Low Urinary Cortisol Research Articles

Urinary cortisol is lower in pregnant women with higher pre-pregnancy BMI.

Although cortisol levels increase during normal pregnancy, particularly high levels of cortisol or stress have been associated with adverse maternal/child outcomes. Obesity is associated with altered cortisol metabolism, but there is limited information on pregnancy-related changes in cortisol in pregnant women with overweight/obesity. The objective of this study was to examine weekly measures of urinary cortisol and perceived stress throughout ~10-36 weeks gestation, if levels differ by pre-pregnancy BMI categories, and whether concurrent measures of urinary cortisol and perceived stress are associated. Longitudinal observational data from Healthy Mom Zone, a gestational weight management intervention, and an ancillary fetal growth study were combined. Pregnant women with normal (n=7), overweight (n=11), or obese (n=14) pre-pregnancy BMI were recruited at >8 weeks gestation. Overnight urinary cortisol and Perceived Stress Scale were measured weekly from ~10-36 weeks gestation. Higher pre-pregnancy BMI was associated with overall lower urinary cortisol throughout gestation, but rate of increase in urinary cortisol across pregnancy was similar across weight status groups. Women with obesity reported higher levels of overall perceived stress than normal weight women. Regardless of weight status, perceived stress was not associated with gestational age or cortisol. Although women with obesity reported higher perceived stress, they had lower urinary cortisol than women with normal BMI, and gestation-related increases in cortisol were similar across weight groups and unrelated to perceived stress, suggesting that physiological factors that drive increases in cortisol as pregnancy may outweigh effects of stress and adiposity. https://clinicaltrials.gov/ct2/show/NCT03945266, identifier (NCT03945266).

Maternal Age at Holocaust Exposure and Maternal PTSD Independently Influence Urinary Cortisol Levels in Adult Offspring.

Background: Parental traumatization has been associated with increased risk for the expression of psychopathology in offspring, and maternal posttraumatic stress disorder (PTSD) appears to increase the risk for the development of offspring PTSD. In this study, Holocaust-related maternal age of exposure and PTSD were evaluated for their association with offspring ambient cortisol and PTSD-associated symptom expression.Method: Ninety-five Holocaust offspring and Jewish comparison subjects received diagnostic and psychological evaluations, and 24 h urinary cortisol was assayed by RIA. Offspring completed the parental PTSD questionnaire to assess maternal PTSD status. Maternal Holocaust exposure was identified as having occurred in childhood, adolescence, or adulthood and examined in relation to offspring psychobiology.Results: Urinary cortisol levels did not differ for Holocaust offspring and comparison subjects but differed significantly in offspring based on maternal age of exposure and maternal PTSD status. Increased maternal age of exposure and maternal PTSD were each associated with lower urinary cortisol in offspring, but did not exhibit a significant interaction. In addition, offspring PTSD-associated symptom severity increased with maternal age at exposure and PTSD diagnosis. A regression analysis of correlates of offspring cortisol indicated that both maternal age of exposure and maternal PTSD were significant predictors of lower offspring urinary cortisol, whereas childhood adversity and offspring PTSD symptoms were not.Conclusion: Offspring low cortisol and PTSD-associated symptom expression are related to maternal age of exposure, with the greatest effects associated with increased age at exposure. These effects are relatively independent of the negative consequences of being raised by a trauma survivor. These observations highlight the importance of maternal age of exposure in determining a psychobiology in offspring that is consistent with increased risk for stress-related pathology.

An angiotensin-1 converting enzyme polymorphism is associated with allostatic load mediated by C-reactive protein, interleukin-6 and cortisol

Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects of adaptation to change or stress throughout the lifespan. AL is operationalized by a composite index of multiple biomarkers. Accordingly, genes, behavior and environment contribute to AL. To determine if individual differences in AL may be influenced by inherent genetic variation, we calculated an allostatic load index (ALI) for 182 Caucasian subjects derived from a population-based study of chronic fatigue syndrome. Nearly 65% of the subjects in this study sample reported fatiguing illness. ALI was calculated based on 11 measures representing metabolic, cardiovascular, inflammatory, hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) activities. Subjects were dichotomized into high (ALI > or = 3) or low (ALI < 3) AL groups, and the association between high AL and 129 polymorphisms in 32 genes related to the HPA axis, neurotransmission, inflammation, cardiovascular and metabolic functions were evaluated. Polymorphisms in angiotensin-1 converting enzyme (ACE), corticotropin-releasing hormone receptor 1 (CRHR1), and serotonin receptors (HTR3A and HTR4) were associated with AL (p=0.0007-0.0486), but only one polymorphism, rs4968591, in ACE remained significant after correction for multiple comparisons. The T allele of ACE rs4968591 was more common in subjects with high AL (67.5%) than in subjects with low AL (49.3%) (p=0.0007), and this effect appeared independent of age, sex, body mass index and fatigue status. Additionally, high interleukin-6 (IL-6; p(trend)=0.04), and C-reactive protein (CRP; p(trend)=0.01) levels, as well as low urinary cortisol levels in females (p=0.03) were associated with the T allele, which may result in allele-specific binding of the transcription factor, E2F1. Our results suggest a role for ACE in the bidirectional communication between the central nervous and immune systems in response to stress. Further studies will be needed (a) to replicate the association between AL and ACE polymorphisms in population studies designed to differentiate the effects of sex, age and racial/ethnic background, (b) to evaluate the effect of allele-specific binding of E2F1 at rs4968591, and (c) to examine the role of ACE in the co-regulation of CRP, IL-6 and cortisol.

Is there an association between fibromyalgia and below-normal levels of urinary cortisol?

BackgroundAdynamia in fibromyalgia (FM) may be an expression of a functional deficit of the hypothalamic-pituitary-adrenal axis and be associated with below-normal levels of urinary cortisol. Our aim was to demonstrate that urinary cortisol was lower in patients with FM than in healthy subjects.FindingsWe measured urinary cortisol levels for a sample of 47 women aged 29 to 64 years (mean age 53 years), diagnosed with FM 2–3 years previously, and compared the results with those for a control sample of 58 healthy women of a similar age. Samples of 24-hour urine were appropriately collected and levels of urinary cortisol were measured using the fluorescence polarization immunoassay method. The mean cortisol value for the women with FM was 65.40 ± 27.10 μg/L, significantly lower than the mean cortisol level for the control group, at 90.83 ± 38.17 μg/L (p < 0.001).ConclusionOur study confirms that women with FM have significantly lower urinary cortisol levels than healthy women.

Role of Corticotropin-Releasing Hormone Testing in Assessment of Hypothalamic-Pituitary-Adrenal Axis Function in Infants with Congenital Central Hypothyroidism

The Dutch neonatal congenital hypothyroidism (CH) screening program detects infants with CH of central origin (CH-C). These infants have a high likelihood of multiple pituitary hormone deficiencies. ACTH deficiency especially poses an additional risk for brain damage and may be fatal. Our objective was to evaluate different tools for assessment of the integrity of the hypothalamus-pituitary-adrenocortex (HPA) axis in young infants, aiming for a strategy for reliable and timely diagnosis. This is a Dutch nationwide prospective study (enrollment 1994-1996). Patients were included if neonatal CH screening results were indicative of CH-C and HPA axis function could be tested within 6 months of birth. Nine male and three female infants with CH-C and four infants with false-positive screening results or transient hypothyroidism were included in the study. CRH test results, multiple cortisol plasma concentrations, and cortisol excretion in 24-h urine were measured. Six (50%) of the CH-C patients had abnormal CRH test results. Three of them had discordant test results: impaired increase of plasma cortisol in response to CRH, despite substantial increase of plasma ACTH. The other three infants, with concordant impaired responses of both ACTH and cortisol to CRH, had a very low urinary cortisol excretion in comparison with the subjects with normal CRH test results. The CRH test proves to be a fast and reliable tool in the assessment of HPA axis (dys)function. It enables timely diagnosis in (asymptomatic) neonates at risk for serious morbidity and mortality. The discordant response type, which has not been described before, may be an early phase of HPA axis dysfunction. Alternatively, patients with this response type may constitute a separate pathogenetic subset of HPA axis-deficient patients.

Prenatal cortisol, prematurity and low birthweight

Three hundred depressed pregnant women were recruited at approximately 20 weeks gestation. They were then divided by a median split into high and low urinary cortisol level groups. The high cortisol group had higher CES-D depression scores and higher inhibition (BIS) scores prenatally. Their fetuses had smaller head circumference, abdominal circumference, biparietal diameter and fetal weight. The high cortisol group neonates were shorter gestational age and lower birthweight and they had lower Brazelton habituation and higher Brazelton reflex scores. Discriminant function analyses suggested that cortisol levels more accurately classified short gestation and low birthweight groups than CES-D depression scores.

Enclosure choice and well-being in giant pandas: is it all about control?

Behavioral and hormonal data were compared for four giant pandas in two management conditions: (1) panda confined to exhibit area and (2) panda given choice to move freely between exhibit and off-exhibit bedroom areas. Pandas displayed fewer signs of behavioral agitation and lower urinary cortisol in the free choice condition. Time active did not differ between the two conditions. These results suggest that simply offering pandas free access to alternative locations can improve behavioral and hormonal variables that may be related to well-being. Zoo Biol 0:1–7, 2005. © 2005 Wiley-Liss, Inc.

Adrenocortical activity with repeated twice daily dosing of fluticasone propionate and budesonide given via a large volume spacer to asthmatic school children.

BACKGROUND: In a previous single dosing study in asthmatic school children fluticasone propionate produced significantly greater suppression of overnight urinary cortisol excretion than budesonide at high doses of 800 micrograms/day...

Low urinary cortisol excretion in holocaust survivors with posttraumatic stress disorder

Low urinary cortisol excretion in holocaust survivors with posttraumatic stress disorder

Low Urinary Cortisol Excretion in Patients with Posttraumatic Stress Disorder

In the present study, we replicated and extended our previous findings of low urinary free-cortisol levels in PTSD. Cortisol was measured in 16 male patients (nine inpatients, seven outpatients) with posttraumatic stress disorder (PTSD) and in 16 nonpsychiatric control subjects. The mean cortisol level in the PTSD group was significantly lower, and the range narrower, than that observed in control subjects. Low cortisol in PTSD did not seem to be related to the presence or absence of major depressive disorder or to overall psychiatric symptomatology as assessed by the sum Brief Psychiatric Rating Scale score. In the outpatient group, there was a relationship between PTSD symptomatology and cortisol levels. The findings suggests a physiological adaptation of the hypothalamic-pituitary-adrenal axis to chronic stress.

CLINICAL AND STEROID METABOLIC STUDIES IN FOUR SIBLINGS WITH CONGENITAL VIRILIZING ADRENAL HYPERPLASIA

ABSTRACT The present studies were concerned with four siblings suffering from congenital adrenogenital syndrome. Their parents were healthy and not closely related. At first examination the age of the patients varied between 10 and 23 years. They all presented a short stature and marked virilization; blood pressure was normal. All four were genetic females. Three of them were brought up as girls, but one clearly showed male identification. The youngest patient was registered as a boy at birth and brought up as such. None of the case histories revealed signs of cortisol deficiency in spite of low plasma cortisol and low urinary cortisol metabolites. Plasma ACTH was high. Both plasma cortisol and plasma ACTH probably showed normal diurnal variation. Pregnanetriol was a predominant urinary steroid metabolite. There was no indication of a significant secretion of 11-deoxycortisol. Under ordinary salt intake, the urinary aldosterone was higher than in normal subjects, possibly in response to the high production of steroids with natriuretic properties. Following treatment with dexamethasone, the urinary aldosterone decreased and so did cortisol tetra-hydro-derivatives, pregnanetriol and pregnanediol, without any influence on sodium balance. Stimulation with ACTH had no effect on aldosterone production, whereas urinary pregnanetriol and pregnanediol increased markedly, concomitant with a tendency to sodium loss. Angiotensin effectively stimulated aldosterone production, whereas rather larger quantities were needed to obtain a blood pressure response. Plasma testosterone was increased to the levels seen in normal males. Following ACTH there was no further increase in blood testosterone, whereas a marked decrease was seen after dexamethasone. Urinary oestrogens were rather high before treatment and decreased in two patients during treatment with dexamethasone, concomitant with the appearance of urinary gonadotrophins.