Inflammatory diet and preclinical cardiovascular phenotypes in 11-12 year-olds and mid-life adults: A cross-sectional population-based study.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
06 2019
Historique:
received: 12 11 2018
revised: 05 04 2019
accepted: 10 04 2019
pubmed: 3 5 2019
medline: 26 6 2020
entrez: 4 5 2019
Statut: ppublish

Résumé

Pro-inflammatory diet may be a modifiable risk factor for cardiovascular disease. We examine associations of two inflammatory diet scores with preclinical cardiovascular phenotypes at two life course stages. Participants: 1771 children (49% girls) aged 11-12 years and 1793 parents (87% mothers, mean age 43.7 (standard deviation 5.2) years) in the Child Health CheckPoint Study. 23 items in the Australian National Secondary Students' Diet and Activity (NaSSDA) survey were used to derive two inflammatory diet scores based on: 1) published evidence of associations with C-reactive protein (literature-derived score), and 2) empirical associations with CheckPoint's inflammatory biomarker (glycoprotein acetyls, GlycA-derived score). Cardiovascular phenotypes assessed vascular structure (carotid intima-media thickness, retinal vessel calibre) and function (pulse wave velocity, blood pressure). Linear regression models were conducted, adjusted for age, sex, socioeconomic position and child pubertal status, plus a sensitivity analysis also including BMI (z-score for children). In adults, both inflammatory diet scores showed small associations with adverse cardiovascular function and microvascular structure. Per standard deviation higher GlycA-derived diet score, pulse wave velocity was 0.17  m/s faster (95% CI 0.11 to 0.22), mean arterial pressure was 1.85  mmHg (1.34-2.37) higher, and retinal arteriolar calibre was 1.29 μm narrower (-2.10 to -0.49). Adding BMI to models attenuated associations towards null. There was little evidence of associations in children. Our findings support cumulative adverse effects of a pro-inflammatory diet on preclinical cardiovascular phenotypes across the life course. Associations evident by mid-life were not present in childhood, when preventive measures should be instituted.

Sections du résumé

BACKGROUND AND AIMS
Pro-inflammatory diet may be a modifiable risk factor for cardiovascular disease. We examine associations of two inflammatory diet scores with preclinical cardiovascular phenotypes at two life course stages.
METHODS
Participants: 1771 children (49% girls) aged 11-12 years and 1793 parents (87% mothers, mean age 43.7 (standard deviation 5.2) years) in the Child Health CheckPoint Study.
MEASURES
23 items in the Australian National Secondary Students' Diet and Activity (NaSSDA) survey were used to derive two inflammatory diet scores based on: 1) published evidence of associations with C-reactive protein (literature-derived score), and 2) empirical associations with CheckPoint's inflammatory biomarker (glycoprotein acetyls, GlycA-derived score). Cardiovascular phenotypes assessed vascular structure (carotid intima-media thickness, retinal vessel calibre) and function (pulse wave velocity, blood pressure).
ANALYSES
Linear regression models were conducted, adjusted for age, sex, socioeconomic position and child pubertal status, plus a sensitivity analysis also including BMI (z-score for children).
RESULTS
In adults, both inflammatory diet scores showed small associations with adverse cardiovascular function and microvascular structure. Per standard deviation higher GlycA-derived diet score, pulse wave velocity was 0.17  m/s faster (95% CI 0.11 to 0.22), mean arterial pressure was 1.85  mmHg (1.34-2.37) higher, and retinal arteriolar calibre was 1.29 μm narrower (-2.10 to -0.49). Adding BMI to models attenuated associations towards null. There was little evidence of associations in children.
CONCLUSIONS
Our findings support cumulative adverse effects of a pro-inflammatory diet on preclinical cardiovascular phenotypes across the life course. Associations evident by mid-life were not present in childhood, when preventive measures should be instituted.

Identifiants

pubmed: 31048104
pii: S0021-9150(19)30378-8
doi: 10.1016/j.atherosclerosis.2019.04.212
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

93-101

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Addison Davis (A)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Richard Liu (R)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Jessica A Kerr (JA)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Melissa Wake (M)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia; Liggins Institute and Depart of Paediatrics, The University of Auckland, Auckland, New Zealand.

Anneke Grobler (A)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Markus Juonala (M)

Murdoch Children's Research Institute, Parkville, Victoria, Australia; Department of Medicine, University of Turku, Turku, Finland; Division of Medicine, Turku University Hospital, Turku, Finland.

Mengjiao Liu (M)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Louise Baur (L)

The Children's Hospital, Westmead, NSW, Australia; (h)The University of Sydney, Westmead, NSW, Australia.

David Burgner (D)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia; The Royal Children's Hospital, Parkville, Victoria, Australia; Department of Pediatrics, Monash University, Clayton, VIC, Australia.

Kate Lycett (K)

The University of Melbourne, Parkville, Victoria, Australia; Murdoch Children's Research Institute, Parkville, Victoria, Australia; (j)Deakin University, Burwood, VIC, Australia. Electronic address: kate.lycett@mcri.edu.au.

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