Serum cortisol and insulin-like growth factor 1 levels in major depressive disorder and schizophrenia

Abstract

The pathophysiology underlying major depressive disorder (MDD) and schizophrenia is related to endocrine system functions and includes changes in the blood levels of cortisol and insulin-like growth factor 1 (IGF-1). However, these hormones have not been investigated simultaneously in patients with MDD and schizophrenia. We investigated the differences in serum cortisol and IGF-1 levels among patients with MDD and schizophrenia and controls. We included 129 patients with MDD, 71 patients with schizophrenia, and 71 healthy volunteers. Blood tests were performed between 6:00 am and 11:00 am after fasting. Serum cortisol levels were significantly higher in patients with schizophrenia than in patients with MDD and controls. Serum cortisol levels were significantly higher in patients with MDD than in controls. Serum IGF-1 levels were higher in both patient groups than in controls, whereas there was no significant difference between patients with MDD and schizophrenia. Both cortisol and IGF-1 levels were positively correlated with the Hamilton Rating Scale for Depression score in patients with MDD, whereas cortisol level was positively correlated and IGF-1 level was negatively correlated with the Brief Psychiatric Rating Scale score in patients with schizophrenia. The differences in the level of these hormones suggest pathophysiological differences between these disorders.

Protein Plasma Levels of the IGF Signalling System Are Altered in Major Depressive Disorder

“…In some studies, IGF-1 peripheral levels were found to be significantly increased in depression [38][39][40]43,44,49] regardless of ethnicity, since some works were done in Europe [38][39][40]43], North America [44] and Japan [49]. What is more, IGF-1 was found upregulated either when patients were following AD treatments [40,43,49] or not [38,39,44] by the time protein measurements were taken. This may suggest that the levels of IGF-1 might be increased in depression regardless of treatment conditions.…”

“…To the best of our knowledge, this is the first time that IGF-2, IGFBP-5 and IGFBP-7 plasma protein levels have been addressed in depressed patients. On the contrary, in the last few decades, IGF-1 has received far more attention than IGF-2 in the context of depression [38][39][40][41][42][43][44][45][46][47][48][49]. In some studies, IGF-1 peripheral levels were found to be significantly increased in depression [38][39][40]43,44,49] regardless of ethnicity, since some works were done in Europe [38][39][40]43], North America [44] and Japan [49].…”

“…On the contrary, in the last few decades, IGF-1 has received far more attention than IGF-2 in the context of depression [38][39][40][41][42][43][44][45][46][47][48][49]. In some studies, IGF-1 peripheral levels were found to be significantly increased in depression [38][39][40]43,44,49] regardless of ethnicity, since some works were done in Europe [38][39][40]43], North America [44] and Japan [49]. What is more, IGF-1 was found upregulated either when patients were following AD treatments [40,43,49] or not [38,39,44] by the time protein measurements were taken.…”

“…However, to the best of our knowledge, there is no literature available on IGF-2 peripheral levels in major depressive disorders involving human samples. In contrast, peripheral IGF-1 has received far more attention in the last few decades, not just in depression [38][39][40][41][42][43][44][45][46][47][48][49], but also in other mental conditions such as schizophrenia [29,[49][50][51][52][53][54][55][56] and bipolar disorder [57][58][59][60][61][62]. On the other hand, circulating IGFBPs have been less widely studied than their ligand counterparts in the field of psychiatry, and always in a context of their IGF-dependent actions [29][30][31][32]38,55,[63][64][65].…”

The missing hallmark of health: psychosocial adaptation

“…Obesity activates mTORC1 in microglia and astrocytes with disabled autophagy, while rapamycin treatment restores autophagy and reduces depressive and anxiety-like behaviors [ 134 ]. Autophagy inhibition caused by obesity might explain the link between excessive adiposity and ASD, MDD or SCZ [ 135 , 136 ], but the observations suggesting that fasting may improve MDD must be replicated in large randomized studies [ 137 ]. These findings suggest that mTORC1 is hyperactivated in neuropsychiatric diseases, but there are exceptions to this rule.…”