Psychological Stress In Humans Research Articles

The effects of human-robot interaction modality on workers’ mental stress

Advances in robotics have contributed to the prevalence of human-robot collaboration (HRC). Working and interacting with collaborative robots in close proximity can be psychologically stressful. Therefore, it is important to understand the impacts of human-robot interaction (HRI) on mental stress to promote psychological well-being at the workplace. To this end, this study investigated how the HRI presence, complexity, and modality affect psychological stress in humans and discussed possible HRI design criteria during HRC. An experimental setup was implemented in which human operators worked with a collaborative robot on a Lego assembly task, using different interaction paradigms involving pressing buttons, showing hand gestures, and giving verbal commands. The NASA-Task Load Index, as a subjective measure, and the physiological galvanic skin conductance response, as an objective measure, were used to assess the levels of mental stress. The results revealed that the introduction of interactions during HRC helped reduce mental stress and that complex interactions resulted in higher mental stress than simple interactions. Meanwhile, the use of certain interaction modalities, such as verbal commands or hand gestures, led to significantly higher mental stress than pressing buttons, while no significant difference on mental stress was found between showing hand gestures and giving verbal commands.

Kinetics of Plasma Cell-Free DNA under a Highly Standardized and Controlled Stress Induction.

Psychological stress affects the immune system and activates peripheral inflammatory pathways. Circulating cell-free DNA (cfDNA) is associated with systemic inflammation, and recent research indicates that cfDNA is an inflammatory marker that is sensitive to psychological stress in humans. The present study investigated the effects of acute stress on the kinetics of cfDNA in a within-subjects design. Twenty-nine males (mean age: 24.34 ± 4.08 years) underwent both the Trier Social Stress Test (TSST) and a resting condition. Blood samples were collected at two time points before and at 9 time points up to 105 min after both conditions. The cfDNA immediately increased 2-fold after the TSST and returned to baseline levels after 30 min after the test, showing that a brief psychological stressor was sufficient to evoke a robust and rapid increase in cfDNA levels. No associations were detected between perceived stress, whereas subjects with higher basal cfDNA levels showed higher increases. The rapid cfDNA regulation might be attributed to the transient activation of immune cells caused by neuroendocrine-immune activation. Further research is required to evaluate the reliability of cfDNA as a marker of neuroendocrine-immune activation, which could be used for diagnostics purposes or monitoring of treatment progression.

Effect of Combined Ingestion of L-Theanine and L-Arginine for Short-Term Psychological Stress in Young Adults: A Randomized Placebo-Controlled Study.

l-Theanine, the most abundant amino acid component in green tea, has anti-stress effects and refreshes the mental state. A recent study demonstrated that l-arginine, the second most abundant amino acid in green tea, might enhance the anti-stress effects of l-theanine. The aim of this study was to evaluated the effects of combined ingestion of l-theanine and l-arginine on psychological stress in humans. A randomized placebo-controlled trial was conducted including 120 healthy young adults (mean age 22.4 y, 63.3% female). Subjects were randomly assigned to theanine (200 mg l-theanine), combined theanine/arginine (200 mg l-theanine, 50 mg l-arginine), or placebo groups. After consuming a test beverage, we administered a stress-loading test (Uchida-Kraepelin performance test) and performed salivary alpha-amylase activity (sAA) measurements to assess the physiological stress response at 0 min (immediately after), 5 min, and 15 min. The changes in sAA at 15 min after the stress-loading test were -2.75 (11.2) kIU/L in the theanine/arginine group, -0.40 (11.5) kIU/L in the theanine group, and 6.95 (18.6) kIU/L in the placebo group. The values in the theanine/arginine (p=0.007) and theanine (p=0.02) groups differed significantly from those in the placebo group. However, the difference between theanine/arginine and theanine groups, was not statistically significant (p=0.74). From this study, no clear conclusion could be drawn regarding the potentiating effect of theanine and arginine combined ingestion on anti-stress effects in human.

The neuroimmunology of social-stress-induced sensitization.

Myriad clinical findings provide links between chronic stressors, inflammation, and mood disorders. Furthermore, traumatic or chronic exposure to psychological stressors may promote stress sensitization, in which individuals have long-term complications, including increased vulnerability to subsequent stressors. Post-traumatic stress disorder (PTSD) is a clinically relevant example of stress sensitization. PTSD alters neuronal circuitry and mood; however, the mechanisms underlying long-term stress sensitization within this disorder are unclear. Rodent models of chronic social defeat recapitulate several key physiological, immunological, and behavioral responses associated with psychological stress in humans. Repeated social defeat (RSD) uniquely promotes the convergence of neuronal, central inflammatory (microglial), and peripheral immune (monocyte) pathways, leading to prolonged anxiety, social withdrawal, and cognitive impairment. Moreover, RSD promotes stress sensitization, in which mice are highly sensitive to subthreshold stress exposure and recurrence of anxiety weeks after the cessation of stress. Therefore, the purpose of this Review is to discuss the influence of social-defeat stress on the immune system that may underlie stress sensitization within three key cellular compartments: neurons, microglia, and monocytes. Delineating the mechanisms of stress sensitization is critical in understanding and treating conditions such as PTSD.

Genome-Wide mRNA Expression Analysis of Acute Psychological Stress Responses.

Most previous studies have examined the effects of acute psychological stress in humans based on select gene panels. The genomic approach may help identify novel genes that underline biological mechanisms of acute psychological stress responses. This exploratory study aimed to investigate genome-wide transcriptional activity changes in response to acute psychological stress. The sample included 40 healthy women (mean age 31.4 ± 11.6 years). Twenty-two participants had a stress experience induced by the Trier Social Stress Test (experimental group) and 18 did not (control group). Psychological stress levels and hemodynamic changes were assessed before and after the Trier Social Stress Test. Peripheral blood samples obtained before and after the Trier Social Stress Test were processed for mRNA sequencing. Psychological and hemodynamic stress parameters indicated that the Trier Social Stress Test induced moderate levels of stress in the experimental group. Six genes (HCG26, HCP5, HLA-F, HLA-F-AS1, LOC1019287, and SLC22A16) were up-regulated, and fi ve genes (CA1, FBXO9, SNCA, STRADB, and TRMT12) were down-regulated among those who experienced stress induction, compared with the control group. Nine genes of eleven were linked to endocrine system disorders, neurological disease, and organismal injury and abnormalities. Of the genes identifi ed in this study, HCP5, SLC22A16, and SNCA genes have previously been proposed as therapeutic targets for cancer and Parkinson disease. Further studies are needed to examine pathological mechanisms through which these genes mediate eff ects of psychological stress on adverse health outcomes. Such studies may ultimately identify therapeutic targets that enhance biological resilience to adverse eff ects of psychological stress.

The differential modulation of the baroreflex control mechanism in fight, flight or freeze behaviour.

The differential modulation of the baroreflex control mechanism in fight, flight or freeze behaviour.

Effects of Lactococcus lactis subsp. cremoris YRC3780 daily intake on the HPA axis response to acute psychological stress in healthy Japanese men

BackgroundLactococcus lactis subsp. cremoris (YRC3780), which is isolated from kefir, has been associated with anti-allergic effects in humans. However, it remains unknown whether daily intake of YRC3780 attenuates the response to psychological stress in humans in parallel with changes to the gut microbiome. We examined the fundamental role of YRC3780 in the gut microbiome, stress response, sleep, and mental health in humans.MethodsEffects of daily intake of YRC3780 on the hypothalamic-pituitary-adrenal (HPA) axis response to acute psychological stress were investigated in a double-blind, placebo-controlled clinical trial involving 27 healthy young men (mean age and body mass index: 23.5 years and 21.5 kg/m2) who were randomly assigned to placebo (n = 13) or YRC3780 (n = 14) groups. The HPA axis response to acute psychological stress, the diurnal rhythm of HPA axis activity, and gut microbiome were assessed and compared between the two groups.ResultsThe results showed that daily intake of YRC3780 significantly lowered morning salivary cortisol levels compared with placebo. In addition, salivary cortisol levels following a social stress test significantly decreased +40 min after beginning the TSST in the YRC3780-treated group compared to placebo. There were no significant differences between the two groups in terms of actigraphy-based sleep quality, but the subjective sleep quality and mental health were significantly improved in the YRC3780-treated group compared to placebo.ConclusionsOur study suggests that daily intake of YRC3780 improves the HPA axis response to acute psychological stress, which might be associated with a decrease in morning cortisol levels.

The Behavior and Postnatal Development in Infant and Juvenile Rats After Ultrasound-Induced Chronic Prenatal Stress.

Fetal development is susceptible to environmental factors. One such factor is exposure to stress during pregnancy. The present study aimed to investigate the effects of chronic prenatal stress (PS) on the development and behavior of rat offspring during infancy and juvenile ages. Existing approaches to modeling prenatal stress on animals do not correlate with the main type of stress in pregnant women, namely psychological stress. We used a new stress paradigm in the experiment, namely, stress induced by exposure to variable frequency ultrasound (US), which acted on pregnant Wistar rats on gestational days 1–21. This type of stress in rodents can be comparable to psychological stress in humans. We assessed physical development, reflex maturation, motor ability development, anxious behavior, response to social novelty, and social play behavior in male and female offspring. Additionally, we investigated maternal behavior and the effect of neonatal handling (NH) on behavior. Prenatal stress did not affect postnatal developmental characteristics in rat pups, but prenatally stressed rats had higher body weight in early and adult age than controls. Prenatal exposure to a stressor increased anxiety in the open-field test (OF), changed social preferences in the social novelty test (SN), and impaired social play behavior in males. Neonatal handling reduced anxiety and restored social behavior, but evoked hyperactive behavior in rat pups. Maternal behavior did not change. Our study demonstrated for the first time that exposure to variable frequency ultrasound during pregnancy influences offspring development and impairs behavior, correlating with the effects of other types of stress during pregnancy in rodents. This supports the idea of using this exposure to model prenatal stress.

Abstract 12683: Genome-wide Mrna Expression Analysis of Acute Psychological Stress Responses

Introduction: Previous studies have examined effects of acute psychological stress in humans on selected panels of genes. This exploratory study aimed to investigate genome-wide transcriptional activity changes in responses to acute psychological stress. Methods: The sample included 40 healthy women who participated in a previous study (22 who had a stress induced experience (experimental group) and 18 who did not (control group)). The psychological stress was induced by the Trier Social Stress Test (TSST). Psychological stress levels (measured by the Subjective Units of Distress Scale (SUDS) and the state anxiety subscale of the Spielberger State-Trait Anxiety Inventory) and hemodynamic changes (measured by blood pressure (BP) and heart rate (HR)) were assessed before and after the TSST. The peripheral blood samples obtained before and after the TSST were processed for mRNA-sequencing. Results: The mean age of the participants was 31 years (SD 11.6). The psychological and hemodynamic stress parameters indicated that the TSST successfully induced moderate but statistically significant levels of acute psychological stress in the participants of the experimental group. Compared with the participants in the control group, six genes ( BCL2L14, FAM3B, HCG26, HLA-F-AS1, LOC101928710 , and SLC22A16 ) were up-regulated and 9 genes ( ATP2C2, CA1, CRYBG3, FBXO9, HBD, SLC39A9, SNCA, STRADB , and TRMT12 ) were down-regulated among those who experienced stress induction. The IPA analysis identified one network of cell-to-cell signaling and interaction, cellular function and maintenance, and hematological system development and function. Thirteen genes out of 15 were found in this network. Conclusions: The identified genes including FAM3B, BCL2L14, SLC22A16 , and SNCA , have been proposed as the therapeutic targets of diabetes-related CVDs, certain cancers, and Parkinson’s disease, but have not previously been reported to be associated with psychological stress. Future studies are suggested to examine the pathological mechanisms by which the identified genes may mediate the association between psychological stress and adverse health outcome.

Acute psychological stress increases serum circulating cell-free mitochondrial DNA

Intrinsic biological mechanisms transduce psychological stress into physiological adaptation that requires energy, but the role of mitochondria and mitochondrial DNA (mtDNA) in this process has not been defined in humans. Here, we show that similar to physical injury, exposure to psychological stress increases serum circulating cell-free mtDNA (ccf-mtDNA) levels. Healthy midlife adults exposed on two separate occasions to a brief psychological challenge exhibited a 2-3-fold increase in ccf-mtDNA, with no change in ccf-nuclear DNA levels, establishing the magnitude and specificity for ccf-mtDNA reactivity. In cell-based studies, we show that glucocorticoid signaling – a consequence of psychological stress in humans – is sufficient to induce mtDNA extrusion in a time frame consistent with stress-induced ccf-mtDNA increase. Collectively, these findings provide evidence that acute psychological stress induces ccf-mtDNA and implicate neuroendocrine signaling as a potential trigger for ccf-mtDNA release. Further controlled work is needed to confirm that observed increases in ccf-mtDNA result from stress exposure and to determine the functional significance of this effect.

Abstract # 3159 Cytomegalovirus amplifies CD8 + T cell mobilization to psychological stress in humans, via a beta-adrenergic dependent mechanism linked to T-bet/Th1 effector cell differentiation

Psychological stress induces a beta-adrenergic dependent mobilization of CD8 + T lymphocytes (CTL) into the peripheral blood. Here we identified infection with Cytomegalovirus (CMV) as a major determinant of this mobilization, and characterized the cellular and transcriptional alterations that underlie enhanced responsivity. During acute stress (TSST), CMV-positive individuals (N = 35) demonstrated a 3-fold greater CTL mobilization compared to CMV-negative individuals (N = 48). Enhanced CTL mobilization was entirely confined to cells with an effector-memory phenotype (EMRA), which become markedly enriched in CMV-infected individuals. A beta-adrenergic receptor (beta-AR) dependent mechanism was confirmed by studies showing that stress-induced EMRA mobilization; (1) correlated with catecholamine release; (2) was completely abrogated by the beta-AR antagonist propranolol, and; (3) was reproduced by infusion of the beta-AR agonist isoproterenol. Micro-array analyses demonstrated selective 8-fold up-regulation of the beta2-AR gene (ADRB2) in EMRA as well as CMV-specific CTL. Longitudinal analyses confirmed that CMV-infection de novo induced rapid and lasting ADRB2 up-regulation in CTL, in conjunction with a Th1 T-bet/EOMES transcriptional profile. Subsequent studies in vitro replicated that functional beta2-AR expression increased with progressive CTL differentiation assessed as T-bet/Th1 expression. The present study identified a novel mechanism through which host–microbe interactions can regulate immune system responses to stress: CMV-infection induced T-bet differentiation accompanied by beta2-AR upregulation, which hereby enriched the CTL compartment with EMRA cells exhibiting an increased adrenergic sensitivity and enhanced mobilization during stress.

Selection of Neural Oscillatory Features for Human Stress Classification with Single Channel EEG Headset.

A study on classification of psychological stress in humans using electroencephalography (EEG) is presented. The stress is classified using a correlation-based feature subset selection method that efficiently reduces the feature vector length. In this study, twenty-eight participants are involved by filling in the perceived stress scale-10 (PSS-10) questionnaire and their EEG is also recorded in closed eye condition to measure the baseline stress. The recorded data is labelled on the basis of the stress level that is indicated by the participant's PSS score. The feature selection method has shown that, among the EEG oscillations, low beta, high beta, and low gamma are the most significant neural oscillations for classifying human stress. The proposed method not only reduces the time to build a classification model but also improves the classification accuracy up to 78.57% using a single channel wearable EEG device.

Cortisol regulates immune and metabolic processes in murine adipocytes and macrophages through HTR2c and HTR5a serotonin receptors

Epidemiological studies implicate stress as an important factor contributing to the increasing prevalence of metabolic disorders. Studies have correlated visceral obesity and atherosclerosis with hyper-cortisolemia, a sequela of chronic psychological stress in humans and animals. Although several hormonal markers of stress have been associated with various metabolic disorders, the mechanism by which these hormones alter metabolic functions have not been established. We used an in vitro model system, culturing 3T3-L1 pre-adipocytes and RAW 264.7 macrophages in the presence or absence of cortisol, to analyze cell signaling pathways mediating changes in metabolic functions. Our analysis revealed that cortisol up-regulated the expression and function of two serotonin (S) receptors, HTR2c and HTR5a. HTR2c and HTR5a were also directly involved in mediating cortisol enhanced adipogenesis when pre-adipocytes were cultured alone or in the presence of macrophages. Finally, cortisol treatment of pre-adipocytes co-cultured with macrophages enhanced adipogenesis in both macrophages and pre-adipocytes.

The degree of radiation-induced DNA strand breaks is altered by acute sleep deprivation and psychological stress and is associated with cognitive performance in humans.

Sleep deprivation is associated with impaired immune responses, cancer, and morbidity and mortality, and can degrade cognitive performance, although individual differences exist in such responses. Sleep deprivation induces DNA strand breaks and DNA base oxidation in animals, and psychological stress is associated with increased DNA damage in humans. It remains unknown whether sleep deprivation or psychological stress in humans affects DNA damage response from environmental stressors, and whether these responses predict cognitive performance during sleep deprivation. Sixteen healthy adults (ages 29-52 years; mean age ± SD, 36.4 ± 7.1 years; seven women) participated in a 5-day experiment involving two 8 hr time-in-bed (TIB) baseline nights, followed by 39 hr total sleep deprivation (TSD), and two 8-10 hr TIB recovery nights. A modified Trier Social Stress Test was conducted on the day after TSD. The Psychomotor Vigilance Test measured behavioral attention. DNA damage was assessed in blood cells collected at 5 time points, and blood cells were irradiated ex vivo. TSD, alone or in combination with psychological stress, did not induce significant increases in DNA damage. By contrast, radiation-induced DNA damage decreased significantly in response to TSD, but increased back to baseline when combined with psychological stress. Cognitively vulnerable individuals had more radiation-induced DNA strand breaks before TSD, indicating their greater sensitivity to DNA damage from environmental stressors. Our results provide novel insights into the molecular consequences of sleep deprivation, psychological stress, and performance vulnerability. They are important for fields involving sleep loss, radiation exposure, and cognitive deficits, including cancer therapy, environmental toxicology, and space medicine.

Oral lactoferrin influences psychological stress in humans: A single-dose administration crossover study.

Lactoferrin is a secretory protein with various physiological functions. Bovine lactoferrin has been demonstrated to alleviate psychological stresses in rats, but this effect in humans has not yet been assessed. The present study aimed to investigate the changes in psychological stress markers following a calculation task, with either lactoferrin or a placebo orally administered prior to the task. A total of 16 healthy female college students visited Juntendo University, Inzai, Japan following an overnight fast. Subjects were quietly seated for 15 min to stabilize the respiratory rate at 0.25 Hz (one breath every 4 sec). Then, subjects provided saliva, ingested either lactoferrin (800 mg of lactoferrin + soy milk) or a placebo (soy milk), remained seated for another 15 min with respiration rate at 0.25 Hz, and performed a calculation task. The task comprised two sets of 15-min calculations, with a 5-min interval between sets. Each calculation set consisted of various multiplications and divisions using pairs of three-digit numbers. Following the calculation task, saliva was collected again. Heart rate was also monitored to identify the frequency domain of heart-rate variability. The calculation task resulted in increased activity of salivary amylase, and decreased concentration of chromogranin A for both lactoferrin (P=0.028 and P<0.001, respectively) and placebo (P=0.003 and P<0.001, respectively) treatments. The degrees of changes in these salivary markers were similar between the two treatments. Heart rate variability exhibited an increase in the high-frequency (HF) component (P=0.022) and a decrease in low-frequency (LF)/HF and LF/(LF+HF) ratios (both P<0.001) following the calculation task under the placebo condition, demonstrating an upregulation of parasympathetic and a downregulation of sympathetic nervous activities. These changes in parasympathetic (HF) and sympathetic (LF/HF) activities, however, were alleviated by lactoferrin compared with the placebo (P=0.007 and P=0.026, respectively). Collectively these results suggest that oral lactoferrin may mitigate psychological stress in humans.

Ghrelin stimulation by hypothalamic-pituitary-adrenal axis activation depends on increasing cortisol levels.

Ghrelin plasma concentration increases in parallel to cortisol after a standardized psychological stress in humans, but the physiological basis of this interaction is unknown. We aimed to elucidate this question by studying the ghrelin response to pharmacological manipulation of the hypothalamic–pituitary–adrenal (HPA) axis. Six lean, healthy male volunteers were examined under four experimental conditions. Blood samples were collected every 30 min for two sequential periods of two hours. Initially, a baseline period was followed by intravenous injection of a synthetic analog of ACTH (250 μg). Subsequently, a single dose of metyrapone was administered at midnight and in the following morning, blood samples were collected for 2 h, followed by an intravenous injection of hydrocortisone (100 mg) with continued sampling. We show that increased cortisol serum levels secondary to ACTH stimulation or hydrocortisone administration are positively associated with plasma ghrelin levels, whereas central stimulation of the HPA axis by blocking cortisol synthesis with metyrapone is associated with decreased plasma ghrelin levels. Collectively, this suggests that HPA-axis-mediated elevations in ghrelin plasma concentration require increased peripheral cortisol levels, independent of central elevation of ACTH and possibly CRH levels.

Stress and arterial hypertension: ISIAH rat strain

The main views of the issue of stress and hypertension are briefly reviewed. It is well known that stress is one of the major risk factors for cardiovascular disease development. Increase in blood pressure is a typical manifestation of the acute stress response. This fact is the reason to hypothesize that chronic stress causes the development of hypertensive disease. An association of hypertension with psychological stress in humans was shown in several works. In addition, it was demonstrated that hypertension was accompanied by an increase in sympathetic tone. On the other hand, there were many population studies in which no association was found between different types of chronic stress and arterial hyper­tension. Thus, the question is far from being answered. Even in the cases when one managed to obtain a signi­ficant hypertensive effect in experimental studies with emotional stress, it was difficult to explain the mechanisms mediating the formation of stressinduced hypertension. To clarify the situation, one of the authors of this review decided to begin the breeding of a rat strain with increased blood pressure response to emotional stress. This breeding gave rise to inbred rats with persistent stress-induced arterial hypertension. A brief history of the development of the genetic model ofstress-induced arterial hypertension, the ISIAH rat strain, is given. A retrospective review of the studies performed with ISIAH rats is presented. The contribution of genotype changes in the neuroendocrine systems involved in stress and blood pressure regulation to the development ofstress-dependent hypertension in the ISIAH rat strain is shown.

Signal amplification in a microfluidic paper-based analytical device (µ-PAD) by confinement of the fluidic flow

This is a one-step POC biosensor that guarantees rapid assay times, low-cost analysis, simple handling, stability, and is easy to mass product. However, it has several drawbacks such as limited sample volume and relatively low sensitivity. To overcome these disadvantages, we have designed and fabricated the µ-PAD to confine fluid flow by creating a hydrophobic channel in the paper to improve the sensitivity. The channel pattern was drawn by a computer-aided design program and directly printed by a commercially available wax printer which generates the hydrophobic channel pattern. While maintaining a constant sample, absorption, and conjugation pad, the width of the detection pad was reduced from 5 mm to 2 mm at intervals of 1 mm. The intensity of bands from the single- and double-orifice patterns increased identically compared with the device with no orifice. The relative intensity of the signal bands increased from 141 to 158. Also, numerical simulation was performed to validate the experimental result by using lattice Boltzmann method. We observed that the sensitivity was enhanced at a specific detection pad width (3 mm). Therefore, our simple structural change of the channel led to improve the colorimetric intensity. Cortisol, which is a known stress biomarker, was used to validation the device, an enhanced signal was obtained indicating that our device can be used for the detection psychological stress in humans.

Estimation of psychological stress in humans: a combination of theory and practice.

Stress has long been known to increase susceptibility to health disorders. In 2009, American Psychological Association further established association of stress to serious health problems. However, a quantitative and accurate way to evaluate and estimate stress status of individuals is still a big challenge. It has been shown, in large animal models using cattle, that psychological stress can be quantified as well as disease susceptibility could be predicted through biomarker discovery. Taking cue from those studies, we have evaluated and estimated psychological stress level of individuals theoretically and validated experimentally. Various biomarkers have also been identified which can be associated to psychological stress to predict stress status of unknown individuals.

Effects of L-theanine or caffeine intake on changes in blood pressure under physical and psychological stresses

BackgroundL-theanine, an amino acid contained in green tea leaves, is known to block the binding of L-glutamic acid to glutamate receptors in the brain, and has been considered to cause anti-stress effects by inhibiting cortical neuron excitation. Both L-theanine and caffeine, which green tea contains, have been highlighted for their beneficial effects on cognition and mood.MethodsIn this study, we investigated the effects of orally administered L-theanine or caffeine on mental task performance and physiological activities under conditions of physical or psychological stress in humans. Fourteen participants each underwent three separate trials, in which they orally took either L-theanine + placebo, caffeine + placebo, or placebo only.ResultsThe results after the mental tasks showed that L-theanine significantly inhibited the blood-pressure increases in a high-response group, which consisted of participants whose blood pressure increased more than average by a performance of a mental task after placebo intake. Caffeine tended to have a similar but smaller inhibition of the blood-pressure increases caused by the mental tasks. The result of the Profile of Mood States after the mental tasks also showed that L-theanine reduced the Tension-Anxiety scores as compared with placebo intake.ConclusionsThe findings above denote that L-theanine not only reduces anxiety but also attenuates the blood-pressure increase in high-stress-response adults.