Thyroid Function in Anxious and Depressed Patients

Rao, Marie Luise; Vartzopoulos, Dimitrios; Fels, Klaus Werner

doi:10.1055/s-2007-1014580

Cited by 13 publications

(12 citation statements)

References 8 publications

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“…Some studies used syndromal criteria and others used dimensional criteria . In addition, several studies did not include healthy volunteers, and not all studies required that participants have a standard 10–14 day medication‐free period . It should also be noted that some studies did not actually provide a diagnosis, per se, of anxious depression, and instead used scales to measure anxious depressive traits and to make correlations .…”

Section: Discussionsupporting

confidence: 63%

“…Like cortisol, exogenously administered dexamethasone normally works through negative feedback to suppress ACTH, thus decreasing cortisol levels. In 17 women with syndromally defined anxious depression, 50% exhibited impaired suppression of cortisol following dexamethasone challenge, compared to 37% of female subjects with anxiety disorders (PD or GAD; N = 9) and 18% of female subjects with MDD ( N = 12) . This study also examined differences in the thyroid hormone system between the groups.…”

Section: Resultsmentioning

confidence: 99%

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Neurobiology of Anxious Depression: A Review

et al. 2013

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Anxious depression is a common, distinct clinical subtype of major depressive disorder (MDD). This review summarizes current neurobiological knowledge regarding anxious depression. Peer-reviewed articles published January 1970 through September 2012 were identified via PUBMED, EMBASE, and Cochrane Library, using the following key words: anxious depression electroencephalography (EEG), anxious depression functional magnetic resonance imaging (fMRI), anxious depression genetics, anxious depression neurobiology, and anxious melancholia neurobiology. Despite a general dearth of neurobiological research, the results suggest that anxious depression—when defined either syndromally or dimensionally—has distinct neurobiological findings that separate it from non-anxious depression. Structural neuroimaging, EEG, genetics, and neuropsychiatric studies revealed differences in subjects with anxious depression compared to other groups. Endocrine differences between individuals with anxious depression and those with non-anxious depression have also been noted, as evidenced by abnormal responses elicited by exogenous stimulation of the system. Despite these findings, heterogeneity in the definition of anxious depression complicates the results. Because exploring the neurobiology of this depressive subtype is important for improving diagnosis, prognosis, and treatment, enrichment strategies to decrease heterogeneity within the field should be employed for future research.

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Section: Discussionsupporting

confidence: 63%

Section: Resultsmentioning

confidence: 99%

Neurobiology of Anxious Depression: A Review

et al. 2013

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“…Furthermore, the effect of GHRH on sleep endocrine activity is reduced in the early morning hours [Schier et al, 1997]. As TRH secretion seems to be more closely associated with the HPA than with the hypothalamic-pituitary-somatotropic (HPS) axis (see the results of our study) and Rao et al [1989], the responsiveness of this axis to TRH may be increased during the second half of the night.…”

Section: Discussionmentioning

confidence: 56%

“…The circadian variation of TSH secretion, showing low levels during the day and an increase after sleep onset with a maximum at midnight and subsequent returning to basal values until the morning [Souêtre et al, 1986;Wilson et al 1992], provides a further (indirect) argument that the HPT axis activity -and thus TRH -is involved in the regulation of sleep and nocturnal hormone secretion. Additional support for this hypothesis arises from sleep deprivation studies [Baumgartner and Meinhold, 1986;Kasper et al, 1988;Kaschka et al, 1989;Rao et al, 1989] when a further increase in TSH secretion was seen. This observation has led to the controversial interpretation that sleep may exert an inhibitory function on TSH secretion [Parker et al, 1987] or that sleep deprivation is a physiological stimulant of TSH .…”

Section: Introductionmentioning

confidence: 97%

Effects of Thyrotropin-Releasing Hormone on the Sleep EEG and Nocturnal Hormone Secretion in Male Volunteers

Hemmeter¹,

Rothe²,

Güldner³

et al. 1998

Neuropsychobiology

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Various peptides including corticotropin-releasing hormone (CRH) exert selective effects on sleep structure and noctural secretions of cortisol and growth hormone (GH). In animal studies analeptic effects and sleep disturbances after thyrotropin-releasing hormone (TRH) administration have been observed; studies of endocrine function in depressed patients suggest a pathological activity of CRH and TRH as compared with that in healthy volunteers. As the role of TRH in the regulation of the sleep endocrine pattern in humans has not yet been clarified, we performed a study to examine the effects of pulsatile administration of TRH on the sleep EEG pattern and the nocturnal secretions of cortisol and GH in 7 healthy male subjects. The sleep EEG was recorded from 23.00 to 07.00 h, and blood samples were collected every 20 min from 20.00 to 07.00 h for the analysis of GH and cortisol concentrations during intravenous administration of placebo or 4 × 50 µg TRH at 22.00, 23.00, 24.00, and 01.00 h. In contrast to the well-known effects of CRH on the sleep endocrine pattern, TRH exerts only a weak effect on the sleep EEG which is reflected in a slight decrease in sleep efficiency associated with a trend to wakefulness during the night. Furthermore, after TRH administration, the cortisol rise appeared earlier, and a nonsignificant tendency to an increased secretion of cortisol during the first half of the night was found. The GH secretion did not differ significantly after application of TRH or placebo. The activating, albeit weak, effect of TRH on the sleep EEG and nocturnal cortisol secretion in healthy volunteers confirms and adds to the results previously observed in animals. On the basis of these findings, we surmise that TRH may contribute to the disturbed sleep continuity seen in depressed patients, probably acting as a cofactor of CRH in a synergistic manner.

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“…Meller et al (45) discuss that neuroendocrine perturbations are more severe in anxious depression, but point out the ambiguity of the term anxious depression in the literature. Rao et al (46) have studied thyroid measures in depression, anxiety disorders, and anxious depression. This review is limited by its retrospective, qualitative nature, and prospective studies are needed comparing the various groups of antidepressants.…”

Section: Discussionmentioning

confidence: 99%