HOME / PUBLICATIONS /

Posttraumatic Stress Disorder as a Catalyst for the Association Between Metabolic Syndrome and Reduced Cortical Thickness

Citation:

Wolf, E. J., Sadeh, N., Leritz, E. C., Logue, M. W., Stoop, T. B., McGlinchey, R., Milberg, W., et al. (2016). Posttraumatic Stress Disorder as a Catalyst for the Association Between Metabolic Syndrome and Reduced Cortical Thickness. Biol Psychiatry , 80, 363-71.

Date Published:

Sep 1

Abstract:

BACKGROUND: Metabolic syndrome (MetS), defined by a constellation of cardiometabolic pathologies, is highly prevalent among veterans, especially veterans with posttraumatic stress disorder (PTSD), and poses a major risk for adverse health outcomes, including neurodegeneration and mortality. Given this, we evaluated 1) the association between MetS and neural integrity, indexed by cortical thickness; 2) the relationship between PTSD and MetS; and 3) whether PTSD was associated with cortical thickness indirectly through MetS. METHODS: The sample consisted of 346 U.S. military veterans (89.3% male; 71.4% white) who deployed to Iraq, Afghanistan, or both. Neuroimaging data were available for 274 participants. RESULTS: In whole-brain analyses, MetS was negatively associated with cortical thickness in two left and four right hemisphere regions, as follows: bilateral temporal lobe, including temporal pole, fusiform gyrus, and insula, and extending into occipital cortex (left hemisphere) and orbitofrontal cortex (right hemisphere); bilateral precuneus, posterior cingulate, calcarine, and occipital-parietal cortex; and right rostral anterior cingulate cortex and central sulcus/postcentral gyrus. Path models showed that PTSD predicted MetS (β = .19, p < .001), which was associated with reduced cortical thickness (β = -.29 to -.43, all p < .001). CONCLUSIONS: Results from this young veteran sample provide evidence that PTSD confers risk for cardiometabolic pathology and neurodegeneration and raise concern that this cohort may be aging prematurely and at risk for substantial medical and cognitive decline. This study highlights the need to identify the molecular mechanisms linking PTSD to MetS and effective interventions to reduce PTSD-related health comorbidities.

Notes:

1873-2402Wolf, Erika JSadeh, NaomiLeritz, Elizabeth CLogue, Mark WStoop, Tawni BMcGlinchey, ReginaMilberg, WilliamMiller, Mark WCDA-2-067-10S/Intramural VA/United StatesR01 NS086882/NS/NINDS NIH HHS/United StatesR21 MH102834/MH/NIMH NIH HHS/United StatesJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, U.S. Gov't, Non-P.H.S.Biol Psychiatry. 2016 Sep 1;80(5):363-71. doi: 10.1016/j.biopsych.2015.11.023. Epub 2015 Dec 8.