Inflammatory diet and preclinical cardiovascular phenotypes in 11–12 year-olds and mid-life adults: A cross-sectional population-based study
Graphical abstract
Introduction
Inflammation is a central pathogenic mechanism and therapeutic target in atherosclerosis [1]. A pro-inflammatory diet is considered a modifiable risk factor for atherosclerotic cardiovascular disease (CVD) [[2], [3], [4]], and western diets have a particularly high pro-inflammatory potential [5]. Specific food groups, such as refined carbohydrates, red/processed meat and sugar-sweetened beverages, are suggested to promote inflammation [6]. Others, such as fish, fruit, vegetables, and low or non-fat dairy sources, have demonstrated anti-inflammatory effects in both animal and human studies [7]. However, investigating only the pro- or anti-inflammatory elements of diets neglects potential synergistic and antagonistic interactions.
The Dietary Inflammatory Index (DII) is a literature derived score that is widely used to capture both pro- and anti-inflammatory dietary patterns [8]. Although DII scores do not always relate to inflammatory biomarkers or inflammatory-driven diseases [9,10], meta-analytic evidence does imply that, overall, higher (i.e. pro-inflammatory) adult DII scores predict CVD events. Two large meta-analyses including prospective and cross-sectional studies of adults aged 38–69 years from the general population reported that those in the highest DII category, compared to the lowest, had a 20–30% increased risk of cardiovascular mortality and disease [2,11]. A pro-inflammatory diet is also associated with increased cardiovascular risk in early to mid-adulthood. For example, two recent NHANES studies demonstrated that a) among 7880 adults aged ≥20 years (mean age ranged 35–51 years), higher DII scores were associated with increased prevalence of obesity, diabetes, hypertension and hypercholesterolemia [12], and b) among 17,689 adults (mean age 47 years), the odds of higher blood pressure and other cardiometabolic risk factors increased across DII quintiles [13]. Smaller European cohorts report similar results for blood pressure [4].
Cardiovascular risk develops across the life course, with childhood a key period for primordial prevention [14]. In 6-24 year-olds, diet quality is clearly associated with dietary anti-inflammatory potential measured by the DII [15], but very little research has directly examined the relationship between children's inflammatory diets and cardiovascular risk factors and preclinical phenotypes. One recent community-based study reported that children's DII scores were associated with their waist-to-height ratio, but not with body composition, blood pressure or heart rate [16]. Therefore, it is still unknown whether the adverse associations seen in adult studies are already evident in childhood, when early atherosclerosis develops and when adverse risk trajectories are established [17]. We therefore aimed to examine associations of inflammatory diet scores with preclinical phenotypes of cardiovascular structure (carotid intima-media thickness, retinal vessel calibre) and function (pulse wave velocity, blood pressure) in population-based cohorts of 11–12 year-olds and mid-life adults.
Section snippets
Study design and participants
The Child Health CheckPoint study (CheckPoint) was a cross-sectional population-based study nested within the national Longitudinal Study of Australian Children (LSAC). LSAC's initial study design and recruitment are outlined elsewhere [18]. Briefly, LSAC recruited a nationally-representative birth (B) cohort of 5107 infants at age 0–1 years using a two-stage random sampling design, with biennial ‘waves’ of data collection thereafter [19]. CheckPoint was a detailed cross-sectional biophysical
Sample characteristics
Of the 3764 eligible families, 1875 (47% of LSAC wave 6) child-parent pairs participated in CheckPoint. Dietary and preclinical cardiovascular phenotypes were available for 1771 children and 1793 adults. Fig. 1 shows the flow through the study, including the numbers with each of the vascular function and structure measures.
On average, children and adults were aged 11.5 (SD: 0.5) and 43.7 (SD: 5.2) years, respectively, and adults were predominantly female (87.7%, children 49.5% female; Supp
Principal findings
In children aged 11–12 years, there was little evidence that an inflammatory diet was associated with preclinical phenotypes of either vascular function or structure. By mid-life, a pro-inflammatory diet was consistently associated with adverse variations in vascular function (all measures) and microvascular structure (i.e. retinal arteriolar calibre). These associations were small, but are likely to worsen with cumulative exposure to an inflammatory diet. All associations were stronger for the
Conclusions
A pro-inflammatory diet was consistently associated with small adverse variations in preclinical cardiovascular phenotypes of function and microvascular structure in mid-life adults, but not in 11–12 year-olds. These findings support a life course paradigm, where negative impacts of a pro-inflammatory diet on preclinical cardiovascular phenotypes may accumulate so they are detectable by mid-life, and presumably continue to accrue thereafter.
Conflict of interest
The authors declared they do not have anything to disclose regarding conflict of interest with respect to this manuscript.
Financial support
This work has been supported to date by the National Health and Medical Research Council of Australia (NHMRC; 1041352, 1109355), The Royal Children's Hospital Foundation (2014–241), Murdoch Children's Research Institute, The University of Melbourne, National Heart Foundation of Australia (100660), Financial Markets Foundation for Children (2014–055; 2016–310) and Victoria Deaf Education Institute. RL and ML are supported by PhD scholarships: RL by NHMRC (APP1114567) and ML by a Melbourne
Author contributions
Dr Davis initiated this work as part of his student project, made substantial contributions to the conception and design of the study, conducted the analyses, interpreted the data, drafted the article, and revised it critically based on co-author feedback.
Dr Liu contributed to the study design, analysis of the data, interpretation of data, and revised the article critically for important intellectual content.
Dr Kerr co-supervised Dr Davis, made substantial contributions to the conception and
Acknowledgements
This study uses data from the Longitudinal Study of Australian Children (LSAC) and Child Health CheckPoint. LSAC is conducted in partnership between the Department of Social Services, the Australian Institute of Family Studies and the Australian Bureau of Statistics (ABS). The findings and views reported in this paper are those of the author and should not be attributed to DSS, AIFS or the ABS. We thank the LSAC and CheckPoint study participants and families. We also thank the CheckPoint team
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These authors contributed equally to this work as joint senior authors.