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Biomedical subjects

J Mendels

Publications and source records attributed to J Mendels.

At least 109 records · Page 6Linked to original sources
PubMed1976

Neuroendocrine regulation in depression. I. Limbic system-adrenocortical dysfunction.

The regulation of hypothalamopituitary-adrenal (HPA) function in depressed patients was studied by a midnight dexamethasone suppression test. By using an observation period of 24 hours postadministration of dexamethasone, a graded series of abnormal test responses was identified. Depressed patients show abnormal early escape from suppression rather than absolute resistance to HPA suppression by dexamethasone. With increasing severity of depression, this escape occurs progressively more early on the day after administration of dexamethasone. These abnormalities were strongly related to the presence of HPA hyperactivity before dexamethasone was given. The essential disturbance of neuroendocrine regulation in depression is a failure of the normal brain inhibitory influence on the HPA system. This disinhibition of HPA activity suggests that there is an abnormal limbic system drive on the HPA axis in primary depressive illness.

Adrenal Glands↗
PubMed1976

Neuroendocrine regulation in depression. II. Discrimination of depressed from nondepressed patients.

Forty-two patients with endogenomorphic depression (ED) and 42 patients with other psychiatric disorders received an overnight dexamethasone test of hypothalamopituitary-adrenal (HPA) suppressibility. Plasma and urinary cortisol measures showed that the ED patients had significantly greater HPA activity before dexamethasone and less complete HPA suppression after dexamethasone. High cortisol vlaues after dexamethasone correlated strongly with spontaneous HPA disinhibition, as indicated by high baseline midnight plasma cortisol levels. Criteria for defining normal suppression responses were developed. All patients with depressive neuroses and most patients with other nondepressive disorders had completely normal responses to dexamethasone. About half of the ED patients had abnormal responses, whether or not they were receiving other drugs at the time of the test. Drug-free patients with depressive neuroses or other disorders showed no abnormal responses to dexamethasone. The effects of psychotropic drugs on the test require further study. Patients with two or more abnormal cortisol values after administration of dexamethasone were identified correctly as ED at confidence levels close to 100%. The dexamethasone suppression test may be of value as a laboratory aid in the diagnosis of "endogenous" depression.

Adrenal Glands↗
PubMed1976

Urinary free cortisol excretion in depression.

Urinary free cortisol (UFC) excretion was determined in 60 depressed inpatients and in 35 psychiatric inpatients with other disorders. The depressed patients had high daily UFC values, while the other patients excreted normal amounts. Over 40% of the depressed patients had UFC excretions in the range seen in Cushing's disease, while only 6% of the other patients excreted such high amounts of cortisol. Age and sex differences did not account for the results. Among the depressed patients those with depressive neuroses excreted less than unipolar or bipolar depressives. Following treatment, more normal UFC excretion was found in depressed patients. The estimation of UFC and its clinical utility are discussed in detail. UFC determination is a simple and informative indicator of adrenal cortical activation and its application to psychoendocrine studies is recommended.

Adjustment Disorders↗
PubMed1976

Cerebrospinal fluid and plasma free cortisol concentrations in depression.

Cerebrospinal fluid (CSF) cortisol levels were examined in a total group of 65 patients. Those who were not depressed (ND), and those suffering from depressive neuroses (DN) had marginally elevated values. Patients with unipolar depression (UD) and bipolar depression (BD) had levels twice as high as the ND and DN patients. Psychotic UD and BD patients had the highest values, three to four times as high as the ND and DN subjects. A significant reduction of CSF cortisol levels was observed following treatment and recovery. Manic patients had moderately elevated CSF cortisol values. The CSF results were in good agreement with plasma total cortisol levels and with urinary free cortisol excretion. Age and sex effects were not responsible for the observed differences; similar results were found in patient subgroups studied in Australia and in the United States. Preliminary equilibrium dialysis data are presented for plasma and CSF cortisol binding. CSF cortisol was 20% bound and 80% free. Plasma free cortisol levels were in good agreement with CSF free cortisol values. Depressed patients have increased tissue and central nervous system (CNS) exposure to free, physiologically active glucocorticoids. The appearance of severe depressive symptoms which manifest a diurnal rhythm may be determined in part by excesssve CNS exposure to glucocorticoids.

Adjustment Disorders↗
PubMed1976

Lithium in the treatment of depression.

The author reviews the studies of lithium as an antidepressant, evaluates the evidence that there might be specific subgroup of patients for whom it is effective, and reports a study he and his associates conducted that found lithium to be effective for 13 of 21 depressed patients. He concludes that there is convincing, although not conclusive, evidence for an antidepressant effect of lithium and that only by identifying the subgroup of patients for whom it is effective can the continuing uncertainty surrounding lithium's role in affective disorder be resolved. He also calls for a reevaluation of the relationship between mania and depression.

Brain Chemistry↗
PubMed1975

Amine precursors and depression.

The amino acid precursors, levodopa and L-tryptophan, were given to a group of hospitalized depressed patients in a double-blind placebo controlled study. Relatively large doses were not associated with sufficient clinical improvement to allow the patients to leave the hospital. Previous studies using the precursor-load strategy have produced conflicting findings on the use of these compounds for depressed patients.

Adult↗
PubMed1975

Genetic determinant of lithium ion metabolism. II. An in vivo study of lithium ion distribution across erythrocyte membranes.

A study was conducted to determine if membrane factors, known to influence the distribution of sodium ion (Na) and potassium ion (K), also influence lithium ion distribution. Two groups of sheep with genetically determined differences in their cation concentrations were administered lithium chloride for ten days. The low red blood cell (RBC) potassium ion sheep (LK) had a greater RBC lithium ion concentration than the high RBC potassium ion sheep (HK). In vitro incubation of erythrocytes with lithium chloride also produced substantially different RBC lithium ion: plasma lithium ion ratios similar to those seen in the vivo study. Distribution of lithium ion was generally similar to that of Na ion. It seems that lithium ion distribution may be controlled by the same genetic factors that regulate Na ion distribution.

Animals↗