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We investigated whether mood and lifestyle-related indicators of physical health are differentially expressed according to self-reported levels of depressive symptoms among young adults with a current episode of major depression. In a cross-sectional study, we recruited 94 young adults (females = 67, 71.3%; males = 27, 28.7%; aged 18-35 years) with a current episode of major depression. We assessed their mood with the Profile of Mood States (POMS), and Beck Anxiety Inventory-(BAI), sleep with the Pittsburgh Sleep Quality Index (PSQI), physical activity with the Simple Physical Activity Questionnaire (SIMPAQ), and their cardiorespiratory fitness. Participants' depression levels were classified as follows using established cut-points: (a) Mild Depressive Symptoms (MIDS, BDI-II 14-19 points, n = 17), (b) Moderate Depressive Symptoms (MODS, BDI-II 20-28 points, n = 37) or (c) Severe Depressive Symptoms (SEDS, BDI-II 29-63 points, n = 40). As expected, we found that young adults with SEDS, when compared to those with MODS and MIDS, showed higher depressive mood on the POMS, and they exhibited greater anxiety symptoms, lower reported 'vigor' on physical activity measures, worse sleep quality as expressed by their global score sleep; daytime dysfunction; and sleep disturbance, and they showed lower cardiorespiratory fitness. Those with moderate depressive symptoms only differed from those with mild symptoms with respect to hostility, fatigue and mood disturbance. Although there was a gradient whereby worse mental and physical health indicators were more closely related to the SEDS depression categorization, while healthier indicators were associated with the MIDS category, some parameters were not different between the MDD severity groups, particularly when comparing MIDS and MODS. Clinicians treating patients with MDD should consider these factors when designing lifestyle-based interventions.
Subject(s)
Depressive Disorder, Major , Male , Female , Humans , Young Adult , Self Report , Cross-Sectional Studies , Life Style , Exercise , DepressionABSTRACT
Introduction: The understanding of biological responses to psychedelics with antidepressant potential is imperative. Here we report how a set of acute parameters, namely emotional (depressive symptoms), cognitive (psychedelic experience), and physiological (salivary cortisol), recorded during an ayahuasca dosing session, modulated serum brain-derived neurotrophic factor (BDNF), serum cortisol (SC), serum interleukin 6 (IL-6), plasma C-reactive protein (CRP), and salivary cortisol awakening response (CAR). Methods: Results were analyzed 2 days after the psychedelic intervention (ayahuasca) versus placebo in both patients with treatment-resistant depression and healthy volunteers. These measures were assessed as part of a randomized double-blinded, placebo-controlled trial (n = 72). Results: Results revealed that larger reductions of depressive symptoms during the dosing session significantly moderated higher levels of SC in patients. Whereas lesser changes in salivary cortisol levels during the ayahuasca intervention were related to higher BDNF levels in patients with a larger clinical response in the reduction in depressive symptoms. No moderator was found for patient's CAR, IL-6, and CRP responses to ayahuasca and for all biomarker responses to ayahuasca in healthy controls and in the placebo group. Discussion: In summary, some specific emotional and physiological parameters during experimental ayahuasca session were revealed as critical moderators of the improvement of major depression biomarkers, mainly BDNF and SC two days after ayahuasca intake. These findings contribute to paving the way for future studies investigating the biological antidepressant response to psychedelic therapy.
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BACKGROUND: This study aimed to compare the stress tolerance, competitive anxiety, heart rate variability and salivary cortisol before and during successive futsal competitive matches (3 matches in 4 days) in young male futsal players. METHODS: 10 young male futsal players (16.9 ± 0.7 age; 71.0 ± 5.1 kg; 174.9 ± 4.3 cm) were monitored during one training session and across a competitive period with 3 successive matches. External load was determined by the PlayerLoad method, while session rating of perceived exertion was used to calculate the internal training and competitive load. The stress tolerance was examined using Daily Analysis of Life Demand in Athletes questionnaire and the Competitive State Anxiety Inventory was used to analyze the competitive anxiety. The Time and frequency monitoring parameters were used to analyze the vagal cardiac autonomic marker. sC was analyzed using enzyme-linked immunosorbent assay. RESULTS: A generalized estimating equation showed a significant difference for PlayerLoad from M1 to TS, M2 and M3, from M2 to M3 (p < 0.05), and for session rating of perceived exertion from M1 to Ts and M3 (p < 0.05). A difference for sources [χ2 (3) = 1.481, p = 0.68] or symptoms [χ2 (3) = 3.893, p = 0.27] was not found. There was no significant difference in any of the competitive anxiety [cognitive anxiety (F (1.644; 14.799) = 4.6, p = 0.73, Å2 p = 0.28), somatic anxiety (F (2,09; 18,85) = 26.07 p = 0.057; Å2p = 0.27) or self-confidence (F(2.07; 18.85) = 15.875 p = 0.152; Å2p = 0.18)] domains. The HRV parameters (time domain and frequency) and Salivary Cortisol (sC) (χ2 (3) = 4.320 p = 0.229) did not significantly change during the successive matches. CONCLUSION: The competitive scenario in which the players were evaluated did not significantly modify the stress tolerance, or the athletes' state of anxiety, which in turn was not able to promote changes in the cardiac vagal modulation or in the sC levels before the matches.
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ABSTRACT: Mortatti, AL, Oliveira, RSCd, Pinto, JCBdL, Galvão-Coelho, NL, Almeida, RN, Aoki, MS, and Moreira, A. A congested match schedule alters internal match load and affects salivary immunoglobulin A concentration in youth soccer players. J Strength Cond Res 36(6): 1655-1659, 2022-The aim of this study was to analyze the effects of a congested match schedule (CMS) undertaken after a tapering week, on internal match load (IML) and salivary immunoglobulin A (SIgA) concentration in 12 youth soccer players (16.6 ± 0.5 years; 175 ± 8 cm; 65 ± 8 kg) who performed 4 official matches within a 4-day period. Internal match load was determined using the session-rating of perceived exertion method and the competitive strain (CS) and monotony index (MI) were also determined. Saliva sampling was conducted, before the last training day of a tapering week (training) preceding the CMS, 60 minutes before the first match (match-1), and 22 hours after match 4 (postmatch 4). Salivary immunoglobulin A was analyzed by ELISA. The results of the analysis of variance with repeated measures showed a significant difference for IML across the matches (p < 0.001). A significant reduction in SIgA was observed from prematch 1 to postmatch 4 (p = 0.019). Regarding the change in SIgA (ΔSIgA), 58.3% of the players presented values equal/higher than the minimal detectable change. A large within-individual correlation was observed between ΔSIgA and MI and CS (r = 0.71 and r = 0.72: p < 0.01, respectively). The current findings suggest that youth players participating in a CMS may present a decrease in mucosal immunity function. In addition, data suggest that the MI and CS may be used as valuable markers for monitoring competition load during CMS in youth soccer players.
Subject(s)
Soccer , Adolescent , Humans , Immunity, Mucosal , Immunoglobulin A, Secretory , SalivaABSTRACT
The study aim was to analyze the effects of successive matches on the internal match load, stress tolerance, salivary cortisol concentration and countermovement vertical jump height in twelve youth soccer players (16.6 ± 0.5 yr; 175 ± 8 cm; 65 ± 8 kg) who performed four official matches within a four day-period with a 24-h recovery interval between the matches. The internal match load, monotony index and competitive strain, as well as stress tolerance were examined. Saliva samples were collected and countermovement vertical jump height was assessed 60 min pre and 30 min post each match; delta of salivary cortisol and countermovement vertical jump height for each match were analyzed. Salivary cortisol was analyzed using an enzyme-linked immunosorbent assay. The results of ANOVA with repeated measures showed no differences between matches for the internal match load (p > 0.05). The scores of the monotony index and competitive strain were 4.3 (±2.3) and 8104 (±6795) arbitrary units, respectively. There was no difference for stress tolerance between matches (p > 0.05). Delta values of salivary cortisol were not different among the assessed matches (F(3,33) = 1.397, p = 0.351, η2: 0.09); however, delta of countermovement vertical jump height decreased from match 1 to match 4 (F(3,33) = 8.64, p < 0.001, η2: 0.44). The current findings suggest that participating in four successive matches, with 24-h of recovery in between, may not lead to changes in stress tolerance and salivary cortisol of youth players, but it may induce a decrease in players' jumping performance after the fourth match.
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BACKGROUND: Molecular biomarkers are promising tools to be routinely used in clinical psychiatry. Among psychiatric diseases, major depression disorder (MDD) has gotten attention due to its growing prevalence and morbidity. METHODS: We tested some peripheral molecular parameters such as serum mature Brain-Derived Neurotrophic Factor (mBDNF), plasma C-Reactive Protein (CRP), serum cortisol (SC), and the salivary Cortisol Awakening Response (CAR), as well as the Pittsburgh sleep quality inventory (PSQI), as part of a multibiomarker panel for potential use in MDD diagnosis and evaluation of disease's chronicity using regression models, and ROC curve. RESULTS: For diagnosis model, two groups were analyzed: patients in the first episode of major depression (MD: n = 30) and a healthy control (CG: n = 32). None of those diagnosis models tested had greater power than Hamilton Depression Rating Scale-6. For MDD chronicity, a group of patients with treatment-resistant major depression (TRD: n = 28) was tested across the MD group. The best chronicity model (p < 0.05) that discriminated between MD and TRD included four parameters, namely PSQI, CAR, SC, and mBDNF (AUC ROC = 0.99), with 96% of sensitivity and 93% of specificity. CONCLUSION: These results indicate that changes in specific biomarkers (CAR, SC, mBDNF and PSQI) have potential on the evaluation of MDD chronicity, but not for its diagnosis. Therefore, these findings can contribute for further studies aiming the development of a stronger model to be commercially available and used in psychiatry clinical practice.
Subject(s)
Biomarkers/metabolism , Depressive Disorder, Major/blood , Depressive Disorder, Major/diagnosis , Adult , Algorithms , Area Under Curve , Brain-Derived Neurotrophic Factor/blood , C-Reactive Protein/biosynthesis , Case-Control Studies , Female , Humans , Hydrocortisone/blood , Hydrocortisone/metabolism , Male , Middle Aged , Models, Theoretical , Prevalence , Psychiatric Status Rating Scales , Psychiatry/standards , Psychometrics , ROC Curve , Regression Analysis , Saliva/metabolism , Sleep , Time Factors , Young AdultABSTRACT
The comprehension of the pathophysiology of the major depressive disorder (MDD) is essential to the strengthening of precision psychiatry. In order to determine the relationship between the pathophysiology of the MDD and its clinical progression, analyzed by severity of the depressive symptoms and sleep quality, we conducted a study assessing different peripheral molecular biomarkers, including the levels of plasma C-reactive protein (CRP), serum mature brain-derived neurotrophic factor (mBDNF), serum cortisol (SC), and salivary cortisol awakening response (CAR), of patients with MDD (n = 58) and a control group of healthy volunteers (n = 62). Patients with the first episode of MDD (n = 30) had significantly higher levels of CAR and SC than controls (n = 32) and similar levels of mBDNF of controls. Patients with treatment-resistant depression (TRD, n = 28) presented significantly lower levels of SC and CAR, and higher levels of mBDNF and CRP than controls (n = 30). An increased severity of depressive symptoms and worse sleep quality were correlated with levels low of SC and CAR, and with high levels of mBDNF. These results point out a strong relationship between the stages clinical of MDD and changes in a range of relevant biological markers. This can assist in the development of precision psychiatry and future research on the biological tests for depression.
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BACKGROUND: Ayahuasca is a traditional Amazon brew and its potential antidepressant properties have recently been explored in scientific settings. We conducted a double-blind placebo-controlled trial of ayahuasca with treatment-resistant depression patients (n = 28) and healthy controls (n = 45). AIMS: We are evaluating the blood inflammatory biomarkers: C-reactive protein and interleukin 6, as a potential consequence of ayahuasca intake and their correlation with serum cortisol and brain-derived neurotrophic factor levels. Blood samples were collected at pre-treatment and 48 hours after substance ingestion to assess the concentration of inflammatory biomarkers, together with administration of the Montgomery-Åsberg Depression Rating Scale. RESULTS: At pre-treatment, patients showed higher C-reactive protein levels than healthy controls and a significant negative correlation between C-reactive protein and serum cortisol levels was revealed (rho = -0.40, n = 14). C-reactive protein in those patients was not correlated with Montgomery-Åsberg Depression Rating Scale scores. We observed a significant reduction of C-reactive protein levels across time in both patients and controls treated with ayahuasca, but not with placebo. Patients treated with ayahuasca showed a significant correlation (rho = + 0.57) between larger reductions of C-reactive protein and lower depressive symptoms at 48 hours after substance ingestion (Montgomery-Åsberg Depression Rating Scale). No significant result with respect to interleukin 6 and brain-derived neurotrophic factor was found. Furthermore, these biomarkers did not predict the antidepressant response or remission rates observed. CONCLUSIONS: These findings enhance the understanding of the biological mechanisms behind the observed antidepressant effects of ayahuasca and encourage further clinical trials in adults with depression.
Subject(s)
Antidepressive Agents/administration & dosage , Banisteriopsis/chemistry , Depressive Disorder, Treatment-Resistant/drug therapy , Plant Preparations/administration & dosage , Adult , Antidepressive Agents/pharmacology , Biomarkers/metabolism , Case-Control Studies , Depressive Disorder, Major/drug therapy , Depressive Disorder, Major/physiopathology , Depressive Disorder, Treatment-Resistant/physiopathology , Double-Blind Method , Female , Humans , Inflammation/drug therapy , Inflammation/pathology , Male , Plant Preparations/pharmacology , Psychiatric Status Rating Scales , Treatment OutcomeABSTRACT
Sleep disturbance is a symptom consistently found in major depression and is associated with a longer course of illness, reduced response to treatment, increased risk of relapse and recurrence. Chronic insomnia has been associated with changes in cortisol and serum brain-derived neurotrophic factor (BDNF) levels, which in turn are also changed in major depression. Here, we evaluated the relationship between sleep quality, salivary cortisol awakening response (CAR), and serum BDNF levels in patients with sleep disturbance and treatment-resistant major depression (n = 18), and in a control group of healthy subjects with good (n = 21) and poor (n = 18) sleep quality. We observed that the patients had the lowest CAR and sleep duration of all three groups and a higher latency to sleep than the healthy volunteers with a good sleep profile. Besides, low CAR was correlated with more severe depressive symptoms and worse sleep quality. There was no difference in serum BDNF levels between groups with distinct sleep quality. Taken together, our results showed a relationship between changes in CAR and in sleep quality in patients with treatment-resistant depression, which were correlated with the severity of disease, suggesting that cortisol could be a physiological link between sleep disturbance and major depression.
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Serotonergic psychedelics are emerging as potential antidepressant therapeutic tools, as suggested in a recent randomized controlled trial with ayahuasca for treatment-resistant depression. Preclinical and clinical studies have suggested that serum brain-derived neurotrophic factor (BDNF) levels increase after treatment with serotoninergic antidepressants, but the exact role of BDNF as a biomarker for diagnostic and treatment of major depression is still poorly understood. Here we investigated serum BDNF levels in healthy controls (N = 45) and patients with treatment-resistant depression (N = 28) before (baseline) and 48 h after (D2) a single dose of ayahuasca or placebo. In our sample, baseline serum BDNF levels did not predict major depression and the clinical characteristics of the patients did not predict their BDNF levels. However, at baseline, serum cortisol was a predictor of serum BDNF levels, where lower levels of serum BDNF were detected in a subgroup of subjects with hypocortisolemia. Moreover, at baseline we found a negative correlation between BDNF and serum cortisol in volunteers with eucortisolemia. After treatment (D2) we observed higher BDNF levels in both patients and controls that ingested ayahuasca (N = 35) when compared to placebo (N = 34). Furthermore, at D2 just patients treated with ayahuasca (N = 14), and not with placebo (N = 14), presented a significant negative correlation between serum BDNF levels and depressive symptoms. This is the first double-blind randomized placebo-controlled clinical trial that explored the modulation of BDNF in response to a psychedelic in patients with depression. The results suggest a potential link between the observed antidepressant effects of ayahuasca and changes in serum BDNF, which contributes to the emerging view of using psychedelics as an antidepressant. This trial is registered at http://clinicaltrials.gov (NCT02914769).