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Dyslipidaemia-Genotype Interactions with Nutrient Intake and Cerebro-Cardiovascular Disease.

ABSTRACT: A comprehensive understanding of gene-diet interactions is necessary to establish proper dietary guidelines to prevent and manage cardio-cerebrovascular disease (CCD). We investigated the role of genetic variants associated with dyslipidaemia (DL) and their interactions with macro-nutrients for cardiovascular disease using a large-scale genome-wide association study of Korean adults. A total of 58,701 participants from a Korean genome and epidemiology study were included. Their dietary intake was assessed using a food frequency questionnaire. Dyslipidaemia was defined as total cholesterol (TCHL) ≥ 240 mg/dL, high-density lipoprotein (HDL) < 40 mg/dL, low-density lipoprotein (LDL) ≥ 160 mg/dL, triglycerides (TG) ≥ 200 mg/dL, or dyslipidaemia history. Their nutrient intake was classified as follows: protein intake: high ≥ 30%, 30% > moderate ≥ 20%, and 20% > low in daily total energy intake (TEI); carbohydrate intake: high ≥ 60%, 60% > moderate ≥ 50%, and 50% > low; fat intake: high ≥ 40%, 40% > moderate ≥ 30%, and 30% > low. Odds ratios and 95% confidence intervals were calculated after adjusting for age; sex; body mass index (BMI); exercise status; smoking status; alcohol intake; principal component 1 (PC1); principal component 2 (PC2); and intake of carbohydrates, fats, and proteins. This analysis included 20,596 patients with dyslipidaemia and 1027 CCD patients. We found that rs2070895 related to LIPC was associated with HDL-cholesterol. Patients with the minor allele (A) in rs2070895 had a lower risk of CCD than those carrying the reference allele (G) (odds ratio [OR] = 0.8956, p-value = 1.78 × 10^-2). Furthermore, individuals consuming protein below 20% TEI with the LIPC reference allele had a higher risk of CCD than those with the minor allele (interaction p-value 6.12 × 10^-3). Our findings suggest that the interactions of specific polymorphisms associated with dyslipidaemia and nutrients intake can influence CCD.

SUBMITTER: Lee SB

PROVIDER: S-EPMC9312854 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundIn the United Kingdom, the Food Standards Agency-Ofcom nutrient profiling model (FSA-Ofcom model) is used to define less-healthy foods that cannot be advertised to children. However, there has been limited investigation of whether less-healthy foods defined by this model are associated with prospective health outcomes. The objective of this study was to test whether consumption of less-healthy food as defined by the FSA-Ofcom model is associated with cardiovascular disease (CVD).Methods and findingsWe used data from the European Prospective Investigation of Cancer (EPIC)-Norfolk cohort study in adults (n = 25,639) aged 40-79 years who completed a 7-day diet diary between 1993 and 1997. Incident CVD (primary outcome), cardiovascular mortality, and all-cause mortality (secondary outcomes) were identified using record linkage to hospital admissions data and death certificates up to 31 March 2015. Each food and beverage item reported was coded and given a continuous score, using the FSA-Ofcom model, based on the consumption of energy; saturated fat; total sugar; sodium; nonsoluble fibre; protein; and fruits, vegetables, and nuts. Items were classified as less-healthy using Ofcom regulation thresholds. We used Cox proportional hazards regression to test for an association between consumption of less-healthy food and incident CVD. Sensitivity analyses explored whether the results differed based on the definition of the exposure. Analyses were adjusted for age, sex, behavioural risk factors, clinical risk factors, and socioeconomic status. Participants were followed up for a mean of 16.4 years. During follow-up, there were 4,965 incident cases of CVD (1,524 fatal within 30 days). In the unadjusted analyses, we observed an association between consumption of less-healthy food and incident CVD (test for linear trend over quintile groups, p < 0.01). After adjustment for covariates (sociodemographic, behavioural, and indices of cardiovascular risk), we found no association between consumption of less-healthy food and incident CVD (p = 0.84) or cardiovascular mortality (p = 0.90), but there was an association between consumption of less-healthy food and all-cause mortality (test for linear trend, p = 0.006; quintile group 5, highest consumption of less-healthy food, versus quintile group 1, HR = 1.11, 95% CI 1.02-1.20). Sensitivity analyses produced similar results. The study is observational and relies on self-report of dietary consumption. Despite adjustment for known and reported confounders, residual confounding is possible.ConclusionsAfter adjustment for potential confounding factors, no significant association between consumption of less-healthy food (as classified by the FSA-Ofcom model) and CVD was observed in this study. This suggests, in the UK setting, that the FSA-Ofcom model is not consistently discriminating among foods with respect to their association with CVD. More studies are needed to understand better the relationship between consumption of less-healthy food, defined by the FSA-Ofcom model, and indices of health.

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Dyslipidaemia-Genotype Interactions with Nutrient Intake and Cerebro-Cardiovascular Disease.

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