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Muscular temporomandibular disorder (TMD) is a common stress-related condition showing marked comorbidity with depression and fibromyalgia (FM), both of which are associated with dysregulation of cortisol secretion. We measured cortisol levels in 15 women with well-defined TMD and 15 matched controls by sampling blood at 10-minute intervals over 24 hours in a controlled environment. TMD patients showed markedly increased daytime cortisol levels 30% to 50% higher than those of controls (p = 0.0032) and a one-hour phase delay in the timing of maximum cortisol levels (p = 0.048). Increased activation of the stress hormone axis by conscious pain perception is a likely explanation, but the magnitude of the increase could indicate that pain in the facial region acts as a greater stimulus than pain elsewhere in the body. [ABSTRACT FROM AUTHOR]

Many endocrine systems are regulated by pulsatile hormones - hormones that are secreted intermittently in boluses rather than continuously over time. To study pulsatile secretion, blood is drawn every few minutes for an extended period. The result is a time series of hormone concentrations for each individual. The goal is to estimate pulsatile hormone secretion features such as frequency, location, duration, and amount of pulsatile and non-pulsatile secretion and compare these features between groups. Various statistical approaches to analyzing these data have been proposed, but validation has generally focused on one hormone. Thus, we lack a broad understanding of each method's performance. By using simulated data with features seen in reproductive and stress hormones, we investigated the performance of three recently developed statistical approaches for analyzing pulsatile hormone data and compared them to a frequently used deconvolution approach. We found that methods incorporating a changing baseline modeled both constant and changing baseline shapes well; however, the added model flexibility resulted in a slight increase in bias in other model parameters. When pulses were well defined and baseline constant, Bayesian approaches performed similar to the existing deconvolution method. The increase in computation time of Bayesian approaches offered improved estimation and more accurate quantification of estimation variation in situations where pulse locations were not clearly identifiable. Within the class of deconvolution models for fitting pulsatile hormone data, the Bayesian approach with a changing baseline offered adequate results over the widest range of data., (Copyright © 2013 John Wiley & Sons, Ltd.)

Increased plasma cortisol in patients with major depression is a well documented finding, although it is present in only 25-30% of subjects with major depression. However, ACTH and cortisol are secreted in a pulsatile manner, so it is unclear if increased ACTH secretion occurs in depression and if there are changes in the pulsatile components of ACTH secretion. Ten-minute sampling for ACTH and cortisol was performed for 24 hr in 25 premenopausal depressed women, whose age and menstrual cycle day matched control women. As a group, the depressed women demonstrated a trend to increase cortisol secretion (p = 0.089). There was no difference in mean cortisol between the patient group as a whole (8.36 +/- 2.9 microg/dl) and those patients meeting criteria for atypical depression (8.38 +/- 1.9 microg/dl), but patients meeting criteria for endogenous showed increased cortisol (12.17 +/- 4 microg/dl) Mean ACTH was not significantly different between patients and controls. Pulse analyses revealed similar number of secretory events and similar amplitudes for cortisol secretory bursts in patients and controls. The baseline component area under the curve of cortisol secretion was increased at a trend level (p =.064) in depressed patients, and the baseline AUC for ACTH was significantly increased in depressed patients (p =.045). No differences were found in pulsatile components of ACTH secretion between patients and matched controls. Harmonic analyses indicated no significant differences between patients and controls on any detected rhythm for ACTH or cortisol. These data suggest that the pulsatile and circadian components of the HPA axis are normal in premenopausal depressed women and that only 24% of depressed women demonstrate hypercortisolemia.

Background: Stress and corticotropin-releasing hormone inhibit the reproductive axis. We hypothesized that reproductive axis hormone secretion, particularly luteinizing hormone secretion, is inhibited in women with depression, similar to what has been observed to be caused by stress in numerous species., Methods: Blood samples were collected every 10 minutes for 12 hours in 25 untreated premenopausal women with depression and 25 nondepressed women who were matched by age and menstrual cycle day. Samples were assayed for luteinizing hormone, follicle-stimulating hormone, estradiol, and progesterone., Results: The mean plasma estradiol level was 30% lower in the follicular phase in women with depression than in their matched controls: 191 + 136 vs 261 + 169 pmol/L (52 + 37 vs 71 + 46 pg/mL). The half-life of luteinizing hormone was significantly shorter in women with depression than in their matched controls during both the follicular (22% shorter) and luteal (15% shorter) phases., Conclusions: The blood levels of reproductive hormones were mostly normal in women with depression, but the blood level of estradiol was significantly lower. Estradiol is known to affect a number of neurotransmitter systems in the brain. Arch Gen Psychiatry. 2000;57:1157-1162.

Five experiments were conducted to test the hypothesis that PGs mediate the endotoxin-induced inhibition of pulsatile GnRH and LH secretion in the ewe. Our approach was to test whether the PG synthesis inhibitor, flurbiprofen, could reverse the inhibitory effects of endotoxin on pulsatile LH and GnRH secretion in ovariectomized ewes. Exp 1-4 were cross-over experiments in which ewes received either flurbiprofen or vehicle 2 weeks apart. Jugular blood samples were taken for LH analysis throughout a 9-h experimental period. Depending on the specific purpose of the experiment, flurbiprofen or vehicle was administered after 3.5 h, followed by endotoxin, vehicle, or ovarian steroids (estradiol plus progesterone) at 4 h. In Exp 1, flurbiprofen reversed the endotoxin-induced suppression of mean serum LH concentrations and the elevation of body temperature. In Exp 2, flurbiprofen prevented the endotoxin-induced inhibition of pulsatile LH secretion and stimulation of fever, reduced the stimulation of plasma cortisol and progesterone, but did not affect the rise in circulating tumor necrosis factor-alpha. In Exp 3, flurbiprofen in the absence of endotoxin had no effect on pulsatile LH secretion. In Exp 4, flurbiprofen failed to prevent suppression of pulsatile LH secretion induced by luteal phase levels of the ovarian steroids progesterone and estradiol, which produce a nonimmune suppression of gonadotropin secretion. In Exp 5, flurbiprofen prevented the endotoxin-induced inhibition of pulsatile GnRH release into pituitary portal blood. Our finding that this PG synthesis inhibitor reverses the inhibitory effect of endotoxin leads to the conclusion that PGs mediate the suppressive effects of this immune/inflammatory challenge on pulsatile GnRH and LH secretion.