Salivary Cortisol Hypersecretion in Juvenile Depression

Foreman, David; Goodyer, Ian

doi:10.1111/j.1469-7610.1988.tb00719.x

Cited by 17 publications

(11 citation statements)

References 35 publications

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“…To begin with, let us recapitulate this group's work on cortisol, dehydroepiandrosterone (DHEA) and depression in order to see how they arrived at the study just presented. An early case-control study and a small depressed-well follow-up study found evening or night-time hypersecretion of cortisol in depressed children and adolescents (Foreman & Goodyer, 1988 ;. The follow-up study also noted that some individuals were not hypercortisolaemic when depressed, but that hypercortisolaemia was associated with more severe symptomatology.…”

Section: Earlier Studies By Ian Goodyer and His Colleagues Of Effectsmentioning

confidence: 90%

Adolescent depression, cortisol and DHEA

Angold¹

2003

Psychol. Med.

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Since the mid-1980s Ian Goodyer and his colleagues have been engaged in trying to understand the dynamics of the relationship between acute and chronic life stresses and depression in adolescents (Goodyer et al. 1985, 1986). One of the great strengths of their work has been their attention to an array of potential risk factors ranging from the apparently exogenous (such as life events, e.g. Goodyer et al. 1988; Goodyer & Altham, 1991; Goodyer, 1999), through those of uncertain origin (e.g. peer and family relationships and problems, Goodyer et al. 1990), to those that can be regarded as being endogenous to the child (e.g. measures of temperament or endocrine function, Goodyer et al. 1993, 1996, 1998; Herbert et al. 1996). They have then typically attempted to determine how subsets of these factors interact in the generation of disorder (see Goodyer, 2002 for a speculative presentation of his current thinking about the relationships between social adversity and depression). A second characteristic of their research lies in its frequent attention to outcomes over time, as opposed to cross-sectional relationships (e.g. Goodyer et al. 1997a,b). Thirdly, in line with growing evidence that the relationships between environmental stress (and perhaps neuro-anatomical correlates) and depression change as repeated episodes occur (Lewinsohn et al. 1999; Daley et al. 2000), they have distinguished among first, recurrent, remitting and chronic depressive episodes. The group's latest work, presented in this issue (Goodyer et al. 2003), nicely illustrates these characteristics, and their extension to consideration of potential dynamic relations among endocrine parameters in relation to psychopathology.

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Section: Earlier Studies By Ian Goodyer and His Colleagues Of Effectsmentioning

confidence: 90%

Adolescent depression, cortisol and DHEA

Angold¹

2003

Psychol. Med.

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“…Heightened cortisol secretion has been linked to internalizing symptoms, including anxiety and withdrawal (Brown et al 1996; Colomina et al 1997; Schmidt et al 1997; Windle 1994). Baseline and post-dexamethasone elevation in cortisol levels is associated with depression in adults (Nelson et al 1997; Rush et al 1996), adolescents (Foreman and Goodyer 1988), and prepubertal children (Puig-Antioch et al 1989). Conversely, attenuated activity of the HPA system has been identified as a risk factor for antisocial behavior (Susman 2006).…”

Section: Vulnerable Brain Systems In Individuals At Risk For Audmentioning

confidence: 99%

Neural Circuitry Associated with Risk for Alcohol Use Disorders

Tessner

Hill

2009

Neuropsychol Rev

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The core features of risk for alcohol use disorders (AUD), including behavioral disinhibition, affective dysregulation, and executive dysfunction, map onto distinct neural circuits that have been found to be abnormal in the offspring of alcohol dependent individuals. Components of the cerebellothalamocortical system and the extended limbic network may provide the underpinnings for the behavioral and emotional dysfunction observed in individuals at heightened risk for AUD. In addition, abnormalities in these structures appear to be altered in individuals with the predisposition for other psychiatric conditions that may share a similar genetic diathesis. This review proposes several neurobehavioral mechanisms of genetic vulnerability that may account for phenotypic characteristics in individuals at risk for AUD.

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“…Neither depressed pre‐pubertal children nor the majority of post‐pubertal adolescents show marked increases in 24‐hour cortisol output or in loss of negative feedback sensitivity in a non‐stressful environment (Dahl et al, 1989; Puig‐Antich et al, 1989; Birmaher et al, 1992a, 1992b; Dahl et al, 1992a, 1992b). Phasic increase in evening plasma cortisol (Dahl et al, 1991) and evening and morning salivary cortisol measures (Foreman & Goodyer, 1988; Goodyer, Herbert, Moor, & Altham, 1991) have been reported in depressed children and adolescents relative to well controls. In addition, persisting depressive illness is associated with chronic cortisol hypersecretion (Goodyer, Park, & Herbert, 2001; Rao et al, 1996).…”

Section: Cortisol and Depressionmentioning

confidence: 99%