scholarly journals The role of glucocorticoids and corticotropin-releasing hormone regulation on anxiety symptoms and response to treatment

2017 ◽  
Vol 6 (2) ◽  
pp. R1-R7 ◽  
Author(s):  
Greta B Raglan ◽  
Louis A Schmidt ◽  
Jay Schulkin

The stress response has been linked to the expression of anxiety and depression, but the mechanisms for these connections are under continued consideration. The activation and expression of glucocorticoids and CRH are variable and may hold important clues to individual experiences of mood disorders. This paper explores the interactions of glucocorticoids and CRH in the presentation of anxiety and depressive disorders in an effort to better describe their differing roles in each of these clinical presentations. In addition, it focuses on ways in which extra-hypothalamic glucocorticoids and CRH, often overlooked, may play important roles in the presentation of clinical disorders.

2019 ◽  
Vol 9 (4) ◽  
pp. 76 ◽  
Author(s):  
Katherine Young ◽  
Christina Sandman ◽  
Michelle Craske

Emotion regulation skills develop substantially across adolescence, a period characterized by emotional challenges and developing regulatory neural circuitry. Adolescence is also a risk period for the new onset of anxiety and depressive disorders, psychopathologies which have long been associated with disruptions in regulation of positive and negative emotions. This paper reviews the current understanding of the role of disrupted emotion regulation in adolescent anxiety and depression, describing findings from self-report, behavioral, peripheral psychophysiological, and neural measures. Self-report studies robustly identified associations between emotion dysregulation and adolescent anxiety and depression. Findings from behavioral and psychophysiological studies are mixed, with some suggestion of specific impairments in reappraisal in anxiety. Results from neuroimaging studies broadly implicate altered functioning of amygdala-prefrontal cortical circuitries, although again, findings are mixed regarding specific patterns of altered neural functioning. Future work may benefit from focusing on designs that contrast effects of specific regulatory strategies, and isolate changes in emotional regulation from emotional reactivity. Approaches to improve treatments based on empirical evidence of disrupted emotion regulation in adolescents are also discussed. Future intervention studies might consider training and measurement of specific strategies in adolescents to better understand the role of emotion regulation as a treatment mechanism.


2019 ◽  
Author(s):  
Katherine Seaton Young ◽  
Christina F Sandman ◽  
Michelle G. Craske

Emotion regulation skills develop substantially across adolescence, a period characterized by emotional challenges and developing regulatory neural circuitry. Adolescence is also a risk period for the new onset of anxiety and depressive disorders, psychopathologies which have long been associated with disruptions in regulation of positive and negative emotions. This paper reviews current understanding of the role of disrupted emotion regulation in adolescent anxiety and depression, describing findings from self-report, behavioral, peripheral psychophysiological and neural measures. Self-report studies robustly identified associations between emotion dysregulation and adolescent anxiety and depression. Findings from behavioral and psychophysiological studies are mixed, with some suggestion of specific impairments in reappraisal in anxiety. Results from neuroimaging studies broadly implicate altered functioning of amygdala-prefrontal cortical circuitries, although again, findings are mixed regarding specific patterns of neural functioning. Future work may benefit from focusing on designs that contrast effects of specific regulatory strategies, and isolate changes in emotional regulation from emotional reactivity. Greater integration of multiple measures within the same study would also facilitate more reliable evidence of effects observed. Future intervention studies might consider training and measurement of specific strategies in adolescents to better understand the role of emotion regulation as a treatment mechanism.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mareike Ernst ◽  
Antonia M. Werner ◽  
Ana N. Tibubos ◽  
Manfred E. Beutel ◽  
Martina de Zwaan ◽  
...  

Background: Evidence shows that anxiety and depressive disorders play an important role in eating disorder behavior. However, given the epidemiology of eating disorders, there is a need to investigate potentially gender-specific connections.Method: This study tested the associations of anxiety and depression symptoms with eating disorder symptoms and behaviors and explored whether they differed between men and women. Within a population-representative survey (N = 2,510; ages 14–94), participants completed measures of depression symptoms (PHQ-2), anxiety symptoms (GAD-2), and eating disorder symptoms (EDE-Q8). We conducted linear regression analyses of the EDE-Q8 sum score and General Linear Models on the three behaviors overeating, binge eating, and compensatory behaviors (self-induced vomiting/use of laxatives/excessive exercising).Results: Depression and anxiety symptoms were related to more eating disorder symptoms in men and women (irrespective of BMI, age, and income). The association of depression and eating disorder symptoms was slightly stronger in women. Overeating was more common in men and in depressed individuals, whereas compensatory behaviors were more common among anxious individuals, especially anxious women.Conclusion: The study extends previous research by using gender-specific methods in a representative sample. It indicates similarities and differences between men and women regarding disordered eating on a population level.


Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1382
Author(s):  
Lih-Fhung Hiew ◽  
Chi-Him Poon ◽  
Heng-Ze You ◽  
Lee-Wei Lim

TGF-β/Smad signalling has been the subject of extensive research due to its role in the cell cycle and carcinogenesis. Modifications to the TGF-β/Smad signalling pathway have been found to produce disparate effects on neurogenesis. We review the current research on canonical and non-canonical TGF-β/Smad signalling pathways and their functions in neurogenesis. We also examine the observed role of neurogenesis in neuropsychiatric disorders and the relationship between TGF-β/Smad signalling and neurogenesis in response to stressors. Overlapping mechanisms of cell proliferation, neurogenesis, and the development of mood disorders in response to stressors suggest that TGF-β/Smad signalling is an important regulator of stress response and is implicated in the behavioural outcomes of mood disorders.


2021 ◽  
pp. 1-10
Author(s):  
Fiammetta Cosci ◽  
Giovanni A. Fava

Depressive and anxiety disorders are frequently associated. Depression may be a complication of anxiety and anxiety can complicate depression. The nature of their relationship has been a source of controversy. Reviews generally base their conclusions on randomized controlled trials and meta-analyses that refer to the average patient and often clash with the variety of clinical presentations that may occur when anxiety and depression coexist. The aim of this review was to examine the literature according to profiling of subgroups of patients based on clinimetric criteria, in line with the recently developed concept of medicine-based evidence. We critically reviewed the literature pertaining to the specific presentations of anxiety and depression, outlining the advantages and disadvantages of each treatment approach. The following prototypic cases were presented: depression secondary to an active anxiety disorder, depression in patients with anxiety disorders under treatment, anxious depression, anxiety as a residual component of depression, and demoralization secondary to anxiety disorder. We argue that the selection of treatment when anxiety and depression coexist should take into account the modalities of presentation and be filtered by clinical judgment. Very different indications may ensue when the literature is examined according to this perspective.


2017 ◽  
Vol 28 (3) ◽  
pp. 219-233 ◽  
Author(s):  
Anton S. Tsybko ◽  
Tatiana V. Ilchibaeva ◽  
Nina K. Popova

AbstractGlial cell line-derived neurotrophic factor (GDNF) is widely recognized as a survival factor for dopaminergic neurons, but GDNF has also been shown to promote development, differentiation, and protection of other central nervous system neurons and was thought to play an important role in various neuropsychiatric disorders. Severe mood disorders, such as primarily major depressive disorder and bipolar affective disorder, attract particular attention. These psychopathologies are characterized by structural alterations accompanied by the dysregulation of neuroprotective and neurotrophic signaling mechanisms required for the maturation, growth, and survival of neurons and glia. The main objective of this review is to summarize the recent findings and evaluate the potential role of GDNF in the pathogenesis and treatment of mood disorders. Specifically, it describes (1) the implication of GDNF in the mechanism of depression and in the effect of antidepressant drugs and mood stabilizers and (2) the interrelation between GDNF and brain neurotransmitters, playing a key role in the pathogenesis of depression. This review provides converging lines of evidence that (1) brain GDNF contributes to the mechanism underlying depressive disorders and the effect of antidepressants and mood stabilizers and (2) there is a cross-talk between GDNF and neurotransmitters representing a feedback system: GDNF-neurotransmitters and neurotransmitters-GDNF.


2021 ◽  
Vol 12 ◽  
Author(s):  
Valery Krupnik

Depressive, anxiety, and trauma-related disorders have many symptoms in common such as unstable mood, high anxiety, sleep disturbance, impaired concentration among others. This degeneracy creates ambiguity in classifying psychiatric disorders and raises the question of their categorical vs. dimensional nature. Consequently, such ambiguity presents a dilemma for choosing diagnosis-specific vs. trans-diagnostic therapies. In this paper, I build on a theory that considers affective disorders on the continuum of stress response from normative to traumatic. Using an integrative evolutionary-stress response-predictive processing (iESP) model, I arrange affective disorders on a continuum of precision-weighting dysregulation, where depressive, anxiety and trauma-induced disorders have a characteristic pattern of precision-weighting dysregulation. I specifically address the relationship between anxiety and depressive stress responses, exploring the role of anxiety in the dynamics of depressive stress response and the resulting high co-occurrence of anxiety and depression symptoms. Finally, I discuss the model's relevance for therapy of depression.


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
K Mzoughi ◽  
I Zairi ◽  
A Saadaoui ◽  
I Ben Mrad ◽  
S Kraiem

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Anxio-depressive disorders represent one of the psychiatric manifestations most frequently observed in hospitalized patients. Different factors can be involved in the onset or worsening of these disorders. Purpose The aim of our study was to evaluate the prevalence of of anxiety and depression in hospitalized cardiology patients and to determine their predictors. Methods This was a cross-sectional and descriptive study with a prospective data collection that included 150 patients hospitalized in the cardiology department of Habib Thameur hospital between November and December 2016. Anxiety and depression were assessed using the Hospital Anxiety Depression questionnaire validated in Arabic. Results Patients mean age was 60 ± 11.2 years with a gender ratio of 2.7. Seventy-nine percent of the patients had a school education, 85.3% were married and 46% were active workers. Cardiovascular risk factors were dominated by arterial hypertension found in 56.7% of patients, followed by diabetes in 55.3%, dyslipidemia in 54.7% and active smoking in 43.3%. The most frequent reason for hospitalization was acute coronary syndrome, which was found in 52.7% of cases. The mean length of hospital stay was 13.7 ± 9.3 days. The prevalence of anxiety symptoms and depression symptoms was 55.3% and 40%, respectively. In multivariate analysis, age over 65 and active smoking were significantly associated with anxiety symptoms (OR = 0.345, 95% CI 0.150-0.790; p = 0.012 and OR = 0.44, 95% CI, respectively 0.194-0.90; p = 0.045). Independent factors significantly associated with depression symptoms in hospitalized cardiology patients were age greater than 65 years and a hospital stay of more than 7 days (OR = 0.171, respectively, 95% CI 0.067-0.438; p = 0.0001 and OR = 0.462, 95% CI 0.08-0.466; p = 0.001). Conclusion Given the high prevalence of anxiety and depression in patients hospitalized in cardiology, the systematic identification of the factors associated with these disorders would facilitate screening and ensure their early management.


In pathogenesis of the depressed disorders with suicidal behavior an important role belongs not only to мicro- and macrosocial factors but also to the pathology of genes encoding the neuron structures of the central nervous system, as the recent studies have shown. The most studied genes associated with the symptoms of anxiety and depression as well as suicidal behavior are the genes of the serotonin system, the so-called conveyers of serotonin: 5-HTT (SLC6A4), 5-HTR2A, 2a (HTR2A), 2С (HTR2C), TPH1 and ТРН2. The presented analytical review is devoted to the current genetic studies on etiology and dvelopment of depressive disorders with a suicidal behaviour.


2020 ◽  
Vol 24 (1) ◽  
pp. 81-112
Author(s):  
Ilpo Helén

This paper is an analysis of three elements of which depression as the primary target of current Western psychiatry and mental health care is made: the quest of psychiatrists to identify a depressive disease proper; the category of ‘major depression’ as defined by the diagnostic manuals; and the epidemiological view emphasising risk factors of depression. These elements are pivotal to the present understanding and experience of what depression is since they delineate the space of reasoning in which claims about depression are presented, problematised, and disputed. The paper presents how these elements have historically evolved and coalesced, and how depression has been formed and transformed as an object of knowledge and treatment in psychiatry and how the claims about depressive disorders acquire objectivity in the current mental health discussions. The paper also demonstrates how the quest of depression as a neurophysiological disease, consolidation of Major Depression as the diagnostic core of mood disorders, and the central role of the epidemiological notion of risk are both interlocked and discordant with each other in the current depression paradigm. In addition, tendencies of subversion of the depression paradigm are discussed.


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