Nocturnal Cortisol, Thyroid Stimulating Hormone, and Growth Hormone Secretory Profiles in Depressed Adolescents

Kutcher, Stan; Malkin, Dina; Silverberg, Jay; Marton, Peter; Williamson, Peter C.; Malkin, A.; Szalai, John Paul; Katic, Marco

doi:10.1097/00004583-199105000-00009

Cited by 75 publications

(34 citation statements)

References 88 publications

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“…Early studies in children (e.g. Puig-Antich et al, 1984a-c) and adolescents (Kutcher et al, 1988(Kutcher et al, , 1991, reported GH hypersecretion during sleep. However, more recent studies (Dahl et al, 1992a ;DeBellis et al, 1996) found no differences in GH secretion between depressed and normal controls during the night, with one study reporting decreased nocturnal GH secretion in a subgroup of suicidal\in-patient adolescents (Dahl et al, 1992a).…”

Section: Baseline Nocturnal Gh Secretionmentioning

confidence: 99%

“…Several studies including large samples of depressed outpatient children and adolescents have reported that in general depressed children and adolescents have normal plasma cortisol secretion (24 h or nocturnal sampling) when compared with normal controls (Birmaher et al, 1992a,b ;Dahl et al, 1991 ;Kutcher et al, 1991 ;PuigAntich et al, 1989). Goodyear et al (1996) measured cortisol, dehydroepiandrosterone (DHEA), and its sulphate (DHEAS) in saliva (3 times a day over 2 consecutive days) in a sample of children and adolescents with MDD, non-depressed psychiatric and normal controls.…”

Section: Baseline Cortisol and Secretionmentioning

confidence: 99%

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Biological studies in depressed children and adolescents

Birmaher

Heydl

2001

Int. J. Neuropsychopharm.

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The objective was to review the literature on the biological correlates of major depressive disorder (MDD) in children and adolescents. A computerized search for articles published during the last 20 years was done and selected studies presented. To date, examination of growth hormone (GH), prolactin, and cortisol levels after pharmacological stimulation have shown abnormalities in the secretion of these hormones (e.g. blunted GH secretion after the administration of growth hormone releasing hormone). Identical results have been found in never-depressed children at high risk to develop MDD due to high family loading for MDD suggesting that alteration in certain hormonal systems may be trait markers for MDD. Other biological studies (e.g. the hypothalamic-pituitary axis, sleep electroencephalogram) have yielded more inconsistent results with subjects with melancholic symptoms, severe depressions, and older age showing some abnormalities similar to the ones reported in adults with MDD. Factors such age, sex, maturation, psychiatric family history and exposure to stress need to be considered since they also affect the same biological systems associated with the aetiology of MDD. Considerable biological research has been done in youth with MDD. Further research is needed to investigate whether these markers predict the development of new episodes of MDD, recurrences, and treatment response. Also, these and other studies using more sophisticated methods (e.g. functional MRI) aimed at elucidating the interrelationship between biological and other risk factors are needed.

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Section: Baseline Nocturnal Gh Secretionmentioning

confidence: 99%

Section: Baseline Cortisol and Secretionmentioning

confidence: 99%

Biological studies in depressed children and adolescents

Birmaher

Heydl

2001

Int. J. Neuropsychopharm.

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“…Corticotropin-releasing hormone stimulates the secretion of somatostatin, which then inhibits growth hormone (GH) at the level of the pituitary [71]. Initial studies in children and adolescents found that nocturnal hypersecretion of GH significantly differentiated depressed individuals from control individuals [72,73], but more recent studies reported no differences [74,75]. Stimulatory tests of GH secretion have shown more conclusive results.…”

Section: Growth Hormonementioning

confidence: 99%

The roots of depression in adolescent girls: Is menarche the key?

Born¹,

Shea²,

Steiner

2002

Curr Psychiatry Rep

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Before adolescence, the rates of depression are similar in girls and boys (or are slightly higher in boys). Yet with the onset of puberty, the gender proportion of depression dramatically shifts to a two girls to one boy ratio. What, then, is the relationship between menarche and the onset of major depression in early adolescence? Recent literature intimates that vulnerability to depression may be rooted in an intricate meld of genetic traits, normal female hormonal maturational processes, and gender socialization. Information regarding gender differences in the presentation of depressive symptoms is provided along with biologic, psychologic, and sociologic factors contributing to depression in adolescent girls. The burden of illness associated with onset of depression after menarche reinforces the importance of prevention or else expeditious recognition and intervention.

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“…It is therefore noteworthy that largely unremarkable 24-h cortisol secretory patterns have been observed in comparisons of adolescent outpatients with depression to normal controls Kutcher et al, 1991). Consistent with the adolescent findings, no evidence of HPA axis activity was noted in prepubertal depressives by PuigAntich et al (1989).…”

Section: Introductionmentioning

confidence: 69%

Differentiating Depressed Adolescent 24 h Cortisol Secretion in Light of Their Adult Clinical Outcome

Mathew

Coplan

Goetz

et al. 2003

Neuropsychopharmacol

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A clinical follow-up study was performed of adolescent major depressives and normal control subjects approximately 10 years after the subjects had undergone serial cortisol measurements over a 24-h period. In light of their young adulthood clinical status, our objective was to ascertain whether there were any premorbid cortisol abnormalities associated with depressive course of illness. In all, 77 young adults who had received a diagnosis of adolescent major depressive disorder, or were determined to be normal volunteers free of psychiatric diagnosis at index period and during follow-up, were studied. When subjects were adolescents, blood samples were collected for cortisol at 20-min intervals during the 24-h period coinciding with the third consecutive night of sleep EEG. The subjects, in young adulthood at the time of follow-up, were reinterviewed regarding longitudinal course of illness, and the original adolescent cortisol data were analyzed in the light of information obtained. Of the subjects who had experienced at least one lifetime major depressive episode during the follow-up period, the subgroup who would go on to make suicide attempts during the follow-up period secreted significantly greater levels of cortisol in the 4, 6, and 12 h prior to sleep onset. Conversely, this same subgroup exhibited reduced cortisol levels 2-4 h following sleep onset. Adolescents who are at risk to make suicide attempts appear to display significant elevations of cortisol prior to sleep onset, a time when the hypothalamic-pituitary-adrenal (HPA) axis is normally most quiescent. Dysregulation of the HPA axis, combined with dysfunction of sleep-onset mechanisms previously reported in this same cohort, might serve as premorbid biological substrates that predict suicide attempts during follow-up.

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Nocturnal Cortisol, Thyroid Stimulating Hormone, and Growth Hormone Secretory Profiles in Depressed Adolescents

Cited by 75 publications

References 88 publications

Biological studies in depressed children and adolescents

Biological studies in depressed children and adolescents

The roots of depression in adolescent girls: Is menarche the key?

Differentiating Depressed Adolescent 24 h Cortisol Secretion in Light of Their Adult Clinical Outcome

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