Inflammation as a predictive biomarker for response to omega-3 fatty acids in major depressive disorder: a proof-of-concept study
Rapaport MH, Nierenberg AA, Schettler PJ, Kinkead B, Cardoos A, Walker R, Mischoulon D
Molecular psychiatry · 208 citas
Etiquetas de revisión
Vínculos de autores con la industriaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institute of Mental Health
- Gobierno
- NIMH NIH HHS
- Autores
- Al menos un autor declara un vínculo económico con la industria
- Subvenciones
- National Institute of Mental Health (R01 MH074085); National Institute of Mental Health (5R01MH74085); National Institute of Mental Health (R01 MH073765)
Según 2 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2015-03-24 · Mol Psychiatry · vol. 21 · número 1 · págs. 71–79
- Editorial
- Springer Nature
- Citado
- 265 citas · más que el 100% de estudios similares · 24.6× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 50 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Fatty Acid Research and Health · Tryptophan and brain disorders · Treatment of Major Depression
- Palabras clave
- major depressive disorder, omega-3 fatty acids, eicosapentaenoic acid, docosahexaenoic acid, inflammation, inflammatory markers, treatment response prediction, interleukin-6, C-reactive protein, leptin, adiponectin, treatment moderators
- MeSH
- humans, leptin, docosahexaenoic acids, eicosapentaenoic acid, c-reactive protein, interleukin-6, treatment outcome, double-blind method, psychiatric status rating scales, dietary supplements, adult, aged, middle aged, female, male, interleukin 1 receptor antagonist protein, young adult, biomarkers, major depressive disorder
7 autores
- Mark Hyman Rapaport🇺🇸 · autor de correspondenciaEmory University
- Andrew Alan Nierenberg🇺🇸Harvard University; Massachusetts General Hospital
- Pamela J. Schettler🇺🇸Emory University
- Becky L. Kinkead🇺🇸Emory University
- Amber Cardoos🇺🇸Harvard University; Massachusetts General Hospital
- Rosemary Walker🇺🇸Harvard University; Massachusetts General Hospital
- David Mischoulon🇺🇸Harvard University; Massachusetts General Hospital
Resumen
El texto original del estudio, en el idioma en que se publicó.
This study explores whether inflammatory biomarkers act as moderators of clinical response to omega-3 (n-3) fatty acids in subjects with major depressive disorder (MDD). One hundred fifty-five subjects with Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) MDD, a baseline 17-item Hamilton Depression Rating Scale (HAM-D-17) score ⩾ 15 and baseline biomarker data (interleukin (IL)-1ra, IL-6, high-sensitivity C-reactive protein (hs-CRP), leptin and adiponectin) were randomized between 18 May 2006 and 30 June 2011 to 8 weeks of double-blind treatment with eicosapentaenoic acid (EPA)-enriched n-3 1060 mg day(-1), docosahexaenoic acid (DHA)-enriched n-3 900 mg day(-1) or placebo. Outcomes were determined using mixed model repeated measures analysis for 'high' and 'low' inflammation groups based on individual and combined biomarkers. Results are presented in terms of standardized treatment effect size (ES) for change in HAM-D-17 from baseline to treatment week 8. Although overall treatment group differences were negligible (ES=-0.13 to +0.04), subjects with any 'high' inflammation improved more on EPA than placebo (ES=-0.39) or DHA (ES=-0.60) and less on DHA than placebo (ES=+0.21); furthermore, EPA-placebo separation increased with increasing numbers of markers of high inflammation. Subjects randomized to EPA with 'high' IL-1ra or hs-CRP or low adiponectin ('high' inflammation) had medium ES decreases in HAM-D-17 scores vs subjects 'low' on these biomarkers. Subjects with 'high' hs-CRP, IL-6 or leptin were less placebo-responsive than subjects with low levels of these biomarkers (medium to large ES differences). Employing multiple markers of inflammation facilitated identification of a more homogeneous cohort of subjects with MDD responding to EPA vs placebo in our cohort. Studies are needed to replicate and extend this proof-of-concept work.
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