Irene Kürten

Influence of partial sleep deprivation on the secretion of thyrotropin, thyroid hormones, growth hormone, prolactin, luteinizing hormone, follicle stimulating hormone, and estradiol in healthy young women.

The influence of partial sleep deprivation during the second half of the night on the secretion of thyroid stimulating hormone (TSH), thyroxin (T4), free T4 (fT4), triiodothyronine (T3), prolactin (PRL), growth hormone (GH), luteinizing hormone (LH), follicle stimulating hormone (FSH), and estradiol (E2) was investigated in 10 healthy young women. Blood samples were drawn at hourly intervals over a 64-hour period (i.e., 3 consecutive days and nights). During night 2, all subjects were awakened at 1:30 a.m. During partial sleep deprivation, TSH concentrations increased significantly and remained elevated throughout the following day. Levels of T4, fT4, and T3 were enhanced during the partial sleep deprivation hours only, and changes in these hormones seemed to be independent of TSH. PRL levels decreased, LH and E2 concentrations increased, and GH and FSH secretion remained unchanged during partial sleep deprivation. This pattern of change of different endocrine axes during partial sleep deprivation resembles those seen after total sleep deprivation, suggesting that similar neurochemical changes are induced by both forms of antidepressant therapy. The late evening GH peak occurred almost exclusively before the onset of sleep. Partial sleep deprivation did not influence the chronobiological profiles of any of the hormones investigated. The chemical changes underlying these alterations are speculated to involve enhancement of central norepinephrine and dopamine activity with a concomitant increase in the activity of the sympathetic nervous system.

Neuroendocrinological investigations during sleep deprivation in depression I. Early morning levels of thyrotropin, TH, cortisol, prolactin, LH, FSH, estradiol, and testosterone ☆

Measurements of 12 hormones were conducted in patients with major depressive disorder at 8 AM on the morning before and at 8 AM on the morning after total sleep deprivation (SD). Thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), and free T3 (fT3) were measured in 50 patients, free T4 in 39 patients, reverse T3, cortisol, prolactin, luteinizing hormone, and follicle-stimulating hormone in 21, estradiol in 20 (women), and testosterone in 14 (men). After SD, there was a significant rise in TSH, T4, T3, and fT3 concentrations and a significant fall in testosterone levels. The increases in TSH levels were significantly correlated to clinical response. Responders to SD had higher T4, fT4, rT3, and testosterone concentrations before SD. Neither age, gender, polarity, nor antidepressant medication had a clearly significant effect on the response to SD.

Hypothalamic-pituitary-gonadal axis, prolactin, and cortisol in alcoholics during withdrawal and after three weeks of abstinence: comparison with healthy control subjects.

Serum concentrations of luteinizing hormone, follicle-stimulating hormone, testosterone, androstenedione, estradiol, sex hormone-binding globulin, cortisol, and prolactin were measured in 12 male chronic alcoholics once during withdrawal and once after 21 days of abstinence. The results were compared with those of 14 healthy volunteers. During withdrawal, luteinizing hormone, estradiol, and cortisol levels were significantly enhanced. Estradiol and cortisol concentrations fell significantly during abstinence, whereas luteinizing hormone concentrations remained elevated. The results may be interpreted as follows: the well-known inhibitory effect of alcohol on the biosynthesis of testosterone may have led to a compensatory increase in luteinizing hormone secretion, so that normal serum concentrations of testosterone were maintained. On the other hand, peripheral conversion from androstenedione to estradiol via aromatase pathways seemed to be enhanced in chronic alcoholics, at least during withdrawal. Whether this marked increase in estradiol concentrations is implicated in different clinical and psychological symptoms seen in chronic alcoholics remains to be investigated.

The dexamethasone suppression test in depression, in schizophrenia, and during experimental stress

Early escape of plasma cortisol concentrations in the Dexamethasone Suppression Test (DST) has frequently been reported both in depressive illness (e.g., Carroll et al. 1981) and in other psychiatric diseases (e.g., Berger et al. 1982). However, no consensus has yet been reached on the etiology of DST nonsuppression (von Zerssen et al. 1984), or on its clinical relevance as a diagnostic marker for endogenous depression (Carroll et al. 1981) or as a predictor of clinical course, treatment outcome, and relapse in depressive illness (Coryell and Zimmermann 1983; Greden et al. 1983). The purpose of our study was to examine the effects of nonspecific stress factors on the DST. Nonspecific stress is well known to be one cause of excessive cortisol production (Selye 1971), and the DST is used to measure a special form of this excess. To our knowledge, this is the first study in which the DST was conducted in severely ill acute schizophrenics and in healthy volunteers during experimental stress.

Psychological and endocrine abnormalities in refugees from East Germany: Part I. Prolonged stress, psychopathology, and hypothalamic-pituitary-thyroid axis activity

The influence of prolonged psychological stress on hormonal secretion was investigated in 84 East Germany refugees suffering from psychiatric disorders within 6 weeks of their arrival in West Berlin shortly before or after the fall of the Berlin Wall. Before leaving the German Democratic Republic, these patients had already experienced prolonged stress, which continued after migration. In most cases, the diagnosis was anxious-depressive syndrome with vegetative complaints and symptoms of increased arousal. Their formal DSM-III-R diagnoses (American Psychiatric Association, 1987) included adjustment disorders, depressive disorders, and anxiety disorders (the latter including posttraumatic stress disorder). Serum levels of thyroid stimulating hormone (TSH) and thyroid hormones (thyroxine, free thyroxine, triiodothyronine, and reverse triiodothyronine) were measured and compared with those of 20 healthy control subjects. TSH and all thyroid hormone concentrations were significantly reduced in the patient group. Fifty-two of the patients (62%) were in the hypothyroid range but did not show any clinical signs of hypothyroidism. These disturbances in hormonal secretion were not correlated to any psychiatric diagnosis or to the severity of acute or chronic stress. The marked abnormalities in the hypothalamic-pituitary-thyroid axis seen in these refugees differ from those reported in depression and would seem to reflect severe chronic stress rather than specific psychiatric disorders. The underlying neurochemical mechanisms remain to be investigated.

Prolactin in patients with major depressive disorder and in healthy subjects

Prolactin (PRL) levels were investigated in patients with major depressive illness and in healthy subjects. Basal and postdexamethasone levels were measured in 27 patients, and levels after thyrotropin-releasing hormone (TRH) stimulation (delta PRL) were measured in 22 patients. Basal and delta PRL were also determined in 64 age- and sex-matched healthy subjects. Both basal and postdexamethasone PRL levels were normal in depressed patients, with the postdexamethasone levels in particular showing no correlation to postdexamethasone cortisol concentrations. One milligram oral dexamethasone did not influence 4:00 PM PRL levels in 15 healthy subjects. delta PRL was significantly elevated in both male and female patients. These increases were not correlated with severity of illness and are difficult to interpret owing to the complexity of the PRL regulatory system. No significant correlations were found between basal or post-TRH PRL and cortisol, thyroid-stimulating hormone (TSH), thyroid hormones, gonadotropins, or estradiol in the patients. However, surprisingly significant positive correlations between basal PRL and basal cortisol, T4 and reverse T3 occurred in healthy subjects. It is as yet unclear how this finding can be explained and what relevance it has. Women tended to have higher basal PRL concentrations than men, but the difference was not significant in either group. delta PRL was significantly higher in women than in men in both patients and controls. No significant influence of age was found.Prolactin (PRL) levels were investigated in patients with major depressive illness and in healthy subjects. Basal and postdexamethasone levels were measured in 27 patients, and levels after thyrotropin-releasing hormone (TRH) stimulation (delta PRL) were measured in 22 patients. Basal and delta PRL were also determined in 64 age- and sex-matched healthy subjects. Both basal and postdexamethasone PRL levels were normal in depressed patients, with the postdexamethasone levels in particular showing no correlation to postdexamethasone cortisol concentrations. One milligram oral dexamethasone did not influence 4:00 PM PRL levels in 15 healthy subjects. delta PRL was significantly elevated in both male and female patients. These increases were not correlated with severity of illness and are difficult to interpret owing to the complexity of the PRL regulatory system. No significant correlations were found between basal or post-TRH PRL and cortisol, thyroid-stimulating hormone (TSH), thyroid hormones, gonadotropins, or estradiol in the patients. However, surprisingly significant positive correlations between basal PRL and basal cortisol, T4 and reverse T3 occurred in healthy subjects. It is as yet unclear how this finding can be explained and what relevance it has. Women tended to have higher basal PRL concentrations than men, but the difference was not significant in either group. delta PRL was significantly higher in women than in men in both patients and controls. No significant influence of age was found.

Serial dexamethasone suppression tests in psychiatric illness: Part I. A study in Schizophrenia and mania

Weekly dexamethasone suppression tests (DSTs) were performed in 15 patients with schizophrenia (n = 12) and mania (n = 3) until clinical response. At initial evaluation, 53.4% of the patients were nonsuppressors, and 93.3% showed nonsuppression at least once during the treatment period. There was a tendency for DST results to normalize coincident with clinical improvement, although single peaks of DST nonsuppression occurred in several patients irrespective of clinical course. The tests did not prove useful as predictors of recovery or relapse. DST nonsuppression occurred significantly more often in severely ill patients than in moderately ill patients or in patients after recovery, emphasizing the effects of nonspecific stress factors and/or severity of illness on the DST. The cutoff point, established on the basis of DST results in 67 healthy controls, was lower than in other studies, and nonsuppression among healthy controls was associated with low dexamethasone serum levels.

Thyrotropin (TSH) and thyroid hormone concentrations during partial sleep deprivation in patients with major depressive disorder

Thyrotropin (TSH), thyroxine (T4), free T4, triiodothyronine (T3), and free T3 (fT3) concentrations were measured in 25 patients with major depressive disorder at 8 a.m. both before and after partial sleep deprivation (PSD) during the second half of the night. Significant increases in TSH and T3 levels and a corresponding trend in fT3 levels were seen. No convincing correlations occurred between changes in the secretion of any of the hormones and the antidepressant effect of PSD. However, this does not rule out the possibility that the two phenomena, which occur in depression at different anatomical levels with presumably different degrees of disturbance in the respective receptor systems, have common underlying neurochemical mechanisms. Comparison of the effect of the PSD on changes in hormone secretion and mood with the corresponding effects in a sample of depressed patients who underwent total sleep deprivation showed no significant differences between the effects of these two forms of sleep deprivation on either variable.

Prolactin in patients with major depressive disorder and in healthy subjects: III. Investigation of basal and Post-TRH prolactin during different forms of acute and chronic psychological stress

Prolactin (PRL) levels after thyrotropin-releasing hormone (TRH) (delta PRL) were determined 4 times and basal prolactin levels 6 times in 10 healthy medical students before, during, and after a major examination in medicine. No significant differences in basal or delta PRL levels occurred during the examination period. Basal PRL was also measured in 14 doctors of medicine after delivering a paper at a clinical conference and a further 9 doctors both before and after delivering a paper. PRL was measured serially at 20-min intervals in 4 doctors on the day on which they presented the paper. No significant differences in PRL levels were found in any of the tests conducted during this kind of stress as compared with the corresponding values obtained under nonstressful conditions. Increases in PRL before delivering the paper were seen in 3 subjects, but such increases also occurred completely independently of stress. An 18-hr fast did not influence PRL secretion in 11 healthy volunteers. Both the information obtained from a review of the literature on the influence of stress on PRL secretion and our own results strongly suggest that contrary to common opinion, there is no evidence at all that psychological stress affects PRL secretion in man.

The hypothalamic-pituitary-thyroid axis in psychiatric patients and healthy subjects: Parts 1–4: Part 3: The TRH test and thyroid hormone determinations as predictors of therapeutic response and long-term outcome in major depression and schizophrenia☆

Abstract Thyrotropin-releasing hormone (TRH) test results and concentrations of triiodothyronine (T 3 ), free thyroxine (fT 4 ), free T 3 (fT 3 ) did not predict response either to antidepressant drug treatment in general or to a selective norepinephrine reuptake inhibitor (maprotiline) versus a reuptake inhibitor of both norepinephrine and serotonin (clomipramine), respectively, in 31 patients with major depressive disorder. Responders had higher thyroxine (T 4 ) levels on admission than nonresponders. The response to neuroleptic drugs was not predicted by any hormone measurement in the 15 schizophrenic patients. A blunted TRH test result did not predict therapeutic response in either depressed or schizophrenic patients. Changes in either TRH test results or thyroid hormone levels during treatment did not predict relapse in 27 depressed and 12 schizophrenic patients at 6, 12, or 18 months after discharge. The normalization of a blunted TRH test after recovery was also of no value for predicting a stable long-term outcome. Thyroid hormone concentrations on discharge did not predict relapse in depressed patients, but the patients who did not relapse had lower TRH test results on discharge than those who did.