Biomedical subjects

Elizabeth A Young

Publications and source records attributed to Elizabeth A Young.

At least 19 recordsLinked to original sources

PubMed2007

HPA axis activity in patients with panic disorder: review and synthesis of four studies.

Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis may play a role in panic disorder. HPA studies in patients with panic disorder, however, have produced inconsistent results. Seeking to understand the inconsistencies, we reexamined endocrine data from four studies of patients with panic disorder, in light of animal data highlighting the salience of novelty, control, and social support to HPA axis activity. Patients with panic disorder were studied (1) at rest over a full circadian cycle, (2) before and after activation by a panicogenic respiratory stimulant (doxapram) that does not directly stimulate the HPA axis, and (3) before and after a cholecystokinin B (CCK-B) agonist that is panicogenic and does directly stimulate the HPA axis. Patients with panic disorder had elevated overnight cortisol levels, which correlated with sleep disruption. ACTH and cortisol levels were higher in a challenge paradigm (doxapram) than in a resting state study, and paradigm-related ACTH secretion was exaggerated in patients with panic disorder. Panic itself could be elicited without HPA axis activation. Patients with panic disorder showed an exaggerated ACTH response to pentagastrin stimulation, but this response was normalized by prior exposure to the experimental context or psychological preparation to reduce novelty and enhance sense of control. Novelty is one of a number of contextual cues known from animal work to activate the HPA axis. The HPA axis abnormalities seen in patients with panic disorder in the four experiments reviewed here might all be due to exaggerated HPA axis reactivity to novelty cues. Most of the published panic/HPA literature is consistent with the hypothesis that HPA axis dysregulation in panic is due to hypersensitivity to contextual cues. This hypothesis requires experimental testing.

Adolescent↗

PubMed2006

Saliva cortisol and response to dexamethasone in children of depressed parents.

BACKGROUND: Major depression (MDD) is heritable, and children of depressed parents are at higher risk for the development of depression. However, depression in a parent might also act as a stressor leading to increased activation of neuroendocrine stress circuits. To address this question we examined saliva cortisol in children whose parents have a history of MDD. METHODS: We recruited 15 families with one parent with MDD (26 prepubertal children) and 16 control families without history of parental MDD (32 prepubertal children). All parents and children underwent Structured Clinical Interview for DSM-IV and Kiddie Schedule For Affective Disorders And Schizophrenia interviews, respectively. Families were asked to collect morning, afternoon, and bedtime saliva samples for 4 days for 2 weeks. At bedtime of the 3rd day, dexamethasone was administered. Two doses, standard and low, were used in each family. RESULTS: The majority of children demonstrated no psychiatric diagnosis. Children with MDD parents showed higher cortisol basally and higher cortisol after both 25 mg and 5 mg dexamethasone. However, this effect occurred predominantly in children whose parents were currently depressed. There were strong correlations for cortisol between parents and children (r = 52 in depressed; r = 499 in control). CONCLUSIONS: Elevated cortisol and impaired feedback seemed to reflect an environmental effect of MDD in a parent.

Adult↗

PubMed2006

Sex differences in the ACTH response to 24H metyrapone in depression.

Increased hypothalamic-pituitary-adrenal (HPA) axis activation has been observed in major depression. Increased corticotropin-releasing hormone (CRH) is hypothesized to drive corticotropin (ACTH) secretion leading to increased ACTH and cortisol secretion throughout 24H. Contradicting data exist as to whether the increased drive is present throughout the day or is restricted to the late afternoon and evening. To determine if increased HPA axis activation occurs during a specific circadian phase or is found throughout the 24H, we studied 26 healthy drug-free depressed patients and 26 healthy age- and sex-matched control subjects under metyrapone inhibition of cortisol synthesis for 24H beginning at 4 PM. Blood was drawn every 10 min for 24H and assayed for ACTH and cortisol. Gender differences in response to metyrapone were seen in both patients and controls. Depressed women demonstrated increased ACTH concentrations between 4 PM and 10 PM compared to control women. Maximal ACTH response over time was identical between depressed and control women. Depressed men demonstrated significantly decreased ACTH secretion between 4 and 10 PM as well as decreased maximal ACTH response compared to control men or depressed women. These data support an increased evening CRH drive in depressed women, but overall decreased CRH drive in depressed men.

Adrenal Cortex↗

PubMed2006

Disordered adrenocorticotropin secretion in women with major depression.

CONTEXT: Major depression is accompanied by activation of the hypothalamic pituitary axis and evidence of abnormalities in circadian and ultradian hormone rhythms. In addition, diminished negative feedback of cortisol on ACTH has been found. OBJECTIVE: The objective of the study was to compare ACTH and cortisol hormonal patterns in women with major depression with normal control women. DESIGN: This was a case control study. SETTING: The study was conducted at a general clinical research center. PATIENTS AND OTHER PARTICIPANTS: Healthy, drug-free, premenopausal women with major depression and age and menstrual cycle day-matched healthy control women were included in the study. MAIN OUTCOME MEASURE: ACTH and cortisol data were measured every 10 min for 24 h analyzed with approximate entropy and cross-approximate entropy to determine orderliness of hormone secretion and relationship between ACTH and cortisol in terms of feedforward and feedback synchrony. RESULTS: Depressed women manifested increased approximate entropy, indicating more disorderly secretion, of ACTH and elevated forward cross-approximate entropy of ACTH on cortisol, denoting unopposed ACTH drive. CONCLUSIONS: These data support other evidence of hormonal rhythm abnormalities in depression and are compatible with accentuated feedforward drive by ACTH.

Adrenocorticotropic Hormone↗

PubMed2006

Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women.

CONTEXT: There is extensive evidence implicating dysfunctions in stress responses and adaptation to stress in the pathophysiological mechanism of major depressive disorder (MDD) in humans. Endogenous opioid neurotransmission activating mu-opioid receptors is involved in stress and emotion regulatory processes and has been further implicated in MDD. OBJECTIVE: To examine the involvement of mu-opioid neurotransmission in the regulation of affective states in volunteers with MDD and its relationship with clinical response to antidepressant treatment. DESIGN: Measures of mu-opioid receptor availability in vivo (binding potential [BP]) were obtained with positron emission tomography and the mu-opioid receptor selective radiotracer carbon 11-labeled carfentanil during a neutral state. Changes in BP during a sustained sadness challenge were obtained by comparing it with the neutral state, reflecting changes in endogenous opioid neurotransmission during the experience of that emotion. SETTING: Clinics and neuroimaging facilities at a university medical center. PARTICIPANTS: Fourteen healthy female volunteers and 14 individually matched patient volunteers diagnosed with MDD were recruited via advertisement and through outpatient clinics. INTERVENTIONS: Sustained neutral and sadness states, randomized and counterbalanced in order, elicited by the cued recall of an autobiographical event associated with that emotion. Following imaging procedures, patients underwent a 10-week course of treatment with 20 to 40 mg of fluoxetine hydrochloride. MAIN OUTCOME MEASURES: Changes in mu-opioid receptor BP during neutral and sustained sadness states, negative and positive affect ratings, plasma cortisol and corticotropin levels, and clinical response to antidepressant administration. RESULTS: The sustained sadness condition was associated with a statistically significant decrease in mu-opioid receptor BP in the left inferior temporal cortex of patients with MDD and correlated with negative affect ratings experienced during the condition. Conversely, a significant increase in mu-opioid receptor BP was observed in healthy control subjects in the rostral region of the anterior cingulate. In this region, a significant decrease in mu-opioid receptor BP during sadness was observed in patients with MDD who did not respond to antidepressant treatment. Comparisons between patients with MDD and controls showed significantly lower neutral-state mu-opioid receptor BP in patients with MDD in the posterior thalamus, correlating with corticotropin and cortisol plasma levels. Larger reductions in mu-opioid system BP during sadness were obtained in patients with MDD in the anterior insular cortex, anterior and posterior thalamus, ventral basal ganglia, amygdala, and periamygdalar cortex. The same challenge elicited larger increases in the BP measure in the control group in the anterior cingulate, ventral basal ganglia, hypothalamus, amygdala, and periamygdalar cortex. CONCLUSIONS: The results demonstrate differences between women with MDD and control women in mu-opioid receptor availability during a neutral state, as well as opposite responses of this neurotransmitter system during the experimental induction of a sustained sadness state. These data demonstrate that endogenous opioid neurotransmission on mu-opioid receptors, a system implicated in stress responses and emotional regulation, is altered in patients diagnosed with MDD.

Adrenocorticotropic Hormone↗

PubMed2006

The role of corticosterone in human hypothalamic-pituitary-adrenal axis feedback.

OBJECTIVE: In humans, the glucocorticoid corticosterone circulates in blood at 10-20-fold lower levels than cortisol, but is found in higher relative amounts in postmortem brain samples. Access of cortisol and corticosterone to the central nervous system may not be equal. Additionally, the relative affinities for the glucocorticoid and mineralocorticoid receptors differ, such that corticosterone may play a significant role in human brain function. DESIGN: We measured cortisol and corticosterone levels in paired plasma and cerebrospinal fluid (CSF) samples. To test the relative potency of cortisol vs. corticosterone on hypothalamic-pituitary-adrenal (HPA) feedback, subjects underwent a three-phase, single-blind, randomized study assessing the postmetyrapone ACTH response over 3 h to an intravenous bolus of vehicle, cortisol or corticosterone (0.15 mg/kg and 0.04 mg/kg). PARTICIPANTS: Outpatients undergoing diagnostic lumbar puncture who were subsequently deemed to be free of disease. Feedback was tested in healthy male volunteers. MEASUREMENTS: Plasma and CSF corticosterone to cortisol ratio was calculated and the ACTH response over time after the bolus glucocorticoid measured. RESULTS: Plasma corticosterone : cortisol was 0.069 +/- 0.007; CSF corticosterone : cortisol was 0.387 +/- 0.050 (P < 0.001). Cortisol and corticosterone (0.15 mg/kg) suppressed ACTH vs. vehicle (P = 0.002); there was no difference between corticosterone and cortisol. The 0.04 mg/kg dose had no effect on ACTH despite supraphysiological plasma corticosterone levels. CONCLUSIONS: Corticosterone contributes almost 40% of total active glucocorticoids (cortisol and corticosterone) in the CSF. Significant effects on HPA axis suppression were only seen with supraphysiological levels of corticosterone, suggesting that corticosterone is not important in this model of nonstress-induced ACTH hypersecretion, in which the effect of cortisol predominates.

Adrenocorticotropic Hormone↗

PubMed2006

What happened to lithium? Antidepressant augmentation in clinical settings.

OBJECTIVE: Antidepressant augmentation is recommended when patients do not respond to antidepressant monotherapy. However, little is know about antidepressant augmentation in clinical settings and whether these practices reflect the research evidence. METHOD: The authors identified 244,859 patients in Veterans Administration mental health settings with a diagnosis of depression and an antidepressant prescription during fiscal year 2002. Patients with schizophrenia, dementia, or bipolar I disorder were excluded. The authors examined the prevalence and characteristics of antidepressant augmentation during the year, defined as receiving an antidepressant and an augmenting agent (lithium, second-generation antipsychotics, combinations of antidepressants, anticonvulsants, or "other") for >/=60 consecutive days in specified doses for those without other clinical indications. Mixed-effect models were used to examine predictors of augmentation. RESULTS: Some patients (22%) received an augmenting agent. The most commonly used agents were a second antidepressant (11%) and a second-generation antipsychotic (7%). Only 0.5% of the patients received lithium. Whites, younger patients, and those with a prior hospitalization were more likely to receive augmentation. African Americans were more likely to receive antipsychotic augmentation; whites were more likely to receive lithium. CONCLUSIONS: Antidepressant augmentation is common in clinical settings. Although lithium currently has the most research support, antipsychotic medications and a second antidepressant are the most widely used augmenting agents. Many augmenting agents are used across clinical and demographic groups. Research is needed on the relative effectiveness of these agents, along with efforts to promote the use of agents with the greatest level of research support.

Black or African American↗

PubMed2005

Material hardship alters the diurnal rhythm of salivary cortisol.

BACKGROUND: In the quest for biological mechanisms underlying socioeconomic differences in health outcomes, attention has turned to the role of the hypothalamic-pituitary-adrenocortical axis. As there is some evidence that both acute and chronic stress raise cortisol levels, and material hardship is a stressor, we examined the relationship of chronic material hardship with salivary cortisol levels over the day. METHODS: The data are from a survey of a sample of poor women aged 18-54. Up to four repeated measures of salivary cortisol levels were obtained from 188 women in this sample and modelled as a diurnal profile. Self-reports of a variety of sources of material hardship over the preceding year were combined into a single scale. Specific dimensions of the subjects' cortisol profiles were compared across levels of material hardship. RESULTS: Salivary cortisol varied over the day, and by level of reported material hardship. Upon awakening, salivary cortisol levels were comparable across hardship levels. But soon after waking, women at low levels of hardship experienced both a significantly sharper morning surge and subsequently a sharper decline in salivary cortisol (16.0 and 29.5 nmol/l/h) than women with high hardship levels (5.9 and 24.3 nmol/l/h). These differences in cortisol diurnal pattern tended to be related in a dose-response way to levels of material hardship. CONCLUSIONS: Material hardship among poor women is associated with changes in the diurnal rhythms of cortisol, particularly in the waking response, which is blunted in women with high levels of hardship.

Adolescent↗

PubMed2005

Cognitive modulation of the endocrine stress response to a pharmacological challenge in normal and panic disorder subjects.

CONTEXT: The hypothalamic-pituitary-adrenal (HPA) axis may mediate the deleterious effects of stress on health. It is sensitive to cognitive and emotional aspects of organism-environment interactions, such as familiarity, control, and social support. Scientific study of how such factors moderate human HPA axis activity has been limited. Their relevance to HPA axis disturbances in psychiatric patients is largely unexplored. OBJECTIVE: To determine whether cognitive manipulation can alter HPA axis activity in laboratory studies and whether patients with panic disorder are differentially sensitive to the manipulated factors. DESIGN: Pharmacological activation paradigm (cholecystokinin-B agonist pentagastrin) by which we examined symptom and endocrine effects on subjects randomly assigned to a standard introduction or a cognitive intervention. SETTING: Clinical research center. PARTICIPANTS: Recruited from university clinic and newspaper advertisements. Fourteen patients with panic disorder and 14 controls, individually matched for age and sex. Intervention Half of each group received a 9-minute cognitive intervention designed to reduce novelty, increase cognitive coping, and provide a sense of control. MAIN OUTCOME MEASURES: Corticotropin (ACTH) and cortisol levels. RESULTS: The cognitive intervention significantly reduced cortisol (P = .02) and ACTH (P = .01) levels, despite pentagastrin's robust stimulation of both hormones (P<.001). The intervention effect was evident in patients and controls, who did not differ in basal HPA axis activity or response to pentagastrin. They did differ in panic symptom responses, which were unaffected by the intervention, and in ACTH effects of the intervention. Patients' exaggerated anxiety responses to pentagastrin were normalized by the intervention. CONCLUSIONS: Cognitive/emotional manipulation can substantially modulate HPA axis responses to pharmacological activation in humans, and HPA disturbances in panic disorder may be secondary to manipulable cognitive/emotional sensitivities. Further study of such factors as novelty, control, and coping may help clarify the origins of HPA axis disturbance in psychiatric disorders and the mediators linking psychosocial stress to disease.

Adaptation, Psychological↗

PubMed2005

Gender differences in depression: findings from the STAR*D study.

BACKGROUND: Epidemiologic research consistently reports gender differences in the rates and course of major depressive disorder (MDD). The STAR*D (Sequenced Treatment Alternatives to Relieve Depression) multicenter trial provides a unique opportunity to explore gender differences in outpatients with nonpsychotic MDD. METHODS: This sample included the first 1500 outpatients with MDD who enrolled in STAR*D. Nearly two-thirds of the sample (62.8%) were women. Baseline sociodemographic factors, comorbidities, and illness characteristics were analyzed by gender. RESULTS: Women (62.8% of the sample) had a younger age at onset of the first major depressive episode. They commonly reported concurrent symptoms consistent with anxiety disorders, somatoform disorder, and bulimia as well as atypical symptoms. Alcohol and drug abuses were more common in men. LIMITATIONS: This report is a subpopulation of the entire STAR*D sample. These exploratory analyses aimed to identify potential gender differences for further hypothesis testing. CONCLUSIONS: The gender-specific rate of MDD in this study population is proportional to rates found in community samples with a 1.7:1 prevalence of MDD in women vs. men which argues against increased treatment seeking in women.

Adolescent↗

PubMed2005

Modeling cortisol rhythms in a population-based study.

The aim of these analyses was to develop and describe easily implementable, yet information rich, approaches for analysis of the temporal profile of cortisol in human populations. A typical waking profile of cortisol in a sample of women aged 15-44 was parameterized by a piecewise linear regression model, implemented as a mixed model to accommodate repeated observations among individuals. The model was extended to distinguish characteristic cortisol profiles of obese women from those of non-obese women. Sharp inflection points for the diurnal profile of cortisol were noted at 30 and 75 min past awakening. Obese women showed a slight tendency to have a less sharply rising and declining response to awakening than non-obese women.

Adolescent↗

PubMed2005

Interaction of brain noradrenergic system and the hypothalamic-pituitary-adrenal (HPA) axis in man.

BACKGROUND: Numerous interactions between the brainstem locus coeruleus system and the HPA axis have been shown in experimental animals. This relationship is less well characterized in humans and little is known about the influence of psychiatric disorders, which disturb one of these systems, on this relationship. METHODS: Untreated subjects with pure MDD (n = 13), MDD with comorbid anxiety disorders (n = 17), and pure anxiety disorders (n = 15) were recruited by advertising. Age and sex matched control subjects were recruited for each subject with a psychiatric diagnosis (n = 45). All subjects underwent a social stressor, the Trier Social Stress Test (TSST), and blood was collected for ACTH assay. These same subjects also underwent a clonidine challenge study for assessment of growth hormone release as a marker of tonic noradrenergic activation. RESULTS: Examining log transformed area under the curve response for each hormone, a significant negative relationship (simple regression) was observed between systems in normal subjects. This relationship was preserved in anxiety subjects. However, both pure depressed and comorbid depressed and anxiety subjects demonstrated disruption of this relationship. CONCLUSIONS: Under normal circumstances, noradrenergic systems can influence the magnitude of the HPA axis response to stress. However, in subjects with major depression, HPA axis activation appears autonomous of noradrenergic influence.

Adrenocorticotropic Hormone↗

PubMed2005

The pattern of growth hormone secretion during the menstrual cycle in normal and depressed women.

OBJECTIVE: Major depression is associated to altered hypothalamic-pituitary function. Stress is linked to elevated cortisol as well as menstrual cycle disturbance; however, there is no known relationship between depression and menstrual cycle disruption. The aim of this study was to investigate changes of growth hormone (GH) secretion during the menstrual cycle in normal and depressed women. DESIGN: Case-control study. PATIENTS AND METHODS: Nineteen women affected with depression and 24 normal controls were included. The two groups had comparable body mass index (BMI), and age (29.4 +/- 9.8 vs. 28.6 +/- 9.7 years). Nine depressed and 10 controls were studied in the follicular phase, while 10 depressed and 14 controls were studied in the luteal phase of the cycle. GH was sampled every 10 min for 24 h, and the data were analysed by the cluster pulse detection method. RESULTS: There was no difference in 24-h mean GH concentrations between depressed and control subjects (P = 0.93), even after accounting for menstrual cycle phase (P = 0.38). GH pulse frequency was higher during the follicular phase of the cycle (P = 0.032), and nocturnal GH was higher in the follicular phase of the cycle (P = 0.05, and after adjusting for 24-h GH, P = 0.0138) regardless of whether the subjects were depressed or healthy. CONCLUSIONS: In studies of GH secretion in women with or without depression, it is necessary to control for the phase of menstrual cycle.

Adult↗

PubMed2005

The health of poor women under welfare reform.

OBJECTIVES: We compared the health of single mothers affected by welfare reform with the health of a nationally representative sample of women to document the prevalence of poor health as single mothers experience the effects of welfare reform. METHODS: We compared risk factors and measures of health among women randomly sampled from the welfare rolls with similar data from a nationally representative sample of women. RESULTS: Women in our welfare recipient sample had higher rates of elevated glycosylated hemoglobin (> or = 6%; prevalence ratio [PR]=4.87; 95% confidence interval [CI]=2.69, 7.04), hypertension (systole > or = 140 or diastole > or = 90; PR=2.36; 95% CI = 1.47, 3.24), high body mass index ( > or = 30; PR = 1.78; 95% CI = 1.49, 2.08), and high-density lipoprotein cholesterol (< or = 35 mg/dL; PR=1.91; 95% CI=1.17, 2.65); lower peak expiratory flow; and less physical functioning. Current smoking rates were higher (PR = 1.85; 95% CI = 1.50, 2.19) and smoking cessation rates were lower (PR=0.62; 95% CI=0.37, 0.86) than in the national sample. CONCLUSIONS: Current and former welfare recipients bear a substantial burden of illness. Further studies are necessary to interpret our findings of worsened health in the wake of welfare reform.

Adult↗

PubMed2005

Clinical predictors of suicide in primary major depressive disorder.

OBJECTIVE: Follow-up studies of patients with depressive disorders have identified only a few replicable predictors of suicide and have not explored possible interactions between them. The following analysis takes advantage of a large cohort of depressed patients given detailed, structured interviews 2 decades ago. METHOD: The data set on which this analysis is based was collected between 1976 and 1990. Research personnel administered the Schedule for Affective Disorders and Schizophrenia to 785 adults who had major depressive disorder (Research Diagnostic Criteria) but who lacked other Axis I disorders. The current analysis used the National Death Index to determine mortality status as of 2003. RESULTS: One in 4 of the 134 deaths were by suicide for an overall suicide rate of 4.2%. In comparison to the remaining 752 patients, the 33 who died by suicide were more likely to have been inpatients and to have had a history of suicide attempts at the time of baseline assessment. They had also expressed more hopelessness and had higher ratings of suicidal tendency. The last of these variables was the most robust by far and, when tested with other predictors in regression analyses, was the only one to retain significance (p < .0001). No interactions between predictors emerged. As in an earlier, similar study, the suicidal tendency rating was predictive of suicides that occurred after the first year of follow-up, which suggests that suicidal tendencies comprise a trait that persists across episodes. CONCLUSION: A global rating of suicidality appears to be the single most important predictor of eventual suicide in patients with major depressive disorder.

Adult↗

PubMed2004

Anxious and depressive disorders and their comorbidity: effect on central nervous system noradrenergic function.

BACKGROUND: Although comorbidity of anxiety with depression is common, investigations of physiologic abnormalities related specifically to comorbidity are rare. This study examined relationships of DSM-IV-defined depression, anxiety, and their comorbidity to noradrenergic function measured by blunting of the growth hormone (GH) response to the alpha2 adrenoreceptor agonist (and imidazoline receptor agent) clonidine and by blood pressure and symptom responses. METHODS: Fifteen subjects with pure social anxiety or panic disorder, 15 with pure major depression, and 18 with both depression and anxiety were compared with healthy control subjects matched for age and gender. Other factors known to affect GH (weight, menstrual status, prior antidepressant, or other drug exposure) were controlled. RESULTS: Anxiety produced GH blunting, but depression was associated with normal GH responses. The comorbid state did not affect results beyond the impact of anxiety. Preclonidine stress-related GH elevations were observed, to the greatest degree in anxious subjects. Relevant symptom, but not blood pressure, changes were significantly associated with blunting. CONCLUSIONS: With use of pure depression and anxiety groups and careful control of other factors known to affect GH, these results demonstrate central nervous system noradrenergic dysfunction in anxiety disorders. In contrast to less rigorously controlled studies, noradrenergic function in depression was normal.

Adrenergic alpha-Agonists↗

PubMed2004

Saliva cortisol in posttraumatic stress disorder: a community epidemiologic study.

BACKGROUND: Stress activates the hypothalamic-pituitary-adrenal (HPA) axis, so it was expected that posttraumatic stress disorder (PTSD) would be associated with activation of this axis; however, studies have found both increased and decreased cortisol in PTSD. To address this question, we collected saliva cortisol at home in a subsample of a longitudinal epidemiologic sample. METHODS: Six hundred eighty-four persons randomly selected from the total sample of 913 were requested to collect saliva samples upon awakening and in the early evening. Of these, 538 responded with samples, 516 of whom met inclusion criteria. These were 68 exposed to trauma with lifetime PTSD, 265 exposed to trauma with no PTSD, and 183 never exposed to trauma. RESULTS: In a comparison of these three groups, lifetime PTSD revealed elevated evening saliva cortisol compared with exposed/no PTSD. When lifetime comorbidity with major depressive disorder (MDD) was included in the analysis, only persons with comorbid PTSD and MDD showed this evening elevation in cortisol. Persons with PTSD alone (never MDD) showed normal saliva cortisol levels, as did subjects with lifetime MDD alone. CONCLUSIONS: Neither exposure to trauma nor PTSD alone is associated with alterations in saliva cortisol; however, elevated cortisol is found in PTSD comorbid with lifetime MDD.

Adult↗

PubMed2004

Effect of comorbid anxiety disorders on the hypothalamic-pituitary-adrenal axis response to a social stressor in major depression.

BACKGROUND: Major depressive disorder (MDD) is often complicated by anxiety symptoms, and anxiety disorders occur in approximately 30% of mood cases. This study examined the influence of anxiety comorbidity on the hypothalamic-pituitary-adrenal (HPA) axis response to stress in patients with MDD. METHODS: Untreated subjects with pure MDD (n = 15), MDD with comorbid anxiety disorders (n = 18), and pure anxiety disorders (n = 15) were recruited by advertising. Age- and gender-matched control subjects were recruited for each subject with a psychiatric diagnosis (n = 48). All subjects underwent a social stressor, the Trier Social Stress Test (TSST), and blood was collected for adrenocorticotropic hormone (ACTH) and cortisol assay. RESULTS: When all depressed patients (n = 33) were compared with their matched control subjects (n = 33), they showed a significantly greater ACTH response to the stressor; however, this exaggerated ACTH response was exclusively due to the depressed group with comorbid anxiety disorders. A similar but nonsignificant effect was observed in the cortisol response. Subjects with pure mood or pure anxiety disorders showed normal ACTH and cortisol responses to the TSST. All patient groups showed similar levels of TSST-induced anxiety. CONCLUSIONS: Comorbid anxiety disorders might play a role in the increased activation of the HPA axis observed in patients with major depression.

Adrenocorticotropic Hormone↗