scholarly journals Parental history of depression or anxiety and the cortisol awakening response

2010 ◽  
Vol 197 (3) ◽  
pp. 180-185 ◽  
Author(s):  
Sophie A. Vreeburg ◽  
Catharina A. Hartman ◽  
Witte J. G. Hoogendijk ◽  
Richard van Dyck ◽  
Frans G. Zitman ◽  
...  

BackgroundIt is unclear whether altered hypothalamic–pituitary–adrenal (HPA) axis regulation, which frequently accompanies depression and anxiety disorders, represents a trait rather than a state factor.AimsTo examine whether HPA axis dysregulation represents a biological vulnerability for these disorders, we compared cortisol levels in unaffected people with and without a parental history of depressive or anxiety disorders. We additionally examined whether possible HPA axis dysregulations resemble those observed in participants with depression or anxiety disorders.MethodData were from the Netherlands Study of Depression and Anxiety. Within the participants without a lifetime diagnoses of depression or anxiety disorders, three groups were distinguished: 180 people without parental history, 114 with self-reported parental history and 74 with CIDI-diagnosed parental history. These groups were additionally compared with people with major depressive disorder or panic disorder with agoraphobia (n = 1262). Salivary cortisol samples were obtained upon awakening, and 30, 45 and 60 min later.ResultsAs compared with unaffected participants without parental history, unaffected individuals with diagnosed parental history of depression or anxiety showed a significantly higher cortisol awakening curve (effect size (d) = 0.50), which was similar to that observed in the participants with depression or anxiety disorders. Unaffected people with self-reported parental history did not differ in awakening cortisol levels from unaffected people without parental history.ConclusionsUnaffected individuals with parental history of depression or anxiety showed a higher cortisol awakening curve, similar to that of the participants with depression or anxiety disorders. This suggests that a higher cortisol awakening curve reflects a trait marker, indicating an underlying biological vulnerability for the development of depressive and anxiety disorders.

Author(s):  
Jennifer Gillies

An important causal factor of depression is family history ¾ there is compelling evidence that Major Depressive Disorder (MDD) is familial. Although the connection between a maternal history of depression and offspring risk is well established, paternal history has been largely ignored in research thus far. The first goal of this study is to examine differences in the clinical profile of MDD across parental depression history groups (i.e., both-parent history versus maternal history only versus paternal history only versus no parental history).  Based on previous findings, I predict that the severity of the clinical course of MDD (as operationalized by a higher severity of depression and anxiety symptoms, an increased likelihood of recurrence, and a greater likelihood of a comorbid anxiety disorder) will be highest for offspring with a both-parent history of depression, followed by those with a maternal history only, followed by individuals with a paternal history only, and lastly by offspring with no parental history of depression. The second goal is to determine if the group differences hypothesized above are further moderated by offspring sex. To date, very little is known about how parental history influences the clinical presentation of MDD in depressed offspring. This study will contribute to a limited body of research, and is unique in that it will include four parental history groups as well as offspring sex in its analyses. The study will use a quasi-archival sample of approximately 250 participants between 12 and 29 years of age, who have been diagnosed with MDD.


2012 ◽  
Vol 42 (9) ◽  
pp. 1815-1823 ◽  
Author(s):  
N. Messerli-Bürgy ◽  
G. J. Molloy ◽  
A. Wikman ◽  
L. Perkins-Porras ◽  
G. Randall ◽  
...  

BackgroundDepressed mood following an acute coronary syndrome (ACS) is a risk factor for future cardiac morbidity. Hypothalamic–pituitary–adrenal (HPA) axis dysregulation is associated with depression, and may be a process through which depressive symptoms influence later cardiac health. Additionally, a history of depression predicts depressive symptoms in the weeks following ACS. The purpose of this study was to determine whether a history of depression and/or current depression are associated with the HPA axis dysregulation following ACS.MethodA total of 152 cardiac patients completed a structured diagnostic interview, a standardized depression questionnaire and a cortisol profile over the day, 3 weeks after an ACS. Cortisol was analysed using: the cortisol awakening response (CAR), total cortisol output estimated using the area under the curve method, and the slope of cortisol decline over the day.ResultsTotal cortisol output was positively associated with history of depression, after adjustment for age, gender, marital status, ethnicity, smoking status, body mass index (BMI), Global Registry of Acute Cardiac Events (GRACE) risk score, days in hospital, medication with statins and antiplatelet compounds, and current depression score. Men with clinically diagnosed depression after ACS showed a blunted CAR, but the CAR was not related to a history of depression.ConclusionsPatients with a history of depression showed increased total cortisol output, but this is unlikely to be responsible for associations between depression after ACS and later cardiac morbidity. However, the blunted CAR in patients with severe depression following ACS indicates that HPA dysregulation is present.


Author(s):  
Ayu Laela Fitriyani ◽  
◽  
Setyo Sri Rahardjo ◽  
Bhisma Murti ◽  
◽  
...  

ABSTRACT Background: Chronic exposure to organophosphate pesticides can increase the risk of neuropsychiatric disorders, including depression and anxiety. Unsafe behavior from farmers will endanger the health of farmers, especially in the form of neuropsychiatric disorders (depression and anxiety). This study aimed to analyze the effects of pesticide exposure and psychosocial determinants on depression and anxiety. Subjects and Method: A retrospective cohort study was conducted in Sukoharjo, Central Java. The study population was rice farmers. A sample of 200 rice farmers who use organophospate pesticide was selected by fixed exposure sampling. The dependent variable was neuropsychiatry (anxiety and depression). The independent variables were exposure to organophospate pesticide, had family history of depression, loss and grief, post trauma, work stress, and the use of personal protective equipment (PPE). The data were collected by questionnaire and analyzed by a multiple linear regression. Results: The risk of depression increased with high exposure to organophospate pesticide (b= 0.15; 95% CI= 0.05 to 0.26; p= 0.005), had family history of depression (b= 5.10; 95% CI= 2.60 to 7.60; p<0.001), loss and grief (b= 2.94; 95% CI= 0.76 to 5.11; p= 0.008), post trauma (b= 2.57; 95% CI= 0.24 to 4.89; p= 0.031), and work stress (b= 0.16; 95% CI= 0.05 to 0.27; p= 0.005). The risk of depression decreased with the use of PPE (b= -0.69; 95% CI= -1.32 to -0.076; p= 0.028). The risk of anxiety increased with high exposure to organophospate pesticide (b= 0.13; 95% CI= 0.02 to 0.24; p= 0.025), post trauma (b= 5.96; 95% CI= 3.48 to 8.44; p<0.001), loss and grief (b= 3.39; 95% CI= 1.07 to 5.71; p<0.001), had family history of depression (b= 2.95; 95% CI= 0.29 to 5.62; p= 0.004), and work stress (b= 0.19; 95% CI= 0.07 to 0.30; p=0.002). The risk of anxiety decreased with the use of PPE (b= -0.09; 95% CI= -1.57 to -0.024; p=0.008). Conclusion: The risk of depression increases with high exposure to organophospate pesticide, family history of depression, loss and grief, post trauma, and work stress. The risk of depression decreases with the use of PPE. The risk of anxiety increases with high exposure to organophospate pesticide, post trauma, loss and grief, had family history of depression, and work stress. The risk of anxiety decreases with the use of PPE. Keywords: Neuropsychiatry disorder, depression, anxiety Correspondence: Ayu Laela Fitriyani. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: [email protected]. Mobile: +625796333986. DOI: https://doi.org/10.26911/the7thicph.01.48


1997 ◽  
Vol 46 (3) ◽  
pp. 255-262 ◽  
Author(s):  
Gill Livingston ◽  
Vivienne Watkin ◽  
Brian Milne ◽  
Monica V Manela ◽  
Cornelius Katona

2017 ◽  
Vol 208 ◽  
pp. 103-109 ◽  
Author(s):  
Brandon L. Goldstein ◽  
Greg Perlman ◽  
Roman Kotov ◽  
Joan E. Broderick ◽  
Keke Liu ◽  
...  

2017 ◽  
Vol 9 (1) ◽  
pp. 34-49 ◽  
Author(s):  
Indriono Hadi ◽  
Fitri Wijayanti ◽  
Reni Devianti Usman ◽  
Lilin Rosyanti

Depression is a condition of a person feeling sad, disappointed when experiencing a change, loss, failure and becoming pathological when unable to adapt. Depression is a condition that affects a person affectively, physiologically, cognitively and behaviorally thus changing the usual patterns and responses. Major Depressive Disorder is a heterogeneous disease characterized by feelings of depression, anhedonia, changes in cognitive function, changes in sleep, changes in appetite, guilt that occur over two weeks, described with a loss of interest or pleasure in the usual activity and is a disease with neurobiological consequences involving structural, functional and molecular changes in some areas of the brain. Maladaptive neural responses, social, psychological, and physiological rejections interact with each other with other susceptibility factors, such as a history of depression, life stress levels, genetic factors, will increase a person's susceptibility to depression. Catatan PenerbitPolekkes Kemenkes Kendari menyatakan tetap netral sehubungan dengan klaim dari perspektif atau buah pikiran yang diterbitkan dan dari afiliasi institusional manapun.


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