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A neurobiological link between transportation noise exposure and metabolic disease in humans.
Osborne, Michael T; Naddaf, Nicki; Abohashem, Shady; Radfar, Azar; Ghoneem, Ahmed; Dar, Tawseef; Wang, Ying; Patrich, Tomas; Oberfeld, Blake; Tung, Brian; Pitman, Roger K; Mehta, Nehal N; Shin, Lisa M; Lo, Janet; Rajagopalan, Sanjay; Koenen, Karestan C; Grinspoon, Steven K; Fayad, Zahi A; Tawakol, Ahmed.
Afiliación
  • Osborne MT; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: mosborne@mgh.harvard.edu.
  • Naddaf N; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA. Electronic address: nicki.naddaf@stonybrookmedicine.edu.
  • Abohashem S; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: sabohashem@mgh.harvard.edu.
  • Radfar A; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: azar.radfar@jhsmiami.org.
  • Ghoneem A; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA. Electronic address: ahmed.ghoneem@lahey.org.
  • Dar T; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: tawseef.dar@jhsmiami.org.
  • Wang Y; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA. Electronic address: ywang88@mgh.harvard.edu.
  • Patrich T; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA. Electronic address: tomy@patrich.com.
  • Oberfeld B; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA. Electronic address: blake_oberfeld@hms.harvard.edu.
  • Tung B; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA. Electronic address: btung@student.nymc.edu.
  • Pitman RK; Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: roger_pitman@hms.harvard.edu.
  • Mehta NN; Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Dr., Building 10, Room 5-5140, Bethesda, MD 02814, USA. Electronic address: nehal.mehta@nih.gov.
  • Shin LM; Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA; Department of Psychology, Tufts University, 490 Boston Ave., Medford, MA 02155, USA. Electronic address: lisa.shin@tufts.edu.
  • Lo J; Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: jlo@mgh.harvard.edu.
  • Rajagopalan S; Department of Cardiovascular Medicine, Case Western Reserve University, 11100 Euclid Ave., Cleveland, OH 44106, USA. Electronic address: sxr647@case.edu.
  • Koenen KC; Department of Epidemiology, Harvard University T.H. Chan School of Public Health, 677 Huntington Ave., Kresge Building, 505, Boston, MA 02115, USA. Electronic address: kkoenen@hsph.harvard.edu.
  • Grinspoon SK; Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: sgrinspoon@mgh.harvard.edu.
  • Fayad ZA; BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, 1470 Madison Ave., New York, NY 10029, USA. Electronic address: zahi.fayad@mssm.edu.
  • Tawakol A; Cardiac Imaging Research Center, Massachusetts General Hospital, 165 Cambridge St., Suite 400, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St., Boston, MA 02114, USA. Electronic address: atawakol@mgh.harvard.edu.
Psychoneuroendocrinology ; 131: 105331, 2021 09.
Article en En | MEDLINE | ID: mdl-34183223
ABSTRACT

BACKGROUND:

Chronic transportation noise exposure associates with cardiovascular events through a link involving heightened stress-associated neurobiological activity (as amygdalar metabolic activity, AmygA) on 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT). Increased AmygA also associates with greater visceral adipose tissue (VAT) and type 2 diabetes mellitus (DM). While relationships between noise exposure and VAT and DM have been reported, the underlying mechanisms remain incompletely understood. We tested whether (1) transportation noise exposure associates with greater (a) baseline and gains in VAT and (b) DM risk, and (2) heightened AmygA partially mediates the link between noise exposure and these metabolic diseases.

METHODS:

VAT was measured in a retrospective cohort (N = 403) who underwent clinical 18F-FDG-PET/CT. AmygA was measured in those with brain imaging (N = 238). Follow-up VAT was remeasured on available imaging (N = 67). Among individuals (N = 224) without baseline DM, incident DM was adjudicated over 2 years from clinical records. Noise (24-h average) was modeled at each individual's home address. Linear regression, survival, and mediation analyses were employed.

RESULTS:

Higher noise exposure (upper tertile vs. others) associated with greater baseline VAT (standardized ß [95% confidence interval (CI)]= 0.230 [0.021, 0.438], p = 0.031), gains in VAT (0.686 [0.185, 1.187], p = 0.008 adjusted for baseline VAT), and DM (hazard ratio [95% CI]=2.429 [1.031, 5.719], p = 0.042). The paths of ↑noise exposure→↑AmygA→↑baseline VAT and ↑noise exposure→↑AmygA→↑subsequent DM were significant (p < 0.05).

CONCLUSIONS:

Increased transportation noise exposure associates with greater VAT and DM. This relationship is partially mediated by stress-associated neurobiological activity. These findings suggest altered neurobiology contributes to noise exposure's link to metabolic diseases.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Diabetes Mellitus Tipo 2 / Grasa Intraabdominal / Ruido del Transporte Tipo de estudio: Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: Psychoneuroendocrinology Año: 2021 Tipo del documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Diabetes Mellitus Tipo 2 / Grasa Intraabdominal / Ruido del Transporte Tipo de estudio: Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: Psychoneuroendocrinology Año: 2021 Tipo del documento: Article