Biomedical subjects

T F Sadow

Publications and source records attributed to T F Sadow.

3 recordsLinked to original sources

PubMed1996

Adrenal gland volume in major depression: relationship to basal and stimulated pituitary-adrenal cortical axis function.

We measured adrenal gland volume and both baseline and stimulated pituitary and adrenal cortical hormones in 35 unmedicated, major depressives and 35 individually matched normal control subjects. Mean adrenal volume in the depressives was significantly larger, by about 38%, than the adrenal volume of their matched controls. Basal plasma adrenocorticotropic hormone (ACTH)1-39 was significantly lower, and basal plasma cortisol was significantly higher, in the patients. In contrast, basal plasma ACTH determined by radioimmunoassay (RIA) was not significantly different between the two groups. The ACTH response to ovine corticotropin-releasing hormone (oCRH), whether measured specifically as ACTH1-39 or by the less-specific RIA, was highly significantly lower in the depressives than in the controls. However, neither the cortisol response to oCRH nor its response to low-dose ACTH 1-24 differed significantly between groups. In both groups of subjects, correlations between adrenal gland volume and all the hormone measures were low, and none represented more than 4% shared variance. In the patients, adrenal volume did not correlate significantly with duration of the present episode, lifetime number of episodes, melancholic subtype, Hamilton Depression Scale total score, or the Hamilton suicidality item. However, adrenal volume was significantly positively related to the somatization factor of the Hamilton scale, which was almost totally accounted for by the specific items of somatic symptoms and somatic anxiety.

Adolescent↗

PubMed1995

Adrenal gland volume in major depression. Increase during the depressive episode and decrease with successful treatment.

BACKGROUND: Hyperactivity of the pituitary-adrenocortical axis is the most prominent neuroendocrine abnormality in major depression. It is state-related, returning to normal with resolution of the depressive episode. Adrenal gland enlargement also has been reported in patients with major depression and has been hypothesized as an index of cumulative lifetime depression. However, whether or not adrenal enlargement decreases with successful treatment of depression has not yet been studied, to our knowledge. We, therefore, determined adrenal gland volume in patients with major depression before and after treatment and in matched normal controls, and compared adrenal size with functional indexes of pituitary-adrenocortical activity. METHODS: Adrenal volumes were measured by magnetic resonance imaging in nine adult and two adolescent patients with major depression during their illness and during full remission when medication had been stopped for at least 1 month, and in nine adult and two adolescent normal control subjects individually matched to the patients. Basal, 4 to 7 PM plasma corticotropin 1-39 and cortisol levels, and corticotropin 1-39 and cortisol responses to administration of ovine corticorelin and lowdose cosyntropin also were measured. RESULTS: Mean adrenal gland volume was significantly larger, by about 70% in the patients while depressed than after successful treatment, and it also was significantly larger, again by about 70%, than the mean adrenal gland volume of their matched controls. After treatment, the mean adrenal volume of the patients decreased and was no longer significantly different from that of their controls at baseline. The magnitude of the decrease was significantly positively correlated with the duration of the depressive episode. Basal, late-afternoon plasma corticotropin 1-39 levels were significantly lower in the patients while depressed than in their matched controls, but basal plasma cortisol levels did not differ significantly among the three groups, nor did the corticotropin 1-39 and cortisol responses to corticorelin or the cortisol response to cosyntropin. Correlations between adrenal gland volume and basal corticotropin and cortisol levels, and the corticotropin and cortisol responses to hormone challenge, were not consistently in the expected direction in any of the three groups of subjects. CONCLUSIONS: Adrenal gland enlargement occurring during an episode of major depression appears to be state-dependent, in that it reverts to the normal size range during remission after treatment. It thus does not appear to be an index of cumulative lifetime depression. The lack of a discernible relationship between adrenal volume and pituitary-adrenocortical activity remains to be explained and might be related to noncorticotropin influences on the adrenal gland, including other tropic hormones and/or neural mechanisms.

Adolescent↗

PubMed1992

Effects of hypothalamic peptides on the aging brain.

The hypothalamic peptide hormones, TRH, LHRH (GnRH), CRH, GHRH, and GHIRH (somatostatin), influence the release of the anterior pituitary hormones, which in turn promote the release of target endocrine gland hormones and other metabolites. These latter compounds feed back to the brain to help control the secretion of the hypothalamic hormones. This is a dynamic interaction that is influenced by the aging process: Most of these hormones systems become less responsive with advancing age, due to decreased function of peptide-containing secretory neurons, a loss of hormone receptor sensitivity, and/or a reduction in the output of the target endocrine glands. That the hypothalamic peptides themselves can influence brain function is supported by the fact that most are found in areas of the brain other than the hypothalamus and that receptors for them exist in these other areas. For example, CRH is contained in a number of central neural systems that can influence behavior, including limbic areas, the hypothalamus, locus coeruleus, median raphé nuclei, and cortical interneurons. CRH has been shown to be anxiogenic in animal models, and its effect can be blocked by CRH receptor antagonists. CRH content in the locus coeruleus is particularly increased by stress and may influence norepinephrine neurotransmitter function in this structure. In aging there is a gradual reduction of the sensitivity of the brain to the negative feedback of corticosteroids, such that CRH secretion becomes somewhat increased under basal conditions. The behavioral effects of this change are unclear, however, as is the influence of stress-related activation of CRH, ACTH, and glucocorticoid secretion on behavior in the elderly. Other hypothalamic peptides have different patterns of change with aging, and some are markedly altered in pathological conditions; for example, in Alzheimer's disease the content of CRH and somatostatin in certain brain areas is decreased. However, whether the changes in hypothalamic peptides precede or follow the pathological behavioral changes, and how they participate in the changes, is still unclear.

Aged↗