scholarly journals Hypothalamic–pituitary–adrenal axis activity in adults who were prenatally exposed to the Dutch famine

2006 ◽  
Vol 155 (1) ◽  
pp. 153-160 ◽  
Author(s):  
Susanne R de Rooij ◽  
Rebecca C Painter ◽  
David I W Phillips ◽  
Clive Osmond ◽  
Robert P J Michels ◽  
...  

Objective: The hypothalamic–pituitary–adrenal (HPA) axis has been proposed to be susceptible to fetal programming, the process by which an adverse fetal environment elicits permanent physiological and metabolic alterations predisposing to disease in later life. It is hypothesized that fetal exposure to poor circumstances alters the set point of the HPA axis, leading to increased HPA axis activity and subsequent increased cortisol concentrations. In this study, we tested the hypothesis that prenatal exposure to famine during different periods of gestation is associated with increased activity of the HPA axis. Design and methods: We assessed plasma cortisol concentrations after a dexamethasone suppression and an ACTH1–24-stimulation test in a group of 98 men and women randomly sampled from the Dutch famine birth cohort. Cohort members were born as term singletons around the 1944–1945 Dutch famine. Results: Cortisol profiles after dexamethasone suppression and ACTH1–24 stimulation were similar for participants exposed to famine during late, mid- or early gestation (P=0.78). Cortisol concentrations after dexamethasone suppression test did not differ between those exposed and those unexposed to famine in utero (mean difference −2% (95% confidence interval (CI) −27 to 23)). Neither peak cortisol concentration (20 nmol/l (95% CI −27 to 66)), cortisol increment (−5 nmol/l (95% CI −56 to 47)) or cortisol area under the curve post-ACTH1–24 injection (4% (95% CI −4 to 12)) differed between exposed and unexposed participants. Conclusions: Prenatal famine exposure does not seem to affect HPA axis activity at adult age, at least not at the adrenal level. This does not exclude altered HPA axis activity at the levels of the hippocampus and hypothalamus.

2021 ◽  
Vol 11 (4) ◽  
pp. 425
Author(s):  
Fabrice Duval ◽  
Marie-Claude Mokrani ◽  
Alexis Erb ◽  
Felix Gonzalez Lopera ◽  
Vlad Danila ◽  
...  

The effects of antidepressants on dopamine (DA) receptor sensitivity in the mesolimbic–hypothalamic system have yielded contradictory results. The postsynaptic DA receptor function was evaluated by the cortisol response to apomorphine (APO; 0.75 mg SC) in 16 drug-free DSM-5 major depressed inpatients and 18 healthy hospitalized control (HC) subjects. Cortisol response to the dexamethasone suppression test (DST) was also measured. After two and four weeks of antidepressant treatment (ADT), the DST and APO test were repeated in all patients. Cortisol response to APO (∆COR) was not influenced by the hypothalamic–pituitary–adrenal (HPA) axis activity, as assessed by the DST. Pre-treatment ∆COR values did not differ significantly between patients and HCs. During ADT, ∆COR values were lower than in HCs at week 2 and 4. After four weeks of treatment, among the eight patients who had blunted ∆COR values, seven were subsequent remitters, while among the eight patients who had normal ∆COR values, seven were non-remitters. Considering the limitations of our study, the results suggest that following chronic ADT, the desensitization of postsynaptic DA receptors connected with the regulation of the HPA axis at the hypothalamic level is associated with clinical remission. These results could reflect increased DA levels in the mesolimbic pathway.


2004 ◽  
Vol 184 (6) ◽  
pp. 496-502 ◽  
Author(s):  
Stuart Watson ◽  
Peter Gallagher ◽  
James C. Ritchie ◽  
I. Nicol Ferrier ◽  
Allan H. Young

BackgroundHypothalamic-pituitary-adrenal (HPA) axis function, as variously measured by the responses to the combined dexamethasone/ corticotrophin-releasing hormone (dex/ CRH) test, the dexamethasone suppression test (DST) and basal cortisol levels, has been reported to be abnormal in bipolar disorder.AimsTo test the hypothesis that HPA axis dysfunction persists in patients in remission from bipolar disorder.MethodSalivary cortisol levels and the plasma cortisol response to the DST and dex/CRH test were examined in 53 patients with bipolar disorder, 27 of whom fulfilled stringent criteria for remission, and in 28 healthy controls. Serum dexamethasone levels were measured.ResultsPatients with bipolar disorder demonstrated an enhanced cortisol response to the dex/CRH test compared with controls (P=0.001). This response did not differ significantly between remitted and non-remitted patients. These findings were present after the potentially confounding effects of dexamethasone levels were accounted for.ConclusionsThe dex/CRH test is abnormal in both remitted and non-remitted patients with bipolar disorder. Thismeasure of HP Aaxis dysfunction is a potential trait marker in bipolar disorder and thus possibly indicative of the core pathophysiological process in this illness.


2002 ◽  
Vol 32 (6) ◽  
pp. 1021-1028 ◽  
Author(s):  
S. WATSON ◽  
P. GALLAGHER ◽  
D. DEL-ESTAL ◽  
A. HEARN ◽  
I. N. FERRIER ◽  
...  

Background. Hypothalamic–pituitary–adrenal (HPA) axis function in patients with chronic depression has previously been shown to be normal when measured using the dexamethasone suppression test (DST). We examined patients with chronic depression using the sensitive dexamethasone/corticotropin releasing hormone (dex/CRH) test and the dexamethasone suppression test (DST) to establish whether HPA axis abnormalities are present in this group. We also compared the sensitivity of the two tests and compared the results with previous studies in depression that have not specifically selected chronic patients.Method. Twenty-nine patients with the chronic subtype of major depressive disorder and 28 matched controls underwent examination of HPA axis function.Results. Neither the cortisol response to the DST or the dex/CRH test differed significantly between the patient and control groups. There was a trend in favour of more patients than controls having an abnormal response to the dex/CRH test (P = 0.052). Neither the patients with an abnormally enhanced response, nor the magnitude of response could be predicted by any illness or demographic variable.Conclusion. The HPA axis is not overtly abnormal in chronic depression. This contrasts with previous findings in acute depression and bipolar disorder and may suggest that the HPA axis abnormalities present in acute depression resolve, but are not accompanied by symptom resolution. Alternatively, a subgroup of depressives with less HPA dysfunction may progress to chronicity. This has implications for treatment and prognosis. The dex/CRH is a more sensitive test of HPA axis function than the DST in patients with chronic depression.


2018 ◽  
Vol 315 (2) ◽  
pp. E316-E325 ◽  
Author(s):  
Kathleen M. Gavin ◽  
Karen L. Shea ◽  
Ellie Gibbons ◽  
Pamela Wolfe ◽  
Robert S. Schwartz ◽  
...  

Sex hormones appear to play a role in the regulation of hypothalamic-pituitary-adrenal (HPA) axis activity. The objective was to isolate the effects of estradiol (E2) on central activation of the HPA axis. We hypothesized that the HPA axis response to corticotropin-releasing hormone (CRH) under dexamethasone (Dex) suppression would be exaggerated in response to chronic ovarian hormone suppression and that physiologic E2 add-back would mitigate this response. Thirty premenopausal women underwent 20 wk of gonadotropin-releasing hormone agonist therapy (GnRHAG) and transdermal E2 (0.075 mg per day, GnRHAG + E2, n = 15) or placebo (PL) patch (GnRHAG + PL, n = 15). Women in the GnRHAG + PL and GnRHAG + E2 groups were of similar age (38 (SD 5) yr vs. 36 (SD 7) yr) and body mass index (27 (SD 6) kg/m2 vs. 27 (SD 6) kg/m2). Serum E2 changed differently between the groups ( P = 0.01); it decreased in response to GnRHAG + PL (77.9 ± 17.4 to 23.2 ± 2.6 pg/ml; P = 0.008) and did not change in response to GnRHAG + E2 (70.6 ± 12.4 to 105 ± 30.4 pg/ml; P = 0.36). The incremental area under the curve (AUCINC) responses to CRH were different between the groups for total cortisol ( P = 0.03) and cortisone ( P = 0.04) but not serum adrenocorticotropic hormone (ACTH) ( P = 0.28). When examining within-group changes, GnRHAG + PL did not alter the HPA axis response to Dex/CRH, but GnRHAG + E2 decreased the AUCINC for ACTH (AUCINC, 1,623 ± 257 to 1,211 ± 236 pg/ml·min, P = 0.004), cortisone (1,795 ± 367 to 1,090 ± 281 ng/ml·min, P = 0.009), and total cortisol (7,008 ± 1,387 to 3,893 ± 1,090 ng/ml·min, P = 0.02). Suppression of ovarian hormones by GnRHAG therapy for 20 wk did not exaggerate the HPA axis response to CRH, but physiologic E2 add-back reduced HPA axis activity compared with preintervention levels.


2021 ◽  
Vol 11 (4) ◽  
pp. 495
Author(s):  
Neus Salvat-Pujol ◽  
Javier Labad ◽  
Mikel Urretavizcaya ◽  
Aida De Arriba-Arnau ◽  
Cinto Segalàs ◽  
...  

Relationships among childhood maltreatment (CM), hypothalamic-pituitary-adrenal (HPA) axis disturbances, major depressive disorder (MDD), poor functionality, and lower quality of life (QoL) in adulthood have been described. We aimed to study the roles of the remission status of depression and HPA axis function in the relationships between CM and functionality and QoL. Ninety-seven patients with MDD and 97 healthy controls were included. The cortisol awakening response, cortisol suppression ratio in the dexamethasone suppression test, and diurnal cortisol slope were assessed. Participants completed measures of psychopathology, CM, functionality, and QoL. Multiple linear regression analyses were performed to study the relationships between CM and functionality and QoL. Only non-remitted MDD patients showed lower functionality and QoL than controls, indicating that depressive symptoms may partly predict functionality and QoL. Cortisol measures did not differ between remitted and non-remitted patients. Although neither HPA axis measures nor depression remission status were consistently associated with functionality or QoL, these factors moderated the effects of CM on functionality and QoL. In conclusion, subtle neurobiological dysfunctions in stress-related systems could help to explain diminished functionality and QoL in individuals with CM and MDD and contribute to the persistence of these impairments even after the remission of depressive symptoms.


2004 ◽  
Vol 36 (05) ◽  
Author(s):  
D Eser ◽  
P Zwanzger ◽  
S Aicher ◽  
C Schüle ◽  
TC Baghai ◽  
...  

2003 ◽  
Vol 18 (7) ◽  
pp. 350-355 ◽  
Author(s):  
Åsa Westrin ◽  
Karin Frii ◽  
Lil Träskman-Bendz

AbstractPrevious research on hypothalamic-pituitary adrenal (HPA) axis-activity in suicide attempter research has shown conflicting outcomes. The design of the present study was to test the influence of personality disorders and concominant axis I diagnoses on the dexamethasone suppression diagnostic test by use of multiple regression analyses. The sample consisted of 184 patients with a recent suicide attempt and 42 healthy controls. As expected, the lowest pre- and postdexamethasone cortisol levels were found in patients with personality disorders axis II, cluster B as compared to the other patients. The results remained significant when analysed for covariance with DSM-III-R axis I diagnoses, age or sex. Whether these low cortisol levels are due to previous experience of extreme stressful events or long-lasting burden, or whether they may be a consequence of biogenetic or psychological predisposal of interest, remains to be elucidated. Axis I comorbidity needs to be further examined.


2007 ◽  
Vol 190 (4) ◽  
pp. 357-358 ◽  
Author(s):  
Jose L. Carrasco ◽  
Marina Díaz-Marsá ◽  
Jose I. Pastrana ◽  
Rosa Molina ◽  
Loreto Brotons ◽  
...  

SummaryHypothalamic–pituitary–adrenal (HPA) axis sensitivity was investigated in 32 non-medicated patients with borderline personality disorder without comorbid post-traumatic syndromes and in 18 normal individuals using a modified dexamethasone suppression test (0.25 mg). Enhanced cortisol suppression was found in the patients v. controls (P < 0.05) and the percentage of participant's with non-suppression was smaller in the patient (34%) than in the control group (89%) (P < 0.01). Baseline cortisol levels in the patients were also lower than in the controls (P < 0.05). The 0.25 mg dexamethasone suppression test reveals increased feedback inhibition of the HPA in borderline personality disorder.


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