PMID- 31307858
OWN - NLM
STAT- MEDLINE
DCOM- 20200914
LR  - 20200914
IS  - 1573-2509 (Electronic)
IS  - 0920-9964 (Linking)
VI  - 213
DP  - 2019 Nov
TI  - Psychotropic medication effects on cortisol: Implications for research and 
      mechanisms of drug action.
PG  - 6-14
LID - S0920-9964(19)30244-0 [pii]
LID - 10.1016/j.schres.2019.06.023 [doi]
AB  - Stress and the hypothalamic-pituitary-adrenal (HPA) axis have been implicated in 
      the etiology of a range psychiatric disorders; abnormalities in cortisol 
      secretion are well documented in mood, anxiety, and psychotic disorders. There 
      is, however, evidence that psychotropic medications affect HPA function, and are 
      often a confound in research on the relation of cortisol secretion with 
      psychiatric symptoms and syndromes. Psychotropic effects are particularly 
      problematic in longitudinal research on individuals at clinical high risk (CHR) 
      for serious mental illness, because they have the potential to obscure 
      neurobiological mechanisms involved in crossing the threshold from CHR states to 
      clinical disorders. This paper reviews the research literature on the relation of 
      cortisol secretion with the three major classes of psychotropic medication that 
      are most often prescribed; antipsychotics, antidepressants, and stimulants. The 
      studies included in this review are those that measured both baseline and 
      post-treatment cortisol. Taken together, most studies of antidepressants find 
      that they are associated with a reduction in both basal and 
      post-dexamethasone-CRH (DEX/CRH) cortisol, although some report no change. 
      Similarly, antipsychotics, both typical and atypical, are found to reduce basal 
      and DEX/CRH cortisol levels in most studies. Psychostimulant medications, in 
      contrast, are associated with an increase in basal cortisol levels or no change. 
      Effects of psychotropics on the cortisol awakening response (CAR) are less 
      consistent. Implications of these effects for clinical research, especially 
      studies of CHR populations, are discussed. Limitations of the research, due to 
      variations in sample demographic and methodologic factors, are noted, and 
      directions for future research are proposed.
CI  - Copyright (c) 2019. Published by Elsevier B.V.
FAU - Subramaniam, Aditi
AU  - Subramaniam A
AD  - Department of Psychology, Emory University, 36 Eagle Row, Atlanta, GA 30322, USA.
FAU - LoPilato, Allison
AU  - LoPilato A
AD  - Department of Psychiatry, Emory University, 12 Executive Park Dr NE #200, 
      Atlanta, GA, USA 30329. Electronic address: allison.lopilato@emory.edu.
FAU - Walker, Elaine F
AU  - Walker EF
AD  - Department of Psychology, Emory University, 36 Eagle Row, Atlanta, GA 30322, USA. 
      Electronic address: psyefw@emory.edu.
LA  - eng
GR  - U01 MH081988/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20190712
PL  - Netherlands
TA  - Schizophr Res
JT  - Schizophrenia research
JID - 8804207
RN  - 0 (Antidepressive Agents)
RN  - 0 (Antipsychotic Agents)
RN  - 0 (Central Nervous System Stimulants)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Antidepressive Agents/*pharmacology
MH  - Antipsychotic Agents/*pharmacology
MH  - Central Nervous System Stimulants/*pharmacology
MH  - Humans
MH  - Hydrocortisone/*metabolism
MH  - Hypothalamo-Hypophyseal System/*drug effects
OTO - NOTNLM
OT  - Antidepressants
OT  - Antipsychotics
OT  - Cortisol
OT  - HPA axis
OT  - Psychostimulants
OT  - Psychotropics
EDAT- 2019/07/17 06:00
MHDA- 2020/09/15 06:00
CRDT- 2019/07/17 06:00
PHST- 2019/02/02 00:00 [received]
PHST- 2019/06/24 00:00 [revised]
PHST- 2019/06/26 00:00 [accepted]
PHST- 2019/07/17 06:00 [pubmed]
PHST- 2020/09/15 06:00 [medline]
PHST- 2019/07/17 06:00 [entrez]
AID - S0920-9964(19)30244-0 [pii]
AID - 10.1016/j.schres.2019.06.023 [doi]
PST - ppublish
SO  - Schizophr Res. 2019 Nov;213:6-14. doi: 10.1016/j.schres.2019.06.023. Epub 2019 
      Jul 12.