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Biology of posttraumatic stress disorder
Yehuda R.. The Journal of clinical psychiatry, 2001-01-01
Topic: Brain proteins, microglia and lab models
Most biological findings in posttraumatic stress disorder (PTSD) are compatible with those of the chronic stress response, such as increased corticotropin-releasing factor (CRF) concentrations, catecholamine depletion within the central nervous system, and reduced hippocampal volume. However, over the last 10 years, biological observations have been made in PTSD that are different from what has been typically associated with chronic stress, notably certain hypothalamic-pituitary-adrenal (HPA) axis findings. In particular, urinary and plasma cortisol levels are considerably lower in PTSD patients than in non-PTSD trauma survivors and normal controls. Furthermore, the circadian pattern of cortisol release from the adrenal glands follows a greater dynamic range in PTSD than in patients with major depression or in normal controls. The reduction in cortisol levels results from an enhanced negative feedback by cortisol, which is secondary to an increased sensitivity of glucocorticoid receptors in target tissues. This HPA axis alteration contrasts with the well-known chronic stress cascade in which CRF release results in erosion of negative feedback and down-regulation of glucocorticoid receptors. Sensitization of the HPA axis is consistent with the clinical picture of hyperreactivity and hyperresponsiveness in PTSD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Yehuda, R. (2001). Biology of posttraumatic stress disorder. The Journal of clinical psychiatry.
Vancouver
Yehuda R. Biology of posttraumatic stress disorder. The Journal of clinical psychiatry. 2001. PMID: 11495096.
BibTeX
@article{yehuda2001-11495096,
author = {Yehuda, R.},
title = {{Biology of posttraumatic stress disorder}},
journal = {The Journal of clinical psychiatry},
year = {2001},
pmid = {11495096}
}
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Key findings
- However, over the last 10 years, biological observations have been made in PTSD that are different from what has been typically associated with chronic stress, notably certain hypothalamic-pituitary-adrenal (HPA) axis findings.
- The reduction in cortisol levels results from an enhanced negative feedback by cortisol, which is secondary to an increased sensitivity of glucocorticoid receptors in target tissues.
- This HPA axis alteration contrasts with the well-known chronic stress cascade in which CRF release results in erosion of negative feedback and down-regulation of glucocorticoid receptors.
Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of clinical psychiatry) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2001 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 11495096) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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