Abstract

Dietary habits of healthy offspring with a positive family history of premature coronary artery disease (P-CAD) have not been studied so far. The aim of this study was twofold: (1) to identify dietary patterns in a sample of young healthy adults with (cases) and without (controls) family history of P-CAD, and (2) to study the association between dietary patterns and family history of P-CAD. The data came from the MAGNETIC case-control study. The participants were healthy adults aged 18–35 years old, with (n = 351) and without a family history of P-CAD (n = 338). Dietary data were collected with food frequency questionnaire FFQ-6. Dietary patterns (DP) were derived using principal component analysis (PCA). The associations between the adherence to DPs and family history of P-CAD were investigated using logistic regression. Two models were created: crude and adjusted for age, sex, smoking status, place of residence, financial situation, education, and physical activity at leisure time. Three DPs were identified: ‘prudent’, ‘westernized traditional’ and ‘dairy, breakfast cereals, and treats’. In both crude and adjusted models, subjects with family history of P-CAD showed higher adherence by 31% and 25% to ‘westernized traditional’ DP (odds ratio (OR) 1.31, 95% confidence interval (95% CI): 1.12–1.53; p < 0.005; per 1 unit of standard deviation (SD) of DP score and adjOR 1.25, 95% CI: 1.06–1.48; p = 0.007; per 1 unit of SD of DP score, respectively). Young healthy adults with family history of P-CAD present unfavorable dietary patterns and are potentially a target group for CAD primary prevention programs.

Highlights

  • Premature coronary artery disease (P-CAD) has a multifactorial etiology and is most likely a mixture of genetic and environmental factors

  • The principal component analysis led to the identification of three dietary patterns explaining 13, 12, and 6% of the variance of consumption in 26 food groups

  • The third dietary pattern was based on frequent consumption of sweetened milk products (0.62); breakfast cereals (0.50); milk; fermented milk drinks, and curd cheese

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Summary

Introduction

Premature coronary artery disease (P-CAD) has a multifactorial etiology and is most likely a mixture of genetic and environmental factors. A robust factor affecting the offspring is myocardial infarction (MI) occurrence before the age of 55 for men and 65 for women [2]. It has been estimated that the age-adjusted odds ratio of cardiovascular events is around 2.5 greater among individuals with family history of P-CAD [1], with a further 10-fold increase if the first-degree relative was affected under the age of 45 [3]. A better understanding of the genetic and environmental background of the disease could result in a substantial progress in successful screening [5]. This resulted in the focus of care provision being diverted from primary care to early diagnosis and pharmacological treatment. As highlighted by Jeemon et al [6], a shift from a ‘reactive’ to a ‘proactive’ approach in the preventative management of patients with family history of

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