Correlations between changes in the hypothalamic-pituitary-adrenal axis and neurochemistry of the anterior cingulate gyrus in postpartum depression
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Updated: Feb 7, 2026

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Published on: June 10, 2013
Marcos Gonçalves de Rezende1, Carlos Eduardo Rosa2, Cybele Garcia-Leal1
1Departments of Neuroscience and Behavior, Ribeirão Preto Medical School, University of São Paulo, Av. dos Bandeirantes, 3900, Ribeirão Preto, SP 14049-900, Brazil.
Background:
This study aimed to investigate associations between indicators of hypothalamic-pituitary-adrenal axis (HPA) functioning and metabolite levels in the anterior cingulate gyrus (ACG) of women with postpartum depression (PPD).
Methods:
The sample (mean age = 28.5 ± 4.6 years) consisted of 20 women with PPD and 19 postpartum euthymic (PPE) women. Brain metabolites were quantified by proton magnetic resonance spectroscopy (1H-MRS). Salivary cortisol samples were collected upon awakening and 30 min and 12 h later, at 20.6 ± 6.6 (PPD) and 23.0 ± 7.4 (PPE) weeks after childbirth.
Results:
There were no significant differences between groups in respect to metabolite levels in the ACG. Compared with PPE, PPD women had less diurnal variation (DVr%). In the PPD group, positive correlations were found between DVr% and myo-inositol (mI/Cr) levels, and between cortisol awakening response (CARi%) and glutamate + glutamine (Glx/Cr) levels. The correlation between CARi% and Glx/Cr remained significant even after controlling for the interval, in weeks, from birth and MR spectroscopy and to hormonal data collection, and the use of contraceptives.
Limitations:
The limitations of the study include the small sample size and the use of oral contraceptives by around half of the sample.
Conclusions:
In the remote postpartum period (mean 21.8 ± 6.9 weeks) and in the presence of depressive episodes, the decreased responsiveness of the HPA axis after awakening and a smaller decrease in cortisol levels over the day were associated with lower levels of metabolites in the ACG. These results may contribute to the development of biological models to explain the etiology of PPD.
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