten (z. B. erhöhte Arzt-, Therapeutenbesuche, Medikamenteneinnahme und Arbeitsunfähigkeit, reduziertes psychisches und physisches Wohlbefinden). Es zeigte sich, dass sowohl Stress, als auch Erschöpfung den Gesundheitszustand über den Verlauf von zwölf Monaten vorhersagt. Bemerkenswert ist, dass der Zusammenhang zwischen Stress und dem Langzeit-Gesundheitszustand vornehmlich durch Erschöpfung vermittelt wurde. Schließlich wurde die Prävalenz von Poststress-Symptomen bei gesunden Personen (2.9%), ambulanten (20%) und stationären Patienten (34,7%) bestimmt. Auch hier war nicht Stress der stärkste Prädiktor für das Auftreten von Poststress-Symptomen, sondern Erschöpfung. Modelle der psychophysiologischen Stressreaktion können die Entstehung von Erschöpfung erklären und die Diagnostik und Behandlung stressbezogener Gesundheitsstörungen verbessern. Die vorgestellte Neuropattern-Erschöpfungsskala ist dabei ein verlässliches und für die Praxis gut geeignetes Instrument, welches zur Indikation und Validierung präventiver und therapeutischer Maßnahmen eingesetzt werden kann. Je nach Erschöpfungsform bieten sich verschiedene Maßnahmen des regenerativen, instrumentellen oder kognitiven Stressmanagements, Nahrungsergänzungsmittel und Pharmakotherapie an.
Pränatal, postnatal und aktuell auftretende chronische Stressbelastung sind bedeutsame Risikofaktoren für mentale und körperliche Beeinträchtigungen im Erwachsenenalter. Ziel dieser Dissertationsschrift ist es, den Einfluss von Stress im Lebenslauf (pränatale, postnatale, aktuelle Stressbelastung) auf verschiedene Erschöpfungsvariablen und Depressivität zu analysieren und mögliche Mediatoreffekte von aktuell auftretendem Stress auf Assoziationen zwischen pränatalem bzw. postnatalem Stress und Erschöpfung bzw. Depressivität zu bestimmen. Zur Prüfung dieser Fragestellung wurden Daten von chronisch gestressten Lehrpersonen (N = 186; 67,70% weiblich) ohne Diagnose für eine psychische Erkrankung sowie von Hausarzt- (N = 473; 59% weiblich) und Klinikpatienten (N = 284; 63,7% weiblich) mit mindestens einer stressbezogenen mentalen Gesundheitsstörung erhoben. Prä-postnataler Stress, subjektive Erschöpfung und Depressivität wurden in allen Stichproben erfasst, aktuelle Stressbelastung und Poststresssymptome in den Patientenstichproben. Zusätzlich wurden konzeptuelle Endophänotypen als psychobiologisches Erschöpfungsmaß in beiden Patientenstichproben sowie Übernachtaktivität des parasympathischen Nervensystems als Maß vagaler Erholung in der Hausarztstichprobe operationalisiert. Bei den Lehrpersonen wurde anhand univariater Varianzanalysen analysiert, ob Lehrkräfte mit frühkindlicher Belastung unterschiedliche Erschöpfungs- bzw. Depressionswerte aufwiesen im Vergleich zu Lehrkräften ohne frühkindliche Belastung. In den Patientenstichproben wurden multiple und binärlogistische Regressionsmodelle verwendet, um Assoziationen zwischen pränatalem, postnatalem sowie aktuellem Stress mit Erschöpfung, Depressivität, den konzeptuellen Endophänotypen der Neuropattern-Diagnostik sowie Übernachtaktivität des parasympathischen Nervensystems (nur bei Hausarztpatienten) zu prüfen. Mögliche Mediatoreffekte aktueller Stressbelastung auf Assoziationen zwischen pränatalem und postnatalem Stress mit Erschöpfung, Depressivität, der konzeptuellen Endophänotypen bzw. der Übernachtaktivität des parasympathischen Nervensystems (nur bei Hausarztpatienten) wurden bestimmt. Ad hoc wurde mittels zusätzlich ein möglicher Moderatoreffekt von pränatalem Stress auf die Assoziation zwischen aktuellem Stress und der Übernachtherzrate getestet. Pränataler Stress war bei sonst gesunden Lehrkräften mit einer stärker ausgeprägten Gratifikationskrise und höherer emotionaler Erschöpfung assoziiert. Postnataler Stress ging mit höheren Werten für Depressivität, Anstrengungs-Belohnungs-Ungleichgewicht, der MBI Gesamtskala, emotionaler Erschöpfung und vitaler Erschöpfung einher. Sowohl bei Hausarzt- als auch bei Klinikpatienten waren aktuelle psychosoziale Belastung und aktuelle Beeinträchtigung durch Lebensereignisse mit Depressivität, Erschöpfung und Poststress assoziiert. Bei Hausarztpatienten sagte aktuelle Stressbelastung eine erhöhte Odds Ratio der Noradrenalin-Hypoaktivität sowie Serotonin-Hyperreaktivität vorher; bei Klinikpatienten für Noradrenalin-Hypoaktivität. Des Weiteren zeigten Hausarztpatienten mit starker psychosozialer Belastung erhöhte parasympathische Aktivität über Nacht. Bei Hausarztpatienten ist hoher pränataler Stress assoziiert mit wahrgenommener psychosozialer Belastung, aktuellen Lebensereignissen und Poststresssymptomen. Pränataler Stress ging mit einer verringerten vagalen Aktivität einher. Weiter ist postnataler Stress assoziiert mit Depressivität, wahrgenommener psychosozialer Belastung, aktuellen Lebensereignissen, Erschöpfung und Poststresssymptomen sowie einem erhöhten Odds Ratio für die Noradrenalin-Hypoaktivität sowie mit CRH-Hyperaktivität. Die Assoziationen zwischen pränatalem bzw. postnatalem Stress und Poststress, Erschöpfung, Depressivität und Noradrenalin-Hypoaktivität wurden signifikant durch aktuelle Stressbelastung mediiert. Die Assoziation zwischen aktuellem Stress und parasympathischer Aktivität über Nacht wurde durch pränatalen Stress moderiert: Bei geringer bis mittlerer nicht aber bei hoher pränataler Belastung ging eine hohe psychosoziale Belastung mit erhöhter Übernachtaktivität des parasympathischen Nervensystems einher. Bei Klinikpatienten zeigten sich keine signifikanten Zusammenhänge zwischen pränatalem bzw. postnatalem Stress und Erschöpfung bzw. Depressivität. Pränataler Stress kann trophotrope Funktionen beeinträchtigen und damit die Vulnerabilität für Erschöpfung und Depressivität erhöhen. Fortgesetzte postnatale und aktuelle Stressbelastung erhöhen den kumulativen Stress im Lebenslauf einer Person und tragen zu psychobiologischen Dysfunktionen sowie Erschöpfung und Depressivität bei.
Academic achievement is a central outcome in educational research, both in and outside higher education, has direct effects on individual’s professional and financial prospects and a high individual and public return on investment. Theories comprise cognitive as well as non-cognitive influences on achievement. Two examples frequently investigated in empirical research are knowledge (as a cognitive determinant) and stress (as a non-cognitive determinant) of achievement. However, knowledge and stress are not stable, what raises questions as to how temporal dynamics in knowledge on the one hand and stress on the other contribute to achievement. To study these contributions in the present doctoral dissertation, I used meta-analysis, latent profile transition analysis, and latent state-trait analysis. The results support the idea of knowledge acquisition as a cumulative and long-term process that forms the basis for academic achievement and conceptual change as an important mechanism for the acquisition of knowledge in higher education. Moreover, the findings suggest that students’ stress experiences in higher education are subject to stable, trait-like influences, as well as situational and/or interactional, state-like influences which are differentially related to achievement and health. The results imply that investigating the causal networks between knowledge, stress, and academic achievement is a promising strategy for better understanding academic achievement in higher education. For this purpose, future studies should use longitudinal designs, randomized controlled trials, and meta-analytical techniques. Potential practical applications include taking account of students’ prior knowledge in higher education teaching and decreasing stress among higher education students.
Acute social and physical stress interact to influence social behavior: the role of social anxiety
(2018)
Stress is proven to have detrimental effects on physical and mental health. Due to different tasks and study designs, the direct consequences of acute stress have been found to be wide-reaching: while some studies report prosocial effects, others report increases in antisocial behavior, still others report no effect. To control for specific effects of different stressors and to consider the role of social anxiety in stress-related social behavior, we investigated the effects of social versus physical stress on behavior in male participants possessing different levels of social anxiety. In a randomized, controlled two by two design we investigated the impact of social and physical stress on behavior in healthy young men. We found significant influences on various subjective increases in stress by physical and social stress, but no interaction effect. Cortisol was significantly increased by physical stress, and the heart rate was modulated by physical and social stress as well as their combination. Social anxiety modulated the subjective stress response but not the cortisol or heart rate response. With respect to behavior, our results show that social and physical stress interacted to modulate trust, trustworthiness, and sharing. While social stress and physical stress alone reduced prosocial behavior, a combination of the two stressor modalities could restore prosociality. Social stress alone reduced nonsocial risk behavior regardless of physical stress. Social anxiety was associated with higher subjective stress responses and higher levels of trust. As a consequence, future studies will need to investigate further various stressors and clarify their effects on social behavior in health and social anxiety disorders.
Background and rationale: Changing working conditions demand adaptation, resulting in higher stress levels in employees. In consequence, decreased productivity, increasing rates of sick leave, and cases of early retirement result in higher direct, indirect, and intangible costs. Aims of the Research Project: The aim of the study was to test the usefulness of a novel translational diagnostic tool, Neuropattern, for early detection, prevention, and personalized treatment of stress-related disorders. The trial was designed as a pilot study with a wait list control group. Materials and Methods: In this study, 70 employees of the Forestry Department Rhineland-Palatinate, Germany, were enrolled. Subjects were block-randomized according to the functional group of their career field, and either underwent Neuropattern diagnostics immediately, or after a waiting period of three months. After the diagnostic assessment, their physicians received the Neuropattern Medical Report, including the diagnostic results and treatment recommendations. Participants were informed by the Neuropattern Patient Report, and were eligible to an individualized Neuropattern Online Counseling account. Results: The application of Neuropattern diagnostics significantly improved mental health and health-related behavior, reduced perceived stress, emotional exhaustion, overcommitment and possibly, presenteeism. Additionally, Neuropattern sensitively detected functional changes in stress physiology at an early stage, thus allowing timely personalized interventions to prevent and treat stress pathology. Conclusion: The present study encouraged the application of Neuropattern diagnostics to early intervention in non-clinical populations. However, further research is required to determine the best operating conditions.
Water-deficit stress, usually shortened to water- or drought stress, is one of the most critical abiotic stressors limiting plant growth, crop yield and quality concerning food production. Today, agriculture consumes about 80-90% of the global freshwater used by humans and about two thirds are used for crop irrigation. An increasing world population and a predicted rise of 1.0-2.5-°C in the annual mean global temperature as a result of climate change will further increase the demand of water in agriculture. Therefore, one of the most challenging tasks of our generation is to reduce the amount water used per unit yield to satisfy the second UN Sustainable Development Goal and to ensure global food security. Precision agriculture offers new farming methods with the goal to improve the efficiency of crop production by a sustainable use of resources. Plant responses to water stress are complex and co-occur with other environmental stresses under natural conditions. In general, water stress causes plant physiological and biochemical changes that depend on the severity and the duration of the actual plant water deficit. Stomatal closure is one of the first responses to plant water stress causing a decrease in plant transpiration and thus an increase in plant temperature. Prolonged or severe water stress leads to irreversible damage to the photosynthetic machinery and is associated with decreasing chlorophyll content and leaf structural changes (e.g., leaf rolling). Since a crop can already be irreversibly damaged by only mild water deficit, a pre-visual detection of water stress symptoms is essential to avoid yield loss. Remote sensing offers a non-destructive and spatio-temporal method for measuring numerous physiological, biochemical and structural crop characteristics at different scales and thus is one of the key technologies used in precision agriculture. With respect to the detection of plant responses to water stress, the current state-of-the-art hyperspectral remote sensing imaging techniques are based on measurements of thermal infrared emission (TIR; 8-14 -µm), visible, near- and shortwave infrared reflectance (VNIR/SWIR; 0.4-2.5 -µm), and sun-induced fluorescence (SIF; 0.69 and 0.76 -µm). It is, however, still unclear how sensitive these techniques are with respect to water stress detection. Therefore, the overall aim of this dissertation was to provide a comparative assessment of remotely sensed measures from the TIR, SIF, and VNIR/SWIR domains for their ability to detect plant responses to water stress at ground- and airborne level. The main findings of this thesis are: (i) temperature-based indices (e.g., CWSI) were most sensitive for the detection of plant water stress in comparison to reflectance-based VNIR/SWIR indices (e.g., PRI) and SIF at both, ground- and airborne level, (ii) for the first time, spectral emissivity as measured by the new hyperspectral TIR instrument could be used to detect plant water stress at ground level. Based on these findings it can be stated that hyperspectral TIR remote sensing offers great potential for the detection of plant responses to water stress at ground- and airborne level based on both TIR key variables, surface temperature and spectral emissivity. However, the large-scale application of water stress detection based on hyperspectral TIR measures in precision agriculture will be challenged by several problems: (i) missing thresholds of temperature-based indices (e.g., CWSI) for the application in irrigation scheduling, (ii) lack of current TIR satellite missions with suitable spectral and spatial resolution, (iii) lack of appropriate data processing schemes (including atmosphere correction and temperature emissivity separation) for hyperspectral TIR remote sensing at airborne- and satellite level.
In order to investigate the psychobiological consequences of acute stress under laboratory conditions, a wide range of methods for socially evaluative stress induction have been developed. The present dissertation is concerned with evaluating a virtual reality (VR)-based adaptation of one of the most widely used of those methods, the Trier Social Stress Test (TSST). In the three empirical studies collected in this dissertation, we aimed to examine the efficacy and possible areas of application of the adaptation of this well-established psychosocial stressor in a virtual environment. We found that the TSST-VR reliably incites the activation of the major stress effector systems in the human body, albeit in a slightly less pronounced way than the original paradigm. Moreover, the experience of presence is discussed as one potential factor of influence in the origin of the psychophysiological stress response. Lastly, we present a use scenario for the TSST-VR in which we employed the method to investigate the effects of acute stress on emotion recognition performance. We conclude that, due to its advantages concerning versatility, standardization and economic administration, the paradigm harbors enormous potential not only for psychobiological research, but other applications such as clinical practice as well. Future studies should further explore the underlying effect mechanisms of stress in the virtual realm and the implementation of VR-based paradigms in different fields of application.
Background
Identifying pain-related response patterns and understanding functional mechanisms of symptom formation and recovery are important for improving treatment.
Objectives
We aimed to replicate pain-related avoidance-endurance response patterns associated with the Fear-Avoidance Model, and its extension, the Avoidance-Endurance Model, and examined their differences in secondary measures of stress, action control (i.e., dispositional action vs. state orientation), coping, and health.
Methods
Latent profile analysis (LPA) was conducted on self-report data from 536 patients with chronic non-specific low back pain at the beginning of an inpatient rehabilitation program. Measures of stress (i.e., pain, life stress) and action control were analyzed as covariates regarding their influence on the formation of different pain response profiles. Measures of coping and health were examined as dependent variables.
Results
Partially in line with our assumptions, we found three pain response profiles of distress-avoidance, eustress-endurance, and low-endurance responses that are depending on the level of perceived stress and action control. Distress-avoidance responders emerged as the most burdened, dysfunctional patient group concerning measures of stress, action control, maladaptive coping, and health. Eustress-endurance responders showed one of the highest levels of action versus state orientation, as well as the highest levels of adaptive coping and physical activity. Low-endurance responders reported lower levels of stress as well as equal levels of action versus state orientation, maladaptive coping, and health compared to eustress-endurance responders; however, equally low levels of adaptive coping and physical activity compared to distress-avoidance responders.
Conclusions
Apart from the partially supported assumptions of the Fear-Avoidance and Avoidance-Endurance Model, perceived stress and dispositional action versus state orientation may play a crucial role in the formation of pain-related avoidance-endurance response patterns that vary in degree of adaptiveness. Results suggest tailoring interventions based on behavioral and functional analysis of pain responses in order to more effectively improve patients quality of life.
This thesis focus on threats as an experience of stress. Threats are distinguished from challenges and hindrances as another dimension of stress in challenge-hindrance models (CHM) of work stress (Tuckey et al., 2015). Multiple disciplines of psychology (e.g. stereotype, Fingerhut & Abdou, 2017; identity, Petriglieri, 2011) provide a variety of possible events that can trigger threats (e.g., failure expe-riences, social devaluation; Leary et al., 2009). However, systematic consideration of triggers and thus, an overview of when does the danger of threats arises, has been lacking to date. The explanation why events are appraised as threats is related to frustrated needs (e.g., Quested et al., 2011; Semmer et al., 2007), but empirical evidence is rare and needs can cover a wide range of content (e.g., relatedness, competence, power), depending on need approaches (e.g., Deci & Ryan, 2000; McClelland, 1961). This thesis aims to shed light on triggers (when) and the need-based mechanism (why) of threats.
In the introduction, I introduce threats as a dimension of stress experience (cf. Tuckey et al., 2015) and give insights into the diverse field of threat triggers (the when of threats). Further, I explain threats in terms of a frustrated need for positive self-view, before presenting specific needs as possible deter-minants in the threat mechanism (the why of threats). Study 1 represents a literature review based on 122 papers from interdisciplinary threat research and provides a classification of five triggers and five needs identified in explanations and operationalizations of threats. In Study 2, the five triggers and needs are ecologically validated in interviews with police officers (n = 20), paramedics (n = 10), teach-ers (n = 10), and employees of the German federal employment agency (n = 8). The mediating role of needs in the relationship between triggers and threats is confirmed in a correlative survey design (N = 101 Leaders working part-time, Study 3) and in a controlled laboratory experiment (N = 60 two-person student teams, Study 4). The thesis ends with a general discussion of the results of the four studies, providing theoretical and practical implications.
Stress gilt als zentrales Gesundheitsrisiko des 21. Jahrhunderts und wird in der Forschung als multidimensionales Konstrukt auf psychologischer und biologischer Ebene untersucht. Wäh-rend die subjektive Wahrnehmung von Stress nicht mit der biologischen Stressreaktivität zu-sammenhängen muss, ist der negative Einfluss stressassoziierter biologischer Prozesse auf Wohlbefinden und Gesundheit gut belegt. Bereits im Grundschulalter zeigen Kinder eine mit Erwachsenen vergleichbare Stressbelastung und gesundheitliche Folgen, Bewältigungsstrategien sind in diesem Alter allerdings noch nicht vollständig entwickelt. Präventionsprogramme im Grundschulalter sollen Kinder in ihren sich entwickelnden Stressbewältigungsfähigkeiten fördern, wobei sowohl emotionsfokussierte und problemorientierte Ansätze als auch soziale Unterstützung wichtige Faktoren darstellen könnten.
Das einleitende Literatur-Review evaluiert bisherige Stresspräventionsstudien und verdeutlicht, dass zwar die Wirksamkeit und Anwendbarkeit von mehrfaktoriellen Stresspräventionsprogrammen im Rahmen psychometrischer Erhebungen gezeigt werden konnten, biologische Prozesse in der Forschung bisher allerdings nicht erhoben und außer Acht gelassen wurden.
Die empirische Untersuchung in Studie 1 zeigt, dass eine multidimensionale psychobiologische Betrachtungsweise sinnvoll ist, indem sowohl die Psychometrie, als auch psychobiologische Prozesse der Stressreaktion miteinbezogen und die Auswirkungen von Stressprävention auf den verschiedenen Ebenen untersucht wurden. Zwei Kurzinterventionen wurden dazu miteinander verglichen und ihre Wirkung auf psychophysiologischen Ebenen (z.B. Kortisol, α-Amylase und Herzrate) in einem Prä-Post Design geprüft. Eine statistisch signifikante Abnahme psychophysiologischer Stressreaktivität, sowie stressassoziierter psychologischer Symptome verdeutlichte die multidimensionale Wirksamkeit von Stressmanagementtrainings.
Studie 2 wurde im Rahmen der Covid-19-Pandemie entworfen. Die in Studie 1 trainierten Kinder wurden mittels Online-Fragebogenerhebung mit einer Kontrollgruppe hinsichtlich ihrer Stressbelastung verglichen. Die Ergebnisse zeigten eine geringere Belastung und vermehrte günstige Bewältigungsstrategien trainierter Kinder im Vergleich zur Kontrollgruppe.
Diese Ergebnisse heben die Relevanz einer multidimensionalen Betrachtung kindlichen Stresses hervor. Es wurde gezeigt, dass Stresspräventionsprogramme auf den unterschiedlichen Ebenen der Stressreaktion wirken und sogar in gesamtgesellschaftlichen Krisensituationen stresspro-tektiv wirken können. Zukünftige Studien sollten Stresspräventionen im Grundschulalter psychophysiologisch evaluieren und deren Wirkung in Längsschnittstudien beurteilen, um das Verständnis der zugrundeliegenden Mechanismen zu verbessern.
Die Effekte diverser Hormone auf das Sozialverhalten von Männern und Frauen sind nicht vollständig geklärt, da eine genaue Messung dieser, sowie eine Ableitung kausaler Zusammenhänge, die Forschung seither vor Herausforderungen stellt. Umso wichtiger sind Studien, welche versuchen für konfundierende Aspekte zu kontrollieren und die hormonellen oder endokrinen Effekte auf das Sozialverhalten und die soziale Kognition zu untersuchen. Während Studien bereits Effekte von akutem Stress auf Sozialverhalten zeigten, sind die zugrundeliegenden neurobiologischen Mechanismen nicht vollständig bekannt, da hierfür ein rein pharmakologischer Ansatz von Nöten wäre. Die wenigen Studien, die einen solchen wählten, zeigen konträre Befunde. Bisherige Untersuchungen mit psychosozialen Stressoren lassen jedoch prosoziale Tendenzen nach Stress sowohl für Männer als auch für Frauen vermuten. Darüber hinaus sind auch Untersuchungen zu weiblichen Geschlechtshormonen und ihrem Einfluss auf Sozialverhalten sowie die soziale Kognition bei Frauen besonders herausfordernd durch die hormonellen Schwankungen während des Menstruationszyklus oder auch Veränderungen durch die Einnahme oraler Kontrazeptiva. Studien die sowohl Zyklusphasen als auch die Effekte von oralen Kontrazeptiva untersuchten, deuten aber bereits auf Unterschiede zwischen den verschiedenen Phasen, sowie Frauen mit natürlichem Zyklus und Einnahme oraler Kontrazeptiva hin.
Der theoretische Teil beschreibt die Grundlagen zur Stressreaktion des Menschen und die hormonellen Veränderungen weiblicher Geschlechtshormone. Folgend, soll ein Kapitel zur aktuellen Forschungslage zu Effekten von akutem Stress auf Sozialverhalten und die soziale Kognition einen Überblick über die bisherige Befundlage schaffen. Die erste empirische Studie, welche die Effekte von Hydrocortison auf das Sozialverhalten und die Emotionserkennung untersucht, soll anschließend in diese aktuelle Befundlage eingeordnet werden und zu der weniger erforschten Sparte der pharmakologischen Studien beitragen. Die zweite empirische Studie befasst sich folgend mit den Effekten weiblicher Geschlechtshormone auf Sozialverhalten und Empathie, genauer wie auch Zyklusphasen und orale Kontrazeptiva (über Hormone vermittelt) einen Einfluss bei Frauen nehmen. Abschließend sollen die Effekte von Stresshormonen bei Männern, und modulierende Eigenschaften weiblicher Geschlechtshormone, Zyklusphasen und oraler Kontrazeptiva bei Frauen, jeweils in Hinblick auf Sozialverhalten und die soziale Kognition diskutiert werden.
Background: Hyperhidrosis (excessive sweating, OMIM %114110) is a complex disorder with multifactorial causes. Emotional strains and social stress increase symptoms and lead to a vicious circle. Previously, we showed significantly higher depression scores, and normal cortisol awakening responses in patients with primary focal hyperhidrosis (PFH). Stress reactivity in response to a (virtual) Trier Social Stress Test (TSST-VR) has not been studied so far. Therefore, we measured sweat secretion, salivary cortisol and alpha amylase (sAA) concentrations, and subjective stress ratings in affected and non-affected subjects in response to a TSST-VR.
Method: In this pilot study, we conducted TSST-VRs and performed general linear models with repeated measurements for salivary cortisol and sAA levels, heart rate, axillary sweat and subjective stress ratings for two groups (diagnosed PFH (n = 11), healthy controls (n = 16)).
Results: PFH patients showed significantly heightened sweat secretion over time compared to controls (p = 0.006), with highest quantities during the TSST-VR. In both groups, sweating (p < 0.001), maximum cortisol levels (p = 0.002), feelings of stress (p < 0.001), and heart rate (p < 0.001) but not sAA (p = 0.068) increased significantly in response to the TSST-VR. However, no differences were detected in subjective ratings, cortisol concentrations and heart rate between PFH patients and controls (pall > 0.131).
Conclusion: Patients with diagnosed PFH showed stress-induced higher sweat secretion compared to healthy controls but did not differ in the stress reactivity with regard to endocrine or subjective markers. This pilot study is in need of replication to elucidate the role of the sympathetic nervous system as a potential pathway involved in the stress-induced emotional sweating of PFH patients.