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1.
IEEE Pulse ; 11(4): 8-13, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32841113

RESUMO

One of the most pernicious side effects of the COVID-19 pandemic is a steep rise in stress and mental health problems. According to a poll by the Kaiser Family Foundation, nearly half of American adults say that worry and stress about the pandemic is hurting their mental health [1]. There are plenty of factors feeding into this phenomenon. People are anxious about getting sick, grieving lost loved ones, and experiencing financial stress, parental stress, and loneliness. The pandemic places additional burdens on essential workers and people of color, both of whom are at greater risk of dying from the disease. COVID-19 itself has been linked to neurological problems as well as anxiety, depression, and sleep disorders [2].


Assuntos
Betacoronavirus , Infecções por Coronavirus , Depressão , Saúde Mental , Pandemias , Pneumonia Viral , Transtornos do Sono-Vigília , Estresse Psicológico , Adulto , Infecções por Coronavirus/economia , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/fisiopatologia , Infecções por Coronavirus/psicologia , Depressão/economia , Depressão/epidemiologia , Depressão/fisiopatologia , Depressão/psicologia , Humanos , Pandemias/economia , Pneumonia Viral/economia , Pneumonia Viral/epidemiologia , Pneumonia Viral/fisiopatologia , Pneumonia Viral/psicologia , Transtornos do Sono-Vigília/economia , Transtornos do Sono-Vigília/epidemiologia , Transtornos do Sono-Vigília/fisiopatologia , Transtornos do Sono-Vigília/psicologia , Estresse Psicológico/economia , Estresse Psicológico/epidemiologia , Estresse Psicológico/fisiopatologia , Estresse Psicológico/psicologia
2.
PLoS One ; 15(8): e0237377, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32785263

RESUMO

BACKGROUND: It is known that bioenergetics of aerobic and resistance exercise are not the same but both can effectively improve depression. However, it is not clear whether and how different types of exercise can influence depression through the same metabolic regulatory system. Metabolomics provides a way to study the correlation between metabolites and changes in exercise and/or diseases through the quantitative analysis of all metabolites in the organism. The objective of this study was to investigate the effects of aerobic and resistance training on urinary metabolites by metabolomics analysis in a rodent model of depression. METHODS: Male Sprague-Dawley rats were given chronic unpredictable mild stress (CUMS) for eight weeks. The validity of the modeling was assessed by behavioral indices. After four weeks of CUMS, the rats that developed depression were randomly divided into a depression control group, an aerobic training group and a resistance training group. There was also a normal control group. From week 5, the rats in the exercise groups were trained for 30 min per day, five days per week, for four weeks. The urine samples were collected pre and post the training program, and analyzed by proton nuclear magnetic resonance (1H-NMR) spectroscopy. RESULTS: Both types of training improved depression-like behavior in CUMS rats. Compared with normal control, 21 potential biomarkers were identified in the urine of CUMS rats, mainly involved in energy, amino acids and intestinal microbial metabolic pathways. Common responses to the training were found in the two exercise groups that the levels of glutamine, acetone and creatine were significantly recalled (all P<0.05) Aerobic training also resulted in changes in pyruvate and trigonelline, while resistance training modified α-Oxoglutarate, citric acid, and trimethylamine oxide (all P<0.05). CONCLUSIONS: Aerobic and resistance training resulted in common effects on the metabolic pathways of alanine-aspartate-glutamate, TCA cycle, and butyric acid. Aerobic training also had effects on glycolysis or gluconeogenesis and pyruvate metabolism, while resistance training had additional effect on intestinal microbial metabolism.


Assuntos
Metabolômica , Estresse Psicológico/metabolismo , Estresse Psicológico/urina , Aerobiose , Animais , Doença Crônica/psicologia , Metabolismo Energético , Masculino , Ratos , Ratos Sprague-Dawley , Treinamento de Resistência , Estresse Psicológico/fisiopatologia
3.
Nat Commun ; 11(1): 4218, 2020 08 24.
Artigo em Inglês | MEDLINE | ID: mdl-32839452

RESUMO

Exposure to social stress and dysregulated serotonergic neurotransmission have both been implicated in the etiology of psychiatric disorders. However, the serotonergic circuit involved in stress vulnerability is still unknown. Here, we explored whether a serotonergic input from the dorsal raphe (DR) to ventral tegmental area (VTA) influences vulnerability to social stress. We identified a distinct, anatomically and functionally defined serotonergic subpopulation in the DR that projects to the VTA (5-HTDR→VTA neurons). Moreover, we found that susceptibility to social stress decreased the firing activity of 5-HTDR→VTA neurons. Importantly, the bidirectional manipulation of 5-HTDR→VTA neurons could modulate susceptibility to social stress. Our findings reveal that the activity of 5-HTDR→VTA neurons may be an essential factor in determining individual levels of susceptibility to social stress and suggest that targeting specific serotonergic circuits may aid the development of therapies for the treatment of stress-related disorders.


Assuntos
Núcleo Dorsal da Rafe/fisiologia , Vias Neurais/fisiologia , Neurônios Serotoninérgicos/fisiologia , Estresse Psicológico/fisiopatologia , Transmissão Sináptica/fisiologia , Área Tegmentar Ventral/fisiologia , Animais , Núcleo Dorsal da Rafe/citologia , Núcleo Dorsal da Rafe/metabolismo , Ácido Glutâmico/metabolismo , Proteínas Luminescentes/genética , Proteínas Luminescentes/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Microscopia Confocal , Neurônios Serotoninérgicos/citologia , Neurônios Serotoninérgicos/metabolismo , Serotonina/metabolismo , Área Tegmentar Ventral/citologia , Área Tegmentar Ventral/metabolismo
5.
JAMA Netw Open ; 3(7): e2014053, 2020 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-32609353

RESUMO

Importance: People exposed to coronavirus disease 2019 (COVID-19) and a series of imperative containment measures could be psychologically stressed, yet the burden of and factors associated with mental health symptoms remain unclear. Objective: To investigate the prevalence of and risk factors associated with mental health symptoms in the general population in China during the COVID-19 pandemic. Design, Setting, and Participants: This large-sample, cross-sectional, population-based, online survey study was conducted from February 28, 2020, to March 11, 2020. It involved all 34 province-level regions in China and included participants aged 18 years and older. Data analysis was performed from March to May 2020. Main Outcomes and Measures: The prevalence of symptoms of depression, anxiety, insomnia, and acute stress among the general population in China during the COVID-19 pandemic was evaluated using the Patient Health Questionnaire-9, Generalized Anxiety Disorder-7, Insomnia Severity Index, and Acute Stress Disorder Scale. Logistic regression analyses were used to explore demographic and COVID-19-related risk factors. Results: Of 71 227 individuals who clicked on the survey link, 56 932 submitted the questionnaires, for a participation rate of 79.9%. After excluding the invalid questionnaires, 56 679 participants (mean [SD] age, 35.97 [8.22] years; 27 149 men [47.9%]) were included in the study; 39 468 respondents (69.6%) were aged 18 to 39 years. During the COVID-19 pandemic, the rates of mental health symptoms among the survey respondents were 27.9% (95% CI, 27.5%-28.2%) for depression, 31.6% (95% CI, 31.2%-32.0%) for anxiety, 29.2% (95% CI, 28.8%-29.6%) for insomnia, and 24.4% (95% CI, 24.0%-24.7%) for acute stress. Participants with confirmed or suspected COVID-19 and their family members or friends had a high risk for symptoms of depression (adjusted odds ratios [ORs], 3.27 [95% CI, 1.84-5.80] for patients; 1.53 [95% CI, 1.26-1.85] for family or friends), anxiety (adjusted ORs, 2.48 [95% CI, 1.43-4.31] for patients; 1.53 [95% CI, 1.27-1.84] for family or friends), insomnia (adjusted ORs, 3.06 [95% CI, 1.73-5.43] for patients; 1.62 [95% CI, 1.35-1.96] for family or friends), and acute stress (adjusted ORs, 3.50 [95% CI, 2.02-6.07] for patients; 1.77 [95% CI, 1.46-2.15] for family or friends). Moreover, people with occupational exposure risks and residents in Hubei province had increased odds of symptoms of depression (adjusted ORs, 1.96 [95% CI, 1.77-2.17] for occupational exposure; 1.42 [95% CI, 1.19-1.68] for Hubei residence), anxiety (adjusted ORs, 1.93 [95% CI, 1.75-2.13] for occupational exposure; 1.54 [95% CI, 1.30-1.82] for Hubei residence), insomnia (adjusted ORs, 1.60 [95% CI, 1.45-1.77] for occupational exposure; 1.20 [95% CI, 1.01-1.42] for Hubei residence), and acute stress (adjusted ORs, 1.98 [95% CI, 1.79-2.20] for occupational exposure; 1.49 [95% CI, 1.25-1.79] for Hubei residence). Both centralized quarantine (adjusted ORs, 1.33 [95% CI, 1.10-1.61] for depression; 1.46 [95% CI, 1.22-1.75] for anxiety; 1.63 [95% CI, 1.36-1.95] for insomnia; 1.46 [95% CI, 1.21-1.77] for acute stress) and home quarantine (adjusted ORs, 1.30 [95% CI, 1.25-1.36] for depression; 1.28 [95% CI, 1.23-1.34] for anxiety; 1.24 [95% CI, 1.19-1.30] for insomnia; 1.29 [95% CI, 1.24-1.35] for acute stress) were associated with the 4 negative mental health outcomes. Being at work was associated with lower risks of depression (adjusted OR, 0.85 [95% CI, 0.79-0.91]), anxiety (adjusted OR, 0.92 [95% CI, 0.86-0.99]), and insomnia (adjusted OR, 0.87 [95% CI, 0.81-0.94]). Conclusions and Relevance: The results of this survey indicate that mental health symptoms may have been common during the COVID-19 outbreak among the general population in China, especially among infected individuals, people with suspected infection, and people who might have contact with patients with COVID-19. Some measures, such as quarantine and delays in returning to work, were also associated with mental health among the public. These findings identify populations at risk for mental health problems during the COVID-19 pandemic and may help in implementing mental health intervention policies in other countries and regions.


Assuntos
Ansiedade , Infecções por Coronavirus , Depressão , Pandemias , Pneumonia Viral , Distúrbios do Início e da Manutenção do Sono , Estresse Psicológico , Adulto , Ansiedade/diagnóstico , Ansiedade/epidemiologia , Ansiedade/fisiopatologia , Betacoronavirus/isolamento & purificação , China/epidemiologia , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/psicologia , Depressão/diagnóstico , Depressão/epidemiologia , Depressão/fisiopatologia , Feminino , Humanos , Masculino , Saúde Mental/estatística & dados numéricos , Entrevista Psiquiátrica Padronizada/estatística & dados numéricos , Pneumonia Viral/diagnóstico , Pneumonia Viral/epidemiologia , Pneumonia Viral/psicologia , Prevalência , Quarentena/psicologia , Retorno ao Trabalho/psicologia , Fatores de Risco , Distúrbios do Início e da Manutenção do Sono/diagnóstico , Distúrbios do Início e da Manutenção do Sono/epidemiologia , Distúrbios do Início e da Manutenção do Sono/fisiopatologia , Estresse Psicológico/diagnóstico , Estresse Psicológico/epidemiologia , Estresse Psicológico/fisiopatologia
6.
Exp Psychol ; 67(2): 132-139, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32729402

RESUMO

Acute stress and chronic stress change the physiology and function of the individual. As one facet, stress and its neuroendocrine correlates - with glucocorticoids in particular - modulate memory in a concerted action. With respect to working memory, impairing effects of acute stress and increased levels of glucocorticoids could be expected, but empirical evidence on moderating effects of cortisol on working memory is ambiguous in human studies. In the current study, we thus aimed to investigate cortisol stress responses and memory performance. Older men and women (32 men, 43 women, aged 61-67 years) underwent the Trier Social Stress Test (TSST) and performed the 2-back task before and after exposure to acute stress. In line with theoretical assumptions, we found that higher cortisol stress responses led to a decline of working memory performance in men. However, the opposite was evident for women, who appeared to benefit from higher stress responses. This effect was evident for accuracy, but not for reaction time. In conclusion, cortisol might mediate working memory alterations with stress in a sex-specific manner in older people. Possible mechanisms and causes for these sex differences put a focus on endocrine changes in the aging population that might lead to differential effects across the lifespan.


Assuntos
Memória de Curto Prazo/fisiologia , Estresse Psicológico/fisiopatologia , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
7.
Neuroscientist ; 26(5-6): 402-414, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32684080

RESUMO

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new pandemic infectious disease that originated in China. COVID-19 is a global public health emergency of international concern. COVID-19 causes mild to severe illness with high morbidity and mortality, especially in preexisting risk groups. Therapeutic options are now limited to COVID-19. The hallmark of COVID-19 pathogenesis is the cytokine storm with elevated levels of interleukin-6 (IL-6), IL-1ß, tumor necrosis factor-alpha (TNF-α), chemokine (C-C-motif) ligand 2 (CCL2), and granulocyte-macrophage colony-stimulating factor (GM-CSF). COVID-19 can cause severe pneumonia, and neurological disorders, including stroke, the damage to the neurovascular unit, blood-brain barrier disruption, high intracranial proinflammatory cytokines, and endothelial cell damage in the brain. Mast cells are innate immune cells and also implicated in adaptive immune response, systemic inflammatory diseases, neuroinflammatory diseases, traumatic brain injury and stroke, and stress disorders. SARS-CoV-2 can activate monocytes/macrophages, dendritic cells, T cells, mast cells, neutrophils, and induce cytokine storm in the lung. COVID-19 can activate mast cells, neurons, glial cells, and endothelial cells. SARS-CoV-2 infection can cause psychological stress and neuroinflammation. In conclusion, COVID-19 can induce mast cell activation, psychological stress, cytokine storm, and neuroinflammation.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/fisiopatologia , Citocinas/imunologia , Mastócitos/imunologia , Doenças do Sistema Nervoso/imunologia , Pneumonia Viral/imunologia , Pneumonia Viral/fisiopatologia , Estresse Psicológico/fisiopatologia , Infecções por Coronavirus/complicações , Humanos , Mastócitos/virologia , Doenças do Sistema Nervoso/complicações , Pandemias , Pneumonia Viral/complicações
8.
Diabetes Metab Syndr ; 14(5): 1043-1051, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32640416

RESUMO

INTRODUCTION: There have been recent mounting concerns regarding multiple reports stating a significantly elevated relative-risk of COVID-19 mortality amongst the Black and Minority Ethnic (BAME) population. An urgent national enquiry investigating the possible reasons for this phenomenon has been issued in the UK. Inflammation is at the forefront of COVID-19 research as disease severity appears to correlate with pro-inflammatory cytokine dysregulation. This narrative review aims to shed light on the novel, pathophysiological role of inflammation in contributing towards the increased COVID-19 mortality risk amongst the BAME population. METHODS: Searches in PubMed, Medline, Scopus, medRxiv and Google Scholar were performed to identify articles published in English from inception to 18th June 2020. These databases were searched using keywords including: 'COVID-19' or 'Black and Minority Ethnic' or 'Inflammation'. A narrative review was synthesized using these included articles. RESULTS: We suggest a novel pathophysiological mechanism by which acute inflammation from COVID-19 may augment existing chronic inflammation, in order to potentiate a 'cytokine storm' and thus the more severe disease phenotype observed in the BAME population. Obesity, insulin resistance, cardiovascular disease, psychological stress, chronic infections and genetic predispositions are all relevant factors which may be contributing to elevated chronic systemic inflammation amongst the BAME population. CONCLUSION: Overall, this review provides early insights and directions for ongoing research regarding the pathophysiological mechanisms that may explain the severe COVID-19 disease phenotype observed amongst the BAME population. We suggest 'personalization' of chronic disease management, which can be used with other interventions, in order to tackle this.


Assuntos
Betacoronavirus/isolamento & purificação , Doenças Cardiovasculares/fisiopatologia , Infecções por Coronavirus/mortalidade , Grupos Étnicos/estatística & dados numéricos , Infecções/fisiopatologia , Inflamação/epidemiologia , Obesidade/fisiopatologia , Pneumonia Viral/mortalidade , Estresse Psicológico/fisiopatologia , Infecções por Coronavirus/fisiopatologia , Infecções por Coronavirus/virologia , Humanos , Incidência , Inflamação/virologia , Pandemias , Pneumonia Viral/fisiopatologia , Pneumonia Viral/virologia , Taxa de Sobrevida , Reino Unido/epidemiologia
9.
Life Sci ; 258: 118107, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32682919

RESUMO

Cognitive impairment has been widely recognized as a common symptom of chronic stress. Ginsenoside Rd (GRd), the major active compound in Panax ginseng, was previously reported in various neurological researches. However, little research is available regarding on the effect of GRd on cognitive improvement in mice subjected to chronic stress. In the present study, we investigated the neuroprotective effects of GRd in chronic restraint stress (CRS)-induced cognitive deficits and explored the potential mechanism in male C57BL/6J mice. Our results demonstrated that oral administration of GRd for 28 days markedly increased the spontaneous alternation in Y-maze and the relative discrimination index in novel object or location recognition tests following CRS. Additionally, GRd treatment considerably increased the antioxidant enzymes activities in the hippocampus. The expression levels of hippocampus and serum inflammation factors in the CRS groups were also counter-regulated by GRd treatment. Meanwhile, GRd treatment could reverse CRS-induced the decrease in phosphorylated phosphoinositide 3-kinase (PI3K), camp-reflecting element binding protein (CREB), brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) expression in the hippocampus. These findings provided evidences that GRd improves cognitive impairment in CRS mice by mitigating oxidative stress and inflammation, while upregulating the hippocampal BDNF-mediated CREB signaling pathway.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/metabolismo , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Ginsenosídeos/uso terapêutico , Restrição Física , Transdução de Sinais , Estresse Psicológico/tratamento farmacológico , Animais , Doença Crônica , Disfunção Cognitiva/sangue , Disfunção Cognitiva/fisiopatologia , Modelos Animais de Doenças , Ginsenosídeos/química , Ginsenosídeos/farmacologia , Hipocampo/efeitos dos fármacos , Hipocampo/enzimologia , Hipocampo/patologia , Hipocampo/fisiopatologia , Inflamação/sangue , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Memória de Curto Prazo/efeitos dos fármacos , Camundongos Endogâmicos C57BL , Modelos Biológicos , Atividade Motora/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Receptor trkB/metabolismo , Transdução de Sinais/efeitos dos fármacos , Estresse Psicológico/sangue , Estresse Psicológico/fisiopatologia
10.
Adv Pharmacol ; 89: 163-194, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32616206

RESUMO

A paradigm shift in the conceptualization of the neurobiology of depression and the serendipitous discovery of ketamine's rapid-acting antidepressant (RAAD) effects has ushered in a new era of innovative research and novel drug development. Since the initial discovery of ketamine's RAAD effects, multiple studies have supported its short-term efficacy for fast-tracked improvements in treatment-resistant depression. Evidence from MRI studies have repeatedly demonstrated functional connectivity alterations in stress- and trauma-related disorders suggesting this may be a viable biomarker of chronic stress pathology (CSP). Human mechanistic studies further support this by coupling functional connectivity to ketamine's RAAD effects including connectivity to glutamate neurotransmission, ketamine to normalized connectivity, and these advantageous normalizations to symptom improvement/ketamine response. This review provides an abridged discussion of the suspected neurobiological underpinnings of ketamine's RAAD effects, highlighting ketamine-induced alterations in prefrontal, striatal, and anterior cingulate cortex functional connectivity in major depressive disorder. We present a model of CSP underscoring the role of synaptic loss and dysconnectivity and discuss how ketamine may be used both as (1) a treatment to restore and normalize these stress-induced neural alterations and (2) a tool to study potential biomarkers of CSP and treatment response. We conclude by noting challenges and future directions including heterogeneity, sex differences, the role of early life stress, and the need for proliferation of new methods, paradigms, and tools that will optimize signal and allow analyses at different levels of complexity, according to the needs of the question at hand, perhaps by thinking hierarchically about both clinical and biological phenotypes.


Assuntos
Transtorno Depressivo Maior/tratamento farmacológico , Transtorno Depressivo Maior/fisiopatologia , Ketamina/uso terapêutico , Rede Nervosa/fisiopatologia , Estresse Psicológico/fisiopatologia , Antidepressivos/farmacologia , Antidepressivos/uso terapêutico , Doença Crônica , Humanos , Ketamina/farmacologia
11.
Am J Physiol Heart Circ Physiol ; 319(2): H488-H506, 2020 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-32618516

RESUMO

Although chronic stress is an important risk factor for cardiovascular diseases (CVD) onset, the underlying mechanisms driving such pathophysiological complications remain relatively unknown. Here, dysregulation of innate stress response systems and the effects of downstream mediators are strongly implicated, with the vascular endothelium emerging as a primary target of excessive glucocorticoid and catecholamine action. Therefore, this review article explores the development of stress-related endothelial dysfunction by focusing on the following: 1) assessing the phenomenon of stress and complexities surrounding this notion, 2) discussing mechanistic links between chronic stress and endothelial dysfunction, and 3) evaluating the utility of various preclinical models currently employed to study mechanisms underlying the onset of stress-mediated complications such as endothelial dysfunction. The data reveal that preclinical models play an important role in our efforts to gain an increased understanding of mechanisms underlying stress-mediated endothelial dysfunction. It is our understanding that this provides a good foundation going forward, and we propose that further efforts should be made to 1) more clearly define the concept of stress and 2) standardize protocols of animal models with specific guidelines to better indicate the mental complications that are simulated.


Assuntos
Doenças Cardiovasculares/etiologia , Endotélio Vascular/fisiopatologia , Estresse Psicológico/complicações , Animais , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Doenças Cardiovasculares/psicologia , Catecolaminas/metabolismo , Doença Crônica , Modelos Animais de Doenças , Endotélio Vascular/metabolismo , Glucocorticoides/metabolismo , Humanos , Sistema Hipotálamo-Hipofisário/metabolismo , Sistema Hipotálamo-Hipofisário/fisiopatologia , Fatores de Risco , Transdução de Sinais , Estresse Psicológico/metabolismo , Estresse Psicológico/fisiopatologia , Estresse Psicológico/psicologia
12.
Encephale ; 46(3S): S93-S98, 2020 Jun.
Artigo em Francês | MEDLINE | ID: mdl-32507556

RESUMO

Although the "panic" word has been abundantly linked to the SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) pandemic in the press, in the scientific literature very few studies have considered whether the current epidemic could predispose to the onset or the aggravation of panic attacks or panic disorder. Indeed, most studies thus far have focused on the risk of increase and aggravation of other psychiatric disorders as a consequence of the SARS-CoV-2 epidemic, such as obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and generalized anxiety disorder (GAD). Yet, risk of onset or aggravation of panic disorder, especially the subtype with prominent respiratory symptoms, which is characterized by a fear response conditioning to interoceptive sensations (e.g., respiratory), and hypervigilance to these interoceptive signals, could be expected in the current situation. Indeed, respiratory symptoms, such as coughs and dyspnea, are among the most commonly associated with the SARS-CoV-2 (59-82% and 31-55%, respectively), and respiratory symptoms are associated with a poor illness prognosis. Hence given that some etiological and maintenance factors associated with panic disorder - i.e., fear conditioning to abnormal breathing patterns attributable or not to the COVID-19 (coronavirus disease 2019), as well as hypervigilance towards breathing abnormalities - are supposedly more prevalent, one could expect an increased risk of panic disorder onset or aggravation following the COVID-19 epidemic in people who were affected by the virus, but also those who were not. In people with the comorbidity (i.e., panic disorder or panic attacks and the COVID-19), it is particularly important to be aware of the risk of hypokalemia in specific at-risk situations or prescriptions. For instance, in the case of salbutamol prescription, which might be overly used in patients with anxiety disorders and COVID-19, or in patients presenting with diarrhea and vomiting. Hypokalemia is associated with an increased risk of torsade de pointe, thus caution is required when prescribing specific psychotropic drugs, such as the antidepressants citalopram and escitalopram, which are first-line treatments for panic disorder, but also hydroxyzine, aiming at anxiety reduction. The results reviewed here highlight the importance of considering and further investigating the impact of the current pandemic on the diagnosis and treatment of panic disorder (alone or comorbid with the COVID-19).


Assuntos
Betacoronavirus , Infecções por Coronavirus/psicologia , Pandemias , Transtorno de Pânico/psicologia , Pneumonia Viral/psicologia , Ansiedade/etiologia , Ansiedade/psicologia , Transtornos de Ansiedade/tratamento farmacológico , Transtornos de Ansiedade/epidemiologia , Transtornos de Ansiedade/fisiopatologia , Transtornos de Ansiedade/psicologia , Catastrofização , Comorbidade , Infecções por Coronavirus/epidemiologia , Dispneia/etiologia , Dispneia/psicologia , Feminino , Humanos , Hipopotassemia/etiologia , Masculino , Transtorno de Pânico/tratamento farmacológico , Transtorno de Pânico/epidemiologia , Transtorno de Pânico/fisiopatologia , Pneumonia Viral/epidemiologia , Psicotrópicos/efeitos adversos , Psicotrópicos/uso terapêutico , Sistema Renina-Angiotensina/fisiologia , Respiração/efeitos dos fármacos , Estresse Psicológico/etiologia , Estresse Psicológico/fisiopatologia , Terminologia como Assunto , Torsades de Pointes/induzido quimicamente , Torsades de Pointes/etiologia
13.
PLoS One ; 15(6): e0235412, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32589644

RESUMO

Exposure to early life adversity is associated with chronic stress and a range of stress-related health problems in adulthood. Since chronic stress debilitates activity in the prefrontal cortex (pFC), maladaptive regulatory strategies in response to stress have been proposed as one explanation for the impact of early life adversity on health outcomes in adulthood. We conducted a study to examine the impact of adverse childhood experiences (ACEs) on cognitive flexibility, a key executive function implicated in activity in the pFC, in a sample of adults (N = 486). Additionally, we investigated whether perceptions of chronic stress in adulthood would mediate the influence of ACEs on cognitive flexibility. However, stress is a subjective experience, and emotion regulation strategies can attenuate the stress response. So, we also examined if individual differences in emotion regulation strategies would modulate the relationship between ACEs and chronic stress. Our results demonstrate that early life adversity, as characterized by ACEs, is associated with decreased cognitive flexibility in adulthood. Additionally, number of ACEs was positively correlated with perceived stress, which in turn was negatively correlated with cognitive flexibility. But, individual differences in the habitual use of emotion regulation strategies moderated the influence of ACEs on chronic stress. Specifically, habitual use of cognitive reappraisal attenuated the stress levels whereas habitual use of expressive suppression exacerbated stress levels. Overall, our study highlights the importance of examining emotion regulation in individuals who have experienced early life adversity.


Assuntos
Experiências Adversas da Infância , Cognição , Regulação Emocional , Percepção , Estresse Psicológico/fisiopatologia , Estresse Psicológico/psicologia , Adulto , Criança , Doença Crônica/psicologia , Feminino , Humanos , Masculino
14.
PLoS One ; 15(6): e0235046, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32579566

RESUMO

Post-ictal emergence of slow wave EEG (electroencephalogram) activity and burst-suppression has been associated with the therapeutic effects of the electroconvulsive therapy (ECT), indicating that mere "cerebral silence" may elicit antidepressant actions. Indeed, brief exposures to burst-suppressing anesthesia has been reported to elicit antidepressant effects in a subset of patients, and produce behavioral and molecular alterations, such as increased expression of brain-derived neurotrophic factor (BDNF), connected with antidepressant responses in rodents. Here, we have further tested the cerebral silence hypothesis by determining whether repeated exposures to isoflurane anesthesia reduce depressive-like symptoms or influence BDNF expression in male Wistar outbred rats (Crl:WI(Han)) subjected to chronic mild stress (CMS), a model which is responsive to repeated electroconvulsive shocks (ECS, a model of ECT). Stress-susceptible, stress-resilient, and unstressed rats were exposed to 5 doses of isoflurane over a 15-day time period, with administrations occurring every third day. Isoflurane dosing is known to reliably produce rapid EEG burst-suppression (4% induction, 2% maintenance; 15 min). Antidepressant and anxiolytic effects of isoflurane were assessed after the first, third, and fifth drug exposure by measuring sucrose consumption, as well as performance on the open field and the elevated plus maze tasks. Tissue samples from the medial prefrontal cortex and hippocampus were collected, and levels of BDNF (brain-derived neurotrophic factor) protein were assessed. We find that isoflurane anesthesia had no impact on the behavior of stress-resilient or anhedonic rats in selected tests; findings which were consistent-perhaps inherently related-with unchanged levels of BDNF.


Assuntos
Antidepressivos/farmacologia , Transtorno Depressivo/prevenção & controle , Isoflurano/farmacologia , Estresse Psicológico/prevenção & controle , Anestésicos Inalatórios , Animais , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Transtorno Depressivo/etiologia , Transtorno Depressivo/fisiopatologia , Modelos Animais de Doenças , Eletroconvulsoterapia/métodos , Eletroencefalografia , Eletrochoque/efeitos adversos , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Hipocampo/fisiopatologia , Humanos , Isoflurano/administração & dosagem , Masculino , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/metabolismo , Córtex Pré-Frontal/fisiopatologia , Ratos Wistar , Estresse Psicológico/etiologia , Estresse Psicológico/fisiopatologia
15.
J Vis Exp ; (159)2020 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-32510516

RESUMO

The insulin tolerance test is commonly used in metabolic studies to assess whole body insulin sensitivity in rodents. It is a relatively simple test that involves measurement of blood glucose levels over time following a single intraperitoneal injection of insulin. Given that it is performed in the conscious state and blood is often collected via a tail snip, it has the potential to elicit a stress response from animals due to anxiety associated with handling and blood collection. As such, a stress-induced rise in blood glucose can occur, making it difficult to detect and interpret the primary endpoint measure, namely an insulin-mediated reduction in blood glucose. This has been seen in many mouse strains, and is quite common in diabetic db/db mice, where glucose levels can increase, rather than decrease, after insulin administration. Here, we describe a method of acclimating mice to handling, injections and blood sampling prior to performing the insulin tolerance test. We find that this lowers stress-induced hyperglycemia and results in data that more accurately reflects whole body insulin sensitivity.


Assuntos
Aclimatação , Artefatos , Hiperglicemia/metabolismo , Hiperglicemia/psicologia , Resistência à Insulina , Estresse Psicológico/complicações , Estresse Psicológico/fisiopatologia , Animais , Glicemia/metabolismo , Hiperglicemia/sangue , Hiperglicemia/complicações , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos
16.
Curr Opin Gastroenterol ; 36(4): 295-303, 2020 07.
Artigo em Inglês | MEDLINE | ID: covidwho-257910

RESUMO

PURPOSE OF REVIEW: The world is experiencing the evolving situation associated with the outbreak of the Corona Virus Disease-2019 (COVID-19) virus, and there is more of need than ever for stress management and self-care. In this article, we will define the physiological, psychological and social aspects, stages, and components of stress reactions in the context of COVID-19, review the relevant literature on stress reactions, and offer some guidance on how to help patients mitigate the physiological and psychological impact of the pandemic through resilience-building techniques. RECENT FINDINGS: There is continued evidence that the fight or flight response involves activation throughout the body at physiological, biochemical and immune levels. This response can be mitigated through increasing parasympathetic nervous system activation as well as cognitive and behavioral interventions. SUMMARY: This article will review the stress, provide a theoretical layout to predict upcoming response, and offer clinicians some practical interventions to employ as the stress of the COVID-19 pandemic continues.


Assuntos
Infecções por Coronavirus/psicologia , Pneumonia Viral/psicologia , Resiliência Psicológica , Estresse Psicológico/terapia , Infecções por Coronavirus/epidemiologia , Gastroenteropatias/prevenção & controle , Gastroenteropatias/psicologia , Trato Gastrointestinal/patologia , Humanos , Sistemas Neurossecretores/fisiopatologia , Pandemias , Pneumonia Viral/epidemiologia , Terapia de Relaxamento , Autocuidado , Estresse Fisiológico , Estresse Psicológico/fisiopatologia
19.
Psychol Trauma ; 12(S1): S255-S257, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32463284

RESUMO

In this commentary we discuss a downstream consequence of increases in stress and anxiety during the COVID-19 pandemic. Stress and anxiety can lead to mind wandering, which in turn competes for limited cognitive resources. We encourage researchers to be understanding and patient concerning the inevitable cognitive impact of the pandemic and subsequent reduced productivity levels from our students, colleagues, and ourselves. (PsycInfo Database Record (c) 2020 APA, all rights reserved).


Assuntos
Ansiedade/fisiopatologia , Atenção/fisiologia , Disfunção Cognitiva/fisiopatologia , Infecções por Coronavirus , Função Executiva/fisiologia , Pandemias , Pneumonia Viral , Psicoterapia , Estresse Psicológico/fisiopatologia , Adulto , Eficiência , Humanos , Atenção Plena , Estudantes , Universidades , Adulto Jovem
20.
Curr Opin Gastroenterol ; 36(4): 295-303, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32398567

RESUMO

PURPOSE OF REVIEW: The world is experiencing the evolving situation associated with the outbreak of the Corona Virus Disease-2019 (COVID-19) virus, and there is more of need than ever for stress management and self-care. In this article, we will define the physiological, psychological and social aspects, stages, and components of stress reactions in the context of COVID-19, review the relevant literature on stress reactions, and offer some guidance on how to help patients mitigate the physiological and psychological impact of the pandemic through resilience-building techniques. RECENT FINDINGS: There is continued evidence that the fight or flight response involves activation throughout the body at physiological, biochemical and immune levels. This response can be mitigated through increasing parasympathetic nervous system activation as well as cognitive and behavioral interventions. SUMMARY: This article will review the stress, provide a theoretical layout to predict upcoming response, and offer clinicians some practical interventions to employ as the stress of the COVID-19 pandemic continues.


Assuntos
Infecções por Coronavirus/psicologia , Pneumonia Viral/psicologia , Resiliência Psicológica , Estresse Psicológico/terapia , Infecções por Coronavirus/epidemiologia , Gastroenteropatias/prevenção & controle , Gastroenteropatias/psicologia , Trato Gastrointestinal/patologia , Humanos , Sistemas Neurossecretores/fisiopatologia , Pandemias , Pneumonia Viral/epidemiologia , Terapia de Relaxamento , Autocuidado , Estresse Fisiológico , Estresse Psicológico/fisiopatologia
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