Search Results (60)

Background/Objectives/Methods: Current research on the link between diet and stroke or myocardial infarction primarily focuses on individual food items. However, people’s eating habits involve complex combinations of various foods. By employing an innovative approach known as the Gaussian graphical model to identify dietary patterns along with the Cox proportional model, the study aimed to identify dietary networks and explore their relationship with the incidence of stroke and/or myocardial infarction in the Korean population. The research utilized data from 84,729 participants in the Korean Genome and Epidemiological Study (KoGES), including the HEXA cohort (61,140 participants), CAVAS cohort (15,419 participants), and Ansan-Ansung cohort (8170 participants). Results: The network identified five dietary patterns or communities consisting of different food groups, while nine food groups did not belong to any community. The High-Protein and Green Tea Community consistently reduced the risk of stroke and myocardial infarction (MI), particularly among females. In most communities, no significant associations with stroke risk were noted in males, and the Rice and High-Calorie Beverages Community was linked to an increased risk of MI in both the total population and females. Conclusions: Dietary patterns derived from network analysis revealed distinct dietary habits in the Korean population, offering new insights into the relationship between diet and the risk of stroke and MI. Full article

Background/Objectives: Colorectal cancer (CRC) is a major health concern in Korea, with its increasing incidence emphasizing the urgent need to identify risk factors. Recent studies suggest that heme iron elevates CRC risk, but evidence remains conflicting. This study examined the associations between total, heme, and non-heme iron intake and the incidence of colorectal, colon, and rectal cancer in Koreans. Methods: Using the Korean Genome and Epidemiology Study Health Examinee (KoGES HEXA) cohort, a large community-based cohort of healthy Koreans, we constructed a database of iron content for foods listed in a validated food frequency questionnaire (FFQ) and assessed dietary iron intake for each participant. Colorectal, colon, and rectal cancer cases were identified via the national cancer registry up to 2018. The association between iron consumption and cancers was evaluated with hazard ratios (HRs) and 95% confidence intervals (95%CIs) using multivariable-adjusted Cox regression. Results: During the 9.1-year median follow-up of 109,908 participants (37,697 men and 71,401 women, median age: 53.8 years), 608 new CRC cases were identified. Moderate total iron consumption in the second quintile (5.00–6.27 mg/day) decreased CRC (HR: 0.75; 95%CI: 0.58–0.97) and colon cancer (HR: 0.71; 95%CI: 0.51–1.00) risk compared to the lowest consumption quintile (1.09–4.99 mg/day), as did non-heme iron intake in the second quintile (4.98–6.24 mg/day) compared to its lowest quintile (1.09–4.97 mg/day) (CRC HR: 0.75; 95%CI: 0.58–0.98; colon cancer HR: 0.70; 95%CI: 0.49–0.98). Conclusions: Moderate total and non-heme iron intake reduced colorectal and colon cancer risk in Koreans, possibly via the displacement of carcinogens and the increased intake of protective micronutrients from plant-based foods. Larger-scale studies may be instrumental in substantiating these results. Full article

Background/Objectives: Metabolic syndrome (MetS) is a growing global health concern, driven in part by increasing rates of overweight and obesity. In Korea, MetS incidence escalates particularly among middle-aged women, eventually surpassing that of men. While protein-rich diets have been associated with improved metabolic health, the impact of protein intake on body weight fluctuations (BWFs) and MetS risk has received limited attention, especially in Korean populations. Methods: Using data from the Korean Genome and Epidemiology Study (KoGES), this study examined whether a higher intake of protein-rich foods is linked to smaller BWF and lower MetS incidence in middle-aged Korean women. Dietary intake was assessed through validated questionnaires, and BWF was calculated based on repeated anthropometric measurements over a long-term follow-up. MetS was defined according to established clinical criteria. Results: Preliminary findings indicated that participants who consumed higher amounts of protein-rich foods, particularly animal-based proteins (e.g., fish, low-fat dairy), tended to exhibit smaller BWFs. Additionally, lower BWF was associated with a reduced risk of MetS, suggesting that stable weight regulation may play a protective role against metabolic dysfunction. Potential mechanisms include the preservation of lean mass, enhanced energy expenditure, and reduced carbohydrate intake when protein consumption is increased. These findings highlight the importance of dietary strategies that optimize protein intake to help minimize BWF and potentially lower MetS risk in middle-aged Korean women. Future research should investigate the specific sources and quality of protein and their long-term effects on metabolic health outcomes in diverse populations. Full article

Background: Sarcopenia and obesity are age-related conditions associated with dietary habits. However, the relationship between eating speed and sarcopenia, particularly in older adults >65 years of age remains unclear. Methods: To investigate the effect of eating speed on the occurrence of sarcopenia, obesity, and sarcopenic obesity, we examined eating speed, socioeconomic factors, and disease history of 6202 patients at baseline and their changes over a 16-year follow-up period. Results: A fast eating speed was significantly associated with a higher risk of developing sarcopenia (normal eating: HR 1.284, 95% CI 1.107–1.490; slow eating: HR 1.583, 95% CI 1.279–1.958). Slower eating was associated with a reduced risk of obesity (normal eating: HR 0.865, 95% CI 0.786–0.952; slow eating: HR 0.680, 95% CI 0.577–0.802). These trends were consistent among participants aged <65 years. Among participants aged ≥65 years, fast eating was associated with a higher incidence of sarcopenia (HR 1.603, 95% CI 1.119–2.298), but no significant relationship existed with obesity (normal eating: HR 0.846, 95% CI 0.623–1.150; slow eating: HR 0.792, 95% CI 0.537–1.168). Conclusions: Slow eating speed decreased the incidence of obesity but increased that of sarcopenia in adults aged <65 years. However, in adults aged ≥65 years, slow eating speeds increased the incidence of sarcopenia but did not reduce the incidence of obesity. Full article

Background: Understanding gene–diet interactions is crucial for establishing dietary guidelines for cardiovascular diseases (CVD). This study analyzed the interaction between dietary intake and six genome-wide association study (GWAS)-identified single nucleotide polymorphisms (SNP) associated with high-density lipoprotein (HDL) cholesterol levels and their impact on CVD risk. Methods: A total of 68,806 participants in the Korean Genome and Epidemiology Study (KoGES) were analyzed. Six target SNPs (LPL: rs17482753; ABCA1: rs1883025; APOA5: rs651821; LIPC: rs1077835; CETP: rs17231506; and LIPG: rs9953437) were extracted from genome-wide SNP genotype data. Dietary intake was assessed using a food frequency questionnaire. SNP genotyping was conducted using the Korea Biobank Array (Korean Chip), a specialized genotyping platform designed for GWAS of blood biochemical traits in the Korean population. SNP–diet interactions on CVD risk were analyzed using generalized linear models (GLM). Results: Among the six SNPs, ABCA1: rs1883025 and APOA5: rs651821 showed significant gene–diet interactions. For rs1883025 (ABCA1), carriers of the T allele exhibited reduced HDL cholesterol levels. However, in the high-protein intake group, individuals with the T/T genotype had a significantly lower risk of ischemic stroke compared to those in the low-protein intake group (interaction p-value = 0.044). For rs651821 (APOA5), carriers of the T allele also had lower HDL cholesterol levels, but individuals with the C/C genotype (wild-type homozygotes) in the low-fat intake group showed a significantly reduced risk of coronary artery disease (interaction p-value = 0.0155). Conclusions: This study suggests potential interactions between polymorphisms associated with low HDL cholesterol and dietary patterns, particularly high-protein and low-fat diets, in relation to CVD risk. These findings highlight the importance of personalized dietary recommendations based on genetic profiles to reduce CVD risk. They provide a basis for future research aimed at developing precision nutrition guidelines and targeted interventions to manage hypo-HDL cholesterolemia and nutrition-related CVD risks. Full article

Background and Objectives: Shift work is associated with an increased risk of acute coronary syndrome (ACS) and higher rates of smoking and alcohol consumption. This study examines how smoking and alcohol intake may influence the effect of shift work on ACS risk, indicating a complex interaction among these factors in individuals engaged in shift work. Materials and Methods: This investigation utilized data from the Korean Genome and Epidemiology Study (KoGES). Shift work was the primary exposure, and the main outcome was ACS, defined as either myocardial infarction or angina pectoris diagnosed from 2003 to 2020. Cox proportional regression analysis was employed to assess the impact of shift work, smoking, and alcohol intake on ACS incidence. Additionally, we performed an interaction analysis to examine the effects of shift work in conjunction with smoking and alcohol intake on ACS incidence. Results: Out of 10,038 participants enrolled during the study period, 3696 (36.8%) met the inclusion criteria. The incidence rate of ACS was 11.88 per 1000 person-years in the shift work group compared to 5.96 per 1000 person-years in the non-shift work group. Using Cox proportional logistic regression, shift work was found to be associated with a hazard ratio (HR) of 1.74 (95% CI, 1.20, 2.53) compared to the non-shift work group. Smoking and alcohol consumption did not exhibit a significant HR for ACS incidence, with HRs of 1.31 (95% CI, 0.98, 1.75) and 0.83 (95% CI, 0.65, 1.07), respectively. In the interaction model, after adjusting for other covariates, shift work was not significantly associated with ACS incidence in current smokers (HR 1.05, 95% CI 0.49, 2.23). However, among non-current smokers, shift work emerged as a significant risk factor for ACS incidence (HR 2.26, 95% CI 1.44, 3.55) (p for interaction < 0.01). No interaction was found between alcohol consumption and shift work in relation to ACS incidence. Conclusions: Shift work is an independent risk factor for acute coronary syndrome (ACS), particularly among non-current smokers. This finding highlights the need to address both lifestyle and occupational factors when developing strategies to mitigate ACS risk among shift workers. Employers and policymakers should consider implementing targeted workplace interventions to reduce this risk. These may include optimizing shift schedules to minimize circadian disruption, providing regular health screenings focused on cardiovascular health, and promoting healthy lifestyle habits such as balanced nutrition, regular physical activity, and stress management programs. Additionally, workplace wellness initiatives could focus on reducing other modifiable risk factors, such as providing resources for smoking cessation and limiting exposure to occupational stressors. Integrating these strategies into occupational health policies can contribute to the early detection and prevention of ACS, ultimately improving the cardiovascular health of shift workers. Full article

Background/Objectives: There is limited evidence on gene-nutrient interaction associated with hypertension (HTN). We examined interactions between genotypes and various nutrients that influenced high blood pressure (BP). Methods: Data were obtained from a total of 50,808 participants from the Korean Genome and Epidemiology Study (KoGES). Dietary intake was assessed by a food frequency questionnaire, and dietary reference intakes (DRIs) were set. We performed genome-wide association analyses (GWAS) and subsequent interaction analyses with genome-wide significant SNPs to identify genomic loci that interact with specific nutrients associated with HTN. Results: We identified one locus near the CUB and Sushi Multiple Domains 1 (CSMD1) gene that showed interaction with dietary iron and vitamin B6 (Vit.B6) intake and significantly influenced HTN risk. Among the individuals consuming iron above DRI (9.5 mg/day for men, 9.25 mg/day for women), carriers of the rs13282715 minor allele (A) at 8p23.2 showed a lower risk of HTN than those who did not (odds ratio [OR] 0.723, 95% confidence interval [CI] (0.644–0.813), p-value 4.858 × 10⁻⁸; interaction p-value 1.336 × 10⁻³). Among the individuals consuming Vit.B6 above DRI (1.5 mg/day for men, 1.4 mg/day for women), carriers of the same variant rs13282715 minor allele (A) also showed a lower risk of HTN (OR 0.733, 95% CI 0.733 (0.656–0.819), p-value 4.121 × 10⁻⁸; interaction p-value 7.183 × 10⁻⁴). Conclusions: We identified a novel gene-nutrient interaction regarding dietary iron and Vit.B6 intake affecting the risk of HTN in Korean adults. This suggests individuals with the variant may benefit from lower HTN risk from dietary intervention of iron and Vit.B6 intake. Further studies with larger diverse populations are warranted to validate our findings. Full article

Insulin resistance is a major indicator of cardiovascular diseases, including hypertension. The Metabolic Score for Insulin Resistance (METS-IR) offers a simplified and cost-effective way to evaluate insulin resistance. This study aimed to identify genetic variants associated with the prevalence of hypertension stratified by METS-IR score levels. Data from the Korean Genome and Epidemiology Study (KoGES) were analyzed. The METS-IR was calculated using the following formula: ln [(2 × fasting blood glucose (FBG) + triglycerides (TG)) × body mass index (BMI)]/ ln [high-density lipoprotein cholesterol (HDL-C)]. The participants were divided into tertiles 1 (T1) and 3 (T3) based on their METS-IR scores. Genome-wide association studies (GWAS) were performed for hypertensive cases and non-hypertensive controls within these tertile groups using logistic regression adjusted for age, sex, and lifestyle factors. Among the METS-IR tertile groups, 3517 of the 19,774 participants (17.8%) at T1 had hypertension, whereas 8653 of the 20,374 participants (42.5%) at T3 had hypertension. A total of 113 single-nucleotide polymorphisms (SNPs) reached the GWAS significance threshold (p < 5 × 10⁻⁸) in at least one tertile group, mapping to six distinct genetic loci. Notably, four loci, rs11899121 (chr2p24), rs7556898 (chr2q24.3), rs17249754 (ATP2B1), and rs1980854 (chr20p12.2), were significantly associated with hypertension in the high-METS-score group (T3). rs10857147 (FGF5) was significant in both the T1 and T3 groups, whereas rs671 (ALDH2) was significant only in the T1 group. The GWASs identified six genetic loci significantly associated with hypertension, with distinct patterns across METS-IR tertiles, highlighting the role of metabolic context in genetic susceptibility. These findings underscore critical genetic factors influencing hypertension prevalence and provide insights into the metabolic–genetic interplay underlying this condition. Full article

Mitochondrial dysfunction is closely linked to obesity and diabetes, with declining lung function in aging increasing diabetes risk, potentially due to elevated serum levels of dioxin-like mitochondria inhibitor substances (MIS) from prolonged exposure to environmental pollutants. However, the mechanisms connecting MIS, mitochondria, lung function, and metabolic disorder remain unclear. In this study, we analyzed data from 1371 adults aged 40–69 years in the 2008 Korean Genome Epidemiologic Study (KoGES) Ansung cohort. We indirectly estimated dioxin-like MIS levels by measuring intracellular ATP (MIS_ATP) and reactive oxygen species (MIS_ROS) in cultured cells treated with the serum of participants. Using correlation analysis and structural equation modeling (SEM), we explored the relationships among MIS, mitochondrial function, body mass index (BMI), and lung function (FEV1 and FVC). Our findings revealed that MIS_ATP was associated with BMI in females and with FVC in males, while MIS_ROS correlated with both BMI and FVC in males, not in females. Significant associations between BMI and FVC were found in the highest MIS subgroup in both sexes. SEM analyses demonstrated that MIS negatively influenced mitochondrial function, which in turn affected BMI and lung function. Age-related declines in lung function were also linked to mitochondrial dysfunction. This study underscores the potential of MIS assays as alternatives for assessing mitochondrial function and highlights the importance of mitochondrial health in metabolic disorders and lung function. Full article

Insights from public DNA methylation data derived from cancer or normal tissues from cancer patients or healthy people can be obtained by machine learning. The goal is to determine methylation patterns that could be useful for predicting the prognosis for cancer patients and correcting lifestyles for healthy people. DNA methylation data were obtained from the DNA of 446 healthy participants from the Korean Genome Epidemiology Study (KoGES) and from the DNA of normal tissues or from cancer tissues of 11 types of carcinomas from The Cancer Genome Atlas (TCGA) database. To correct for the batch effect, R’s ComBat function was used. Using the K-mean clustering (k = 3), the survival rates of the cancer patients and the incidence of chronic diseases were compared between the three clusters for TCGA and KoGES, respectively. Based on the public DNA methylation and clinical data of healthy participants and cancer patients, I present an analysis pipeline that integrates and clusters the methylation data from the two groups. As a result of clustering, CpG sites from gene or genomic regions, such as AFAP1, NINJ2, and HOOK2 genes, that correlated with survival rate and chronic disease are presented. Full article

(1) Background: The relationship between nonalcoholic fatty liver disease (NAFLD) and incident chronic kidney disease (CKD) is unclear, and long-term follow-up data are limited. Therefore, this study aimed to evaluate whether NAFLD, as assessed by the fatty liver index (FLI), could predict the development of CKD in a community-based Korean cohort over 16 years. (2) Methods: Among the 10,030 total participants, 7778 patients without CKD were selected from the Korean Genome and Epidemiology Study (KoGES). The FLI grade ranged from 0 to 100 and was divided into three groups: low (FLI, <30), intermediate (FLI, 30–59), and high (FLI, ≥60). An estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m² or the development of proteinuria was considered to indicate incident CKD. (3) Results: During the 16-year follow-up period, 919 individuals (11.8%) developed CKD. The HRs of incident CKD in the intermediate FLI group (30–59) and high FLI group (≥60) increased compared with the reference low FLI group (<30) after adjusting for potentially confounding variables. NAFLD, as assessed by the FLI, was an independent risk factor for CKD. (4) Conclusions: Our findings suggest that the FLI, a simple surrogate biomarker of fatty liver disease, may be used to identify people at high risk of incident CKD in clinical practice. Full article

The oxidative balance score (OBS) is a novel composite of pro- and anti-oxidative markers for assessing the risk of cardiometabolic diseases and non-alcoholic fatty liver disease (NAFLD). However, it has not yet been established whether the OBS is related to type 2 diabetes mellitus (T2DM), especially in a population without NALFD. Therefore, we aimed to investigate the longitudinal effect of the OBS on T2DM in a large cohort of Korean adults without NALFD. Data were assessed from 9798 participants without NALFD from the Korean Genome and Epidemiology Study-Health Examinees (KoGES-HEXA) cohort. The participants were divided into three groups according to OBS tertiles, identified as T1–T3. We prospectively assessed the hazard ratios (HRs) with 95% confidence intervals (CIs) for new-onset T2DM using multivariable Cox proportional hazard regression models over 6 years following the baseline survey. During the mean 3.5 years of follow-up, 145 individuals (1.48%; 56 men and 89 women) developed T2DM. The HRs of T2DM for the OBS tertiles were 0.79 (95% CI, 0.53–1.18) and 0.60 (95% CI, 0.39–0.93) in the T2 and T3 groups after adjusting for metabolic parameters in subjects without NALFD, respectively; however, the T2 group did not show statistical significance toward a decrease in incident T2DM. A low OBS may be a useful predictive marker in new-onset T2DM for middle-aged and older subjects without NALFD. This implies that the OBS could be an additional valuable tool for assessing the incidence of T2DM among individuals without NAFLD. Full article

Diabetes is characterized by persistently high blood glucose levels and severe complications and affects millions of people worldwide. In this study, we explored the epigenetic landscape of diabetes using data from the Korean Genome and Epidemiology Study (KoGES), specifically the Ansung–Ansan (AS–AS) cohort. Using epigenome-wide association studies, we investigated DNA methylation patterns in patients with type 2 diabetes mellitus (T2DM) and those with normal glucose regulation. Differential methylation analysis revealed 106 differentially methylated probes (DMPs), with the 10 top DMPs prominently associated with TXNIP, PDK4, NBPF20, ARRDC4, UFM1, PFKFB2, C7orf50, and ABCG1, indicating significant changes in methylation. Correlation analysis highlighted the association between the leading DMPs (e.g., cg19693031 and cg26974062 for TXNIP and cg26823705 for NBPF20) and key glycemic markers (fasting plasma glucose and hemoglobin A1c), confirming their relevance in T2DM. Moreover, we identified 62 significantly differentially methylated regions (DMRs) spanning 61 genes. A DMR associated with PDE1C showed hypermethylation, whereas DMRs associated with DIP2C, FLJ90757, PRSS50, and TDRD9 showed hypomethylation. PDE1C and TDRD9 showed a strong positive correlation between the CpG sites included in each DMR, which have previously been implicated in T2DM-related processes. This study contributes to the understanding of epigenetic modifications in T2DM. These valuable insights can be utilized in identifying potential biomarkers and therapeutic targets for effective management and prevention of diabetes. Full article

Several studies have showed that hyperuricemia is related to the development of ischemic heart disease (IHD). There is also growing evidence indicating that hyperuricemia may contribute to the progression of IHD as a pathogenic factor. Ironically, uric acid can be an antioxidant agent, as shown in experimental studies. The aim of our study is to analyse the association between uric acid and IHD with early-stage chronic kidney disease (CKD). Data were assessed from 17,492 participants without cardiovascular disease from the Korean Genome and Epidemiology Study (KoGES) and Korea Health Insurance Review and Assessment (HIRA) data. The subjects were categorized as four groups according to CKD and uric acid levels. We retrospectively evaluated hazard ratios (HRs) with 95% confidence intervals (CIs) for IHD by using multivariate Cox regression analysis over a 4-year period from the baseline survey. During the follow-up, 335 individuals (3.4%; 236 men and 99 women) developed IHD. Compared to the participants without elevated uric acid and early CKD HRs for incident IHD according to uric acid levels and early CKD, the uric acid level was 1.13 (95% CI, 0.86–1.48) in participants with elevated uric acid and without early CKD, 0.99 (95% CI, 0.55–1.77) in participants without elevated uric acid and with early CKD, and 1.65 (95% CI, 1.03–2.66) in participants with elevated uric acid and early CKD after adjusting for confounding metabolic factors. Early CKD and high uric acid levels increased the risk of new-onset IHD (HR, 1.65; 95% CI, 1.03–2.66). Elevated uric acid levels were related to an increased risk of incident IHD in early-stage CKD patients. It is expected that uric acid can be a reliable predictor for IHD, even in early-stage CKD patients; thus, in those with CKD, proactively managing uric acid levels can play a significant role in reducing the risk of cardiovascular disease. Full article

Background: Although knowledge of the genetic factors influencing kidney disease is increasing, epigenetic profiles, which are associated with chronic kidney disease (CKD), have not been fully elucidated. We sought to identify the DNA methylation status of CpG sites associated with reduced kidney function and examine whether the identified CpG sites are associated with CKD development. Method: We analyzed DNA methylation patterns of 440 participants in the Korean Genome and Epidemiology Study (KoGES) with estimated glomerular filtration rates (eGFRs) ≥ 60 mL/min/1.73 m² at baseline. CKD development was defined as a decrease in the eGFR of <60 at any time during an 8-year follow-up period (“CKD prediction” analysis). In addition, among the 440 participants, 49 participants who underwent a second methylation profiling were assessed for an association between a decline in kidney function and changes in the degree of methylation of CpG sites during the 8 years (“kidney function slope” analysis). Results: In the CKD prediction analysis, methylation profiles of a total of 403,129 CpG sites were evaluated at baseline in 440 participants, and increased and decreased methylation of 268 and 189 CpG sites, respectively, were significantly correlated with the development of CKD in multivariable logistic regression. During kidney function slope analysis using follow-up methylation profiles of 49 participants, the percent methylation changes in 913 CpG sites showed a linear relationship with the percent change in eGFR during 8 years. During functional enrichment analyses for significant CpG sites found in the CKD prediction and kidney function slope analyses, we found that those CpG sites represented MAPK, PI3K/Akt, and Rap1 pathways. In addition, three CpG sites from three genes, NPHS2, CHCHD4, and AHR, were found to be significant in the CKD prediction analysis and related to a decline in kidney function. Conclusion: It is suggested that DNA methylation on specific genes is associated with the development of CKD and the deterioration of kidney function. Full article