Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper investigates if the highly selective norepinephrine reuptake inhibitor reboxetine leads to a dose-dependent cortisol release and if this response depends on personality dimensions related to clinical depression in healthy volunteers. Twenty-four male subjects received placebo, 2 mg, or 4 mg reboxetine in a balanced, randomized cross-over study. Cortisol was measured in saliva at six different time-points according to the kinetics of the drug. Furthermore, several measurements of cardiovascular parameters, emotional states, and possible side-effects were obtained. Subjects were divided into two groups scoring above or below the median of a depressiveness questionnaire scale [n = 11, low (D-); n = 13, high (D+)]. Results clearly demonstrated, that reboxetine stimulates cortisol release. Whereas blood pressure was not affected, heart rate increased after 2 and 4 mg but not dose dependently. Subjects reported more non-specific arousal while the dimensions of tiredness-wakefulness and positive-negative emotional states were not affected by the drug. Somatic complaints were low and only non-specific complaints were statistically elevated but of negligible amount. Subjects classified as D+ can be characterized as high responders to the drug. This is especially true not only for cortisol increases but also for changes in heart rate and some ratings on physical complaints. Hot flushes, sweating and a throbbing sensation in blood vessels in the head were observed in D+ but only with the 4 mg dose. The results clearly demonstrate that reboxetine stimulates cortisol release and heart rate and that this is particularly pronounced in subjects scoring high on depression-related personality dimensions. Reboxetine, therefore, is a promising tool for investigating neuroendocrine response to noradrenergic challenge tests. The question whether increased responses in D+ are due to an up-regulation of receptor sensitivity as a consequence of low norepinephrine supply is discussed.
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PMID:Reboxetine in a neuroendocrine challenge paradigm: evidence for high cortisol responses in healthy volunteers scoring high on subclinical depression. 1134 96

Forty-eight-hour rapid cycling is a rare subclass of affective disorders and entails a regular periodic change of moods. The following case study describes the symptoms, therapy, and outcome of a patient suffering from daily switching between mania and depression along with neurobiological findings correlated to the affective cycles. We found alternating reduction and prolongation of sleep duration during manic and depressive days as well as differences in the amount of REM sleep. Cortisol secretion was regularly increased during depressive days. Regarding thyroid-stimulating hormone (TSH) secretion, the circadian rhythm was absent on depressive days. However, the glucose metabolic rate as measured by positron emission tomography (PET) did not differ on manic and depressive days. The patient reached almost complete remission under treatment with lithium.
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PMID:[Neurobiological findings in a patient with 48-hour rapid cycling bipolar affective disorder. A case report]. 1147 28

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal. Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3. untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension). States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome. The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.
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PMID:Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. 1205 88

The Dex/CRH test is one of the most reliable neuroendocrine function tests for hypothalamic-pituitary-adrenocortical (HPA) system dysregulation in depression. Persistent overdrive of HPA system activity after successful antidepressant treatment predicts an enhanced risk for relapse of a depressive episode. As the renin-angiotensin system has been shown to play a role in HPA system activity, we investigated the impact of the angiotensin converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphism, which determines ACE plasma concentrations, on HPA system dysregulation. We performed repeated combined Dex/CRH tests in 115 patients suffering from major depression. Dex/CRH test results were related to the I/D polymorphism within the ACE gene, which was assessed by PCR. Genotype frequencies were comparable to those in the general population (I/I 16.8%, I/D 59.3%, D/D 23.9%). D/D genotypes showed a higher cortisol stimulation during the first Dex/CRH test after admission than homozygous I-allele carriers (repeated measurement ANOVA: P=0.034). Cortisol area under the curve values were highest in those with the D/D genotype (mean+/-SEM [nmol/l*75 min]: 12700+/-2220), intermediate in those with the I/D genotype (9570+/-1000), and lowest in those with the I/I genotype (5160+/-1000; ANOVA: P=0.04). After successful antidepressive treatment and attenuation of HPA system overdrive these differences were no more detectable. The HPA axis stimulating properties of higher ACE and consecutively higher AT-II and/or lower substance P concentrations may be crucial factors for the HPA system hyperactivity during major depressive episodes.
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PMID:Hypothalamic-pituitary-adrenocortical axis dysregulation in patients with major depression is influenced by the insertion/deletion polymorphism in the angiotensin I-converting enzyme gene. 1214 30

Reduced cortisol coupled with elevated catecholamines has been reported for patients with post-traumatic stress disorder (PTSD) precipitated by war and other traumas considered to be "outside the range of usual experiences". It is unclear whether these neuroendocrine abnormalities also occur in PTSD precipitated by more commonly experienced traumas associated with life-threatening illness. Overnight (12-h) urinary cortisol, norepinephrine (NE) and epinephrine (E) were measured in 21 mothers of pediatric cancer survivors with (n = 14) and without PTSD symptoms (n = 7) and in control mothers of healthy children (n = 8). Mothers meeting subthreshold and full PTSD criteria were combined to form the PTSD symptoms group. The PTSD group showed lower total urinary cortisol and a trend for higher total urinary NE than the non-PTSD group, who in turn were no different from controls. There were no significant group effects for E. Cortisol (but not NE) effects remained after controlling for symptoms of co-morbid depression. The finding of reduced cortisol in illness-related PTSD demonstrates neuroendocrine dysregulation similar to that found previously in other types of trauma (e.g., war-related). Future longitudinal studies with repeated urinary collection procedures will be necessary to clarify measurement issues and establish the time course and health implications of the neuroendocrine perturbations.
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PMID:Urinary cortisol and catecholamines in mothers of child cancer survivors with and without PTSD. 1218 16

We examined sleeping problems in women with metastatic breast cancer in relation to depression, social support, and salivary cortisol. Ninety-seven women with metastatic breast cancer were drawn from a larger study on the effects of group therapy on quality of life and survival. This study is based on the baseline assessments conducted prior to randomization into treatment conditions. Sleep, depression symptoms, and social support were assessed by self-reporting. Cortisol was assessed from saliva samples taken over a 3-day period. Medical status and demographic characteristics were also examined in relation to each sleep variable in multiple regression analysis. Most women (63%) reported one or more types of sleep disturbance and 37% reported using sleeping pills in the previous 30 days. Problems with falling to sleep were significantly related to greater pain and depressive symptoms. Problems of waking during the night were significantly associated with greater depression and less education. Problems in waking/getting up were significantly associated with greater depressive symptoms and less social support. Sleepiness during the day was not significantly related to the variables in the regression model. Fewer hours of sleep were significantly associated with metastases to the bone, higher depressive symptoms, and more social support. Women who reported sleeping 9 or more hours per night, compared to those who reported a moderate amount of sleep (6.5-8.5 hours), had significantly lower 9 p.m. cortisol levels. Use of sleeping pills was more frequent among women reporting greater pain and depressive symptoms. These results suggest that women with metastatic breast cancer who are at higher risk for having sleeping problems are those who are less educated, in pain, depressed, have bony metastases, or lack social support.
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PMID:Sleep disturbances in women with metastatic breast cancer. 1239 Mar 59

A bidirectional interaction exists between sleep electroencephalogram (EEG) and endocrine activity in various species including humans. Various hormones (peptides, steroids) were shown to participate in sleep regulation. A keyrole was shown for the reciprocal interaction between sleep-promoting growth hormone-releasing hormone (GHRH) and sleep-impairing corticotropin-releasing hormone (CRH). Changes in the GHRH:CRH ratio result in changes of sleep-endocrine activity. There is good evidence that the change of this ratio in favor of CRH contributes to aberrances of sleep during aging and depression. Besides of GHRH ghrelin and galanin promote SWS, whereas somatostatin is another sleep-impairing factor. NPY acts as a CRH antagonist and induces sleep onset. Prolactin enhances rapid eve-movement sleep (REMS) in rats. SWS is enhanced in patients with prolactinoma. Other studies on the influence of prolactin of human sleep are lacking. There is a controversy whether CRH promotes REMS. In humans vasocactive intestinal polypeptide (VIP) appears to play a role in the temporal organization of sleep, since after VIP administration the NREMS-REMS cycle decelerated. Several neuroactive steroids (pregnenolone, progesterone, allopregnanolone, dehydroepiandrosterone) exert specific effects on sleep EEG via GABAA receptors. Cortisol appears to enhance REMS. Finally gonadal hormones participate in sleep regulation. Estrogen replacement therapy and CRH-1 receptor antagonism in depression are beneficial clinical applications of the basic research presented here.
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PMID:Sleep and endocrine regulation. 1270 62

The present study investigated the acute effects of cortisol administration in normal healthy male volunteers on immediate free recall and recognition of pleasant, unpleasant, and neutral nouns using a between-subjects double-blind design. Two hours after cortisol (10 mg) or placebo administration, impaired recall and recognition of neutral and pleasant words was found in the treatment group, whereas recall and recognition of unpleasant words was similar in both groups. The interaction between treatment and stimulus valence was not mediated by "semantic cohesion," nor does it seem to have been mediated by stimulus arousal. Cortisol did not change mood. The changes with cortisol in recall and recognition of pleasant and unpleasant words parallel those found in depression, a condition that is often accompanied by elevated basal cortisol levels.
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PMID:Acute cortisol effects on immediate free recall and recognition of nouns depend on stimulus valence. 1282 Aug 57

A bidirectional interaction between sleep electroencephalogram and endocrine activity is well established in various species including humans. Various hormones (peptides and steroids) participate in sleep regulation. A key role was shown for the reciprocal interaction between sleep-promoting growth hormone-releasing hormone (GHRH) and sleep-impairing corticotropin-releasing hormone (CRH). Changes in the GHRH : CRH ratio result in changes of sleep-endocrine activity. It is thought that the change of this ratio in favour of CRH contributes to aberrations of sleep during ageing and depression (shallow sleep, blunted GH and elevated cortisol). Besides GHRH, ghrelin and galanin enhance slow wave sleep. Somatostatin is another sleep-impairing factor. Neuropeptide Y acts as a CRH antagonist and induces sleep onset. There are hints that CRH promotes rapid eye movement sleep (REMS). In animals prolactin enhances REMS. In humans vasoactive intestinal polypeptide (VIP) appears to play a role in the temporal organization of sleep as, after VIP, the non-REMS-REMS cycle decelerated. Cortisol appears to enhance REMS. Finally, gonadal hormones participate in sleep regulation. Oestrogen replacement therapy and CRH-1 receptor antagonism in depression are beneficial clinical applications of sleep-endocrine research.
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PMID:Sleep and endocrinology. 1282 39

The effect of hydrocortisone (50 mg/kg body wt i.p.) under beta-adrenergic receptors blockade (four subcutaneous injections of propranolol in single dose of 5 mg/kg body wt with 3 h interval) on phagocytic activity and oxygen dependent microbicidal activity in NBT-test of peripheral blood phagocytic cells in male Wistar rats was investigated. It was established that hydrocortisone stimulated neutrophil phagocytic activity through 6, 24 and 48 h after hormone injection and decreased oxygen-dependent microbicidal activity of phagocytic cells in NBT-test. Hydrocortisone in vitro (500 ng/ml) decreased neutrophil phagocytic activity that indicated on realization of stimulating effect of hydrocortisone in vivo through complex of other indirect mechanisms. Administration of hydrocortisone led to depression of eosinophil phagocytosis and lesser decrease in monocyte phagocytic activity. Hydrocortisone effects were significantly modified under blockade of beta-adrenoceptors that indicated on its mediation by endogenous catecholamines through modulation of beta-adrenoceptor expression.
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PMID:[Effect of hydrocortisone on peripheral blood phagocytic cells under beta-adrenoreceptors blockade]. 1450 72


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