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Objectives: We evaluated the impact of reimbursement for non-face-to-face chronic care management (NFFCCM) on healthcare utilization among Medicare beneficiaries with type 2 diabetes in Louisiana., Methods: We implemented group-based trajectory balancing and propensity score matching to obtain comparable treatment (with NFFCCM) and control (without NFFCCM) groups at baseline. Patients with diabetes with Medicare as their primary payer at baseline were extracted using electronic health records of 3 health systems from Research Action for Health Network, a Clinical Research Network. The study period is from 2013 to early 2020. Our outcomes include general healthcare utilization (outpatient, emergency department, and inpatient encounters) and health utilization related to diabetic complications. We tested each of these outcomes according to multiple treatment definitions and different subgroups., Results: Receiving any NFFCCM was associated with an increase in outpatient visits of 657 (95% confidence interval [CI] 626-687; P < .001) per 1000 patients per month, a decrease in inpatient admissions of 5 (95% CI 2-7; P < .001) per 1000 patients per month, and a decrease in emergency department visits of 4 (95% CI 1-7; P = .005) per 1000 patients per month after 24-month follow-up from initial NFFCCM encounter. Both complex and noncomplex NFFCCM significantly increased visits to outpatient services and inpatient admissions per month. Receiving NFFCCM has a dose-response association with increasing outpatient visits per month., Conclusions: Patients with diabetes in Louisiana who received NFFCCM had more low-cost primary healthcare and less high-cost healthcare utilization in general. The cost savings of NFFCCM in diabetes management could be further explored in the future., (Copyright © 2022. Published by Elsevier Inc.)

Background: Following the high morbidity and mortality due to Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infections in New Orleans, Louisiana, we sought to assess progress toward herd immunity., Methods: Ochsner Health employees and patients who volunteered for Abbott SARS-CoV-2 immunoglobulin G (IgG) antibody test between March 1 and May 1, 2020 were included. We estimated IgG prevalence and used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for variables associated with IgG test status., Results: Of the 13,343 participants with IgG test results, 78.6% were women, 70.6% were non-Hispanic White, 21.1% non-Hispanic Black, 2.9% Hispanic Americans and 5.4% belonged to other races. Overall, 7.99% (95% CI: 7.53-8.45%) of the participants tested IgG positive. In age-, sex- and body mass index (BMI)-adjusted analyses, non-Hispanic Blacks were 2.7-times more likely to test positive than non-Hispanic Whites (OR=2.72; 95% CI: 2.33-3.19). Corresponding ORs (95% CIs) were 1.29 (0.84-1.99) for Hispanic Americans and 1.22 (0.85-1.75) for Other race/ethnicities. Compared to participants in administrative occupations, physician assistants (OR=7.14; 95% CI: 1.72-29.6) and therapists (OR=4.74; 95% CI: 1.49-15.03) were significantly more likely to have IgG antibodies while the association among nurses was not significant (OR=2.35; 95% CI: 0.96-5.77). Relative to 1.40, the test threshold for positivity, our measurements indicate a strong immune response (5.38±1.69), especially among those with a higher BMI., Conclusions: SARS-COV-2 IgG antibodies were prevalent only in 8% of the participants. IgG prevalence was highest among non-Hispanic Blacks and participants with higher BMI but was lower among older participants., Competing Interests: Conflicts of Interest The authors have no financial or other conflicts of interest to disclose., (Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Background and Aims: Data on the relation of egg consumption with risk of type 2 diabetes (T2D) and coronary heart disease (CHD) are limited and inconsistent. Few studies have controlled for overall dietary patterns in egg-T2D or egg-CHD analyses, and it is unclear whether any observed elevated risks of T2D and CHD with frequent egg consumption is real or due to confounding by dietary habits. We tested the hypothesis that frequent egg consumption is associated with a higher risk of T2D and CHD risk after adjustment for overall dietary patterns among adults., Design: We used prospective cohort design to complete time-to-event analyses., Methods: We pooled de novo, harmonized, individual-level analyses from nine US cohorts (n = 103,811). Cox regression was used to estimate hazard ratios separately in each cohort adjusting for age, ethnicity, body mass index (BMI), exercise, smoking, alcohol intake, and dietary patterns. We pooled cohort-specific results using an inverse-variance weighted method to estimate summary relative risks., Results: Median age ranged from 25 to 72 years. Median egg consumption was 1 egg per week in most of the cohorts. While egg consumption up to one per week was not associated with T2D risk, consumption of ≥2 eggs per week was associated with elevated risk [27% elevated risk of T2D comparing 7+ eggs/week with none (95% CI: 16%-37%)]. There was little evidence for heterogeneity across cohorts and we observed similar conclusions when stratified by BMI. Overall, egg consumption was not associated with the risk of CHD. However, in a sensitivity analysis, there was a 30% higher risk of CHD (95% CI: 3%-56%) restricted to older adults consuming 5-6 eggs/week., Conclusions: Our data showed an elevated risk of T2D with egg consumption of ≥2 eggs per week but not with <2 eggs/week. While there was no overall association of egg consumption with CHD risk, the elevated CHD observed with consumption of 5-6 eggs/week in older cohorts merits further investigation., Competing Interests: Disclosures Dr. Djousse received investigator-initiated grant from American Egg Board for current analyses; sponsor had no influence on design, conduct, and interpretation of the results. Other co-authors have no disclosures., (Published by Elsevier Ltd.)

MUFAs are unsaturated FAs with one double bond and are derived from endogenous synthesis and dietary intake. Accumulating evidence has suggested that plasma and erythrocyte MUFA levels are associated with cardiometabolic disorders, including CVD, T2D, and metabolic syndrome (MS). Previous genome-wide association studies (GWASs) have identified seven loci for plasma and erythrocyte palmitoleic and oleic acid levels in populations of European origin. To identify additional MUFA-associated loci and the potential functional variant at each locus, we performed ethnic-specific GWAS meta-analyses and trans-ethnic meta-analyses in more than 15,000 participants of Chinese and European ancestry. We identified novel genome-wide significant associations for vaccenic acid at FADS1/2 and PKD2L1 [log 10 (Bayes factor) ≥ 8.07] and for gondoic acid at FADS1/2 and GCKR [log 10 (Bayes factor) ≥ 6.22], and also observed improved fine-mapping resolutions at FADS1/2 and GCKR loci. The greatest improvement was observed at GCKR , where the number of variants in the 99% credible set was reduced from 16 (covering 94.8 kb) to 5 (covering 19.6 kb, including a missense variant rs1260326) after trans-ethnic meta-analysis. We also confirmed the previously reported associations of PKD2L1 , FADS1/2 , GCKR , and HIF1AN with palmitoleic acid and of FADS1/2 and LPCAT3 with oleic acid in the Chinese-specific GWAS and the trans-ethnic meta-analyses. Pathway-based analyses suggested that the identified loci were in unsaturated FA metabolism and signaling pathways. Our findings provide novel insight into the genetic basis relevant to MUFA metabolism and biology., (Copyright © 2017 by the American Society for Biochemistry and Molecular Biology, Inc.)

Objectives: This study sought to assess whether body mass index (BMI) was associated with subclinical left ventricular (LV) systolic dysfunction in African-American individuals., Background: Higher BMI is a risk factor for cardiovascular disease, including heart failure. Obesity disproportionately affects African Americans; however, the association between higher BMI and LV function in African Americans is not well understood., Methods: Peak systolic circumferential strain (ECC) was measured by tagged cardiac magnetic resonance in 1,652 adult African-American participants of the Jackson Heart Study between 2008 and 2012. We evaluated the association between BMI and ECC in multivariate linear regression and restricted cubic spline analyses adjusted for prevalent cardiovascular disease, conventional cardiovascular risk factors, LV mass, and ejection fraction. In exploratory analyses, we also examined whether inflammation, insulin resistance, or volume of visceral adipose tissue altered the association between BMI and ECC., Results: The proportions of female, nonsmokers, diabetic, and hypertensive participants rose with increase in BMI. In multivariate-adjusted models, higher BMI was associated with worse ECC (β = 0.052; 95% confidence interval: 0.028 to 0.075), even in the setting of preserved LV ejection fraction. Higher BMI was also associated with worse ECC when accounting for markers of inflammation (C-reactive protein, E-selection, and P-selectin), insulin resistance, and volume of visceral adipose tissue., Conclusions: Higher BMI is significantly associated with subclinical LV dysfunction in African Americans, even in the setting of preserved LV ejection fraction., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: DNA methylation is influenced by diet and single nucleotide polymorphisms (SNPs), and methylation modulates gene expression., Objective: We aimed to explore whether the gene-by-diet interactions on blood lipids act through DNA methylation., Design: We selected 7 SNPs on the basis of predicted relations in fatty acids, methylation, and lipids. We conducted a meta-analysis and a methylation and mediation analysis with the use of data from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) consortium and the ENCODE (Encyclopedia of DNA Elements) consortium., Results: On the basis of the meta-analysis of 7 cohorts in the CHARGE consortium, higher plasma HDL cholesterol was associated with fewer C alleles at ATP-binding cassette subfamily A member 1 (ABCA1) rs2246293 (β = -0.6 mg/dL, P = 0.015) and higher circulating eicosapentaenoic acid (EPA) (β = 3.87 mg/dL, P = 5.62 × 10(21)). The difference in HDL cholesterol associated with higher circulating EPA was dependent on genotypes at rs2246293, and it was greater for each additional C allele (β = 1.69 mg/dL, P = 0.006). In the GOLDN (Genetics of Lipid Lowering Drugs and Diet Network) study, higher ABCA1 promoter cg14019050 methylation was associated with more C alleles at rs2246293 (β = 8.84%, P = 3.51 × 10(18)) and lower circulating EPA (β = -1.46%, P = 0.009), and the mean difference in methylation of cg14019050 that was associated with higher EPA was smaller with each additional C allele of rs2246293 (β = -2.83%, P = 0.007). Higher ABCA1 cg14019050 methylation was correlated with lower ABCA1 expression (r = -0.61, P = 0.009) in the ENCODE consortium and lower plasma HDL cholesterol in the GOLDN study (r = -0.12, P = 0.0002). An additional mediation analysis was meta-analyzed across the GOLDN study, Cardiovascular Health Study, and the Multi-Ethnic Study of Atherosclerosis. Compared with the model without the adjustment of cg14019050 methylation, the model with such adjustment provided smaller estimates of the mean plasma HDL cholesterol concentration in association with both the rs2246293 C allele and EPA and a smaller difference by rs2246293 genotypes in the EPA-associated HDL cholesterol. However, the differences between 2 nested models were NS (P > 0.05)., Conclusion: We obtained little evidence that the gene-by-fatty acid interactions on blood lipids act through DNA methylation., (© 2016 American Society for Nutrition.)

Background: Circulating trans fatty acids (TFAs), which cannot be synthesized by humans, are linked to adverse health outcomes. Although TFAs are obtained from diet, little is known about subsequent influences (e.g., relating to incorporation, metabolism, or intercompetition with other fatty acids) that could alter circulating concentrations and possibly modulate or mediate impacts on health., Objective: The objective was to elucidate novel biologic pathways that may influence circulating TFAs by evaluating associations between common genetic variation and TFA biomarkers., Design: We performed meta-analyses using 7 cohorts of European-ancestry participants (n = 8013) having measured genome-wide variation in single-nucleotide polymorphisms (SNPs) and circulating TFA biomarkers (erythrocyte or plasma phospholipids), including trans-16:1n-7, total trans-18:1, trans/cis-18:2, cis/trans-18:2, and trans/trans-18:2. We further evaluated SNPs with genome-wide significant associations among African Americans (n = 1082), Chinese Americans (n = 669), and Hispanic Americans (n = 657) from 2 of these cohorts., Results: Among European-ancestry participants, 31 SNPs in or near the fatty acid desaturase (FADS) 1 and 2 cluster were associated with cis/trans-18:2; a top hit was rs174548 (β = 0.0035, P = 4.90 × 10(-15)), an SNP previously associated with circulating n-3 and n-6 polyunsaturated fatty acid concentrations. No significant association was identified for other TFAs. rs174548 in FADS1/2 was also associated with cis/trans-18:2 in Hispanic Americans (β = 0.0053, P = 1.05 × 10(-6)) and Chinese Americans (β = 0.0028, P = 0.002) but not African Americans (β = 0.0009, P = 0.34); however, in African Americans, fine mapping identified a top hit in FADS2 associated with cis/trans-18:2 (rs174579: β = 0.0118, P = 4.05 × 10(-5)). The association between rs174548 and cis/trans-18:2 remained significant after further adjustment for individual circulating n-3 and n-6 fatty acids, except arachidonic acid. After adjustment for arachidonic acid concentrations, the association between rs174548 and cis/trans-18:2 was nearly eliminated in European-ancestry participants (β-coefficient reduced by 86%), with similar reductions in Hispanic Americans and Chinese Americans., Conclusions: Our findings provide novel evidence for genetic regulation of cis/trans-18:2 by the FADS1/2 cluster and suggest that this regulation may be influenced/mediated by concentrations of arachidonic acid, an n-6 polyunsaturated fat., (© 2015 American Society for Nutrition.)

Very long-chain saturated fatty acids (VLSFAs) are saturated fatty acids with 20 or more carbons. In contrast to the more abundant saturated fatty acids, such as palmitic acid, there is growing evidence that circulating VLSFAs may have beneficial biological properties. Whether genetic factors influence circulating levels of VLSFAs is not known. We investigated the association of common genetic variation with plasma phospholipid/erythrocyte levels of three VLSFAs by performing genome-wide association studies in seven population-based cohorts comprising 10,129 subjects of European ancestry. We observed associations of circulating VLSFA concentrations with common variants in two genes, serine palmitoyl-transferase long-chain base subunit 3 (SPTLC3), a gene involved in the rate-limiting step of de novo sphingolipid synthesis, and ceramide synthase 4 (CERS4). The SPTLC3 variant at rs680379 was associated with higher arachidic acid (20:0 , P = 5.81 × 10(-13)). The CERS4 variant at rs2100944 was associated with higher levels of 20:0 (P = 2.65 × 10(-40)) and in analyses that adjusted for 20:0, with lower levels of behenic acid (P = 4.22 × 10(-26)) and lignoceric acid (P = 3.20 × 10(-21)). These novel associations suggest an inter-relationship of circulating VLSFAs and sphingolipid synthesis., (Copyright © 2015 by the American Society for Biochemistry and Molecular Biology, Inc.)

Background: In 2010, overweight and obesity were estimated to cause 3·4 million deaths, 3·9% of years of life lost, and 3·8% of disability-adjusted life-years (DALYs) worldwide. The rise in obesity has led to widespread calls for regular monitoring of changes in overweight and obesity prevalence in all populations. Comparable, up-to-date information about levels and trends is essential to quantify population health effects and to prompt decision makers to prioritise action. We estimate the global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013., Methods: We systematically identified surveys, reports, and published studies (n=1769) that included data for height and weight, both through physical measurements and self-reports. We used mixed effects linear regression to correct for bias in self-reports. We obtained data for prevalence of obesity and overweight by age, sex, country, and year (n=19,244) with a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs)., Findings: Worldwide, the proportion of adults with a body-mass index (BMI) of 25 kg/m(2) or greater increased between 1980 and 2013 from 28·8% (95% UI 28·4-29·3) to 36·9% (36·3-37·4) in men, and from 29·8% (29·3-30·2) to 38·0% (37·5-38·5) in women. Prevalence has increased substantially in children and adolescents in developed countries; 23·8% (22·9-24·7) of boys and 22·6% (21·7-23·6) of girls were overweight or obese in 2013. The prevalence of overweight and obesity has also increased in children and adolescents in developing countries, from 8·1% (7·7-8·6) to 12·9% (12·3-13·5) in 2013 for boys and from 8·4% (8·1-8·8) to 13·4% (13·0-13·9) in girls. In adults, estimated prevalence of obesity exceeded 50% in men in Tonga and in women in Kuwait, Kiribati, Federated States of Micronesia, Libya, Qatar, Tonga, and Samoa. Since 2006, the increase in adult obesity in developed countries has slowed down., Interpretation: Because of the established health risks and substantial increases in prevalence, obesity has become a major global health challenge. Not only is obesity increasing, but no national success stories have been reported in the past 33 years. Urgent global action and leadership is needed to help countries to more effectively intervene., Funding: Bill & Melinda Gates Foundation., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Whether elevated intakes of trans fatty acids (TFAs) increase the risk of stroke remains unclear. Except for the Women's Health Initiative-Observational Study, most studies that directly assessed the association between TFA intake and stroke yielded null results., Objective: The aim of this study was to investigate the association between TFA intake and stroke incidence., Design: We prospectively investigated the association between TFA intake and stroke incidence in black and white men and women (n = 17,107) from the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort. Participants were recruited between 2003 and 2007 from the continental United States and followed for incident stroke. Diet was assessed by using the Block 1998 food-frequency questionnaire. Cox regression was used to test whether energy-adjusted TFA intake in 1-SD increments was associated with incident stroke., Results: During a median follow-up of 7 y, 479 strokes were identified, including 401 ischemic strokes. Sex modified the association between TFA intake and stroke (P-interaction = 0.06), and thus the results were stratified by sex. In fully adjusted models, a 1-SD (2-g/d) increase in TFA intake was associated with an increased risk of any stroke in men (HR: 1.14; 95% CI: 1.02, 1.28) but not in women (HR: 0.93; 95% CI: 0.79, 1.11). Similarly, our results showed an increased risk of ischemic stroke in men (HR: 1.13; 95% CI: 1.00, 1.28) but not in women (HR: 0.93; 95% CI: 0.77, 1.12)., Conclusions: We show that sex modifies the association between TFA intake and stroke; for every 2-g/d increase in TFA intake, there was a 14% increase in the risk of stroke in men but not in women. Our findings provide further evidence to support the concerted effort to minimize TFAs in the diet.

Background: A high intake of trans fatty acids decreases HDL cholesterol and is associated with increased LDL cholesterol, inflammation, diabetes, cancer, and mortality from cardiovascular disease. The relation between trans fat intake and all-cause mortality has not been established., Objective: The aim of this study was to determine the relation between trans fat intake and all-cause mortality., Design: We used data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study-a prospective cohort study of white and black men and women residing in the continental United States. Energy-adjusted trans fat intake was categorized into quintiles, and Cox-regression was used to evaluate the association between trans fat intake and all-cause mortality., Results: During 7 y of follow-up, there were 1572 deaths in 18,513 participants included in REGARDS. From the first to the fifth quintile of trans fat intake, the mortality rates per 1000 person-years of follow-up (95% CIs) were 12.8 (11.3, 14.5), 14.3 (12.7, 16.2), 14.6 (13.0, 16.5), 19.0 (17.1, 21.1), and 23.6 (21.5, 25.9), respectively. After adjustment for demographic factors, education, and risk factors for mortality, the HRs (95% CIs) for all-cause mortality were 1.00, 1.03 (0.86, 1.23), 0.98 (0.82, 1.17), 1.25 (1.05, 1.48), and 1.24 (1.05, 1.48), respectively (P-trend = 0.004). The population attributable risk due to trans fat intake was 7% (95% CI: 5%, 8%)., Conclusion: Higher trans fat intake is associated with an increased risk of all-cause mortality.

Evidence that physical activity (PA) modulates the association between the fat mass and obesity-associated gene (FTO) and BMI is emerging; however, information about dietary factors modulating this association is scarce. We investigated whether fat and carbohydrate intake modified the association of FTO gene variation with BMI in two populations, including participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study (n = 1069) and in the Boston Puerto Rican Health (BPRHS) study (n = 1094). We assessed energy, nutrient intake, and PA using validated questionnaires. Genetic variability at the FTO locus was characterized by polymorphisms rs9939609 (in the GOLDN) and rs1121980 (in the GOLDN and BPRHS). We found significant interactions between PA and FTO on BMI in the GOLDN but not in the BPRHS. We found a significant interaction between SFA intake and FTO on BMI, which was stronger than that of total fat and was present in both populations (P-interaction = 0.007 in the GOLDN and P-interaction = 0.014 in BPRHS for categorical; and P-interaction = 0.028 in the GOLDN and P-interaction = 0.041 in BPRHS for continuous SFA). Thus, homozygous participants for the FTO-risk allele had a higher mean BMI than the other genotypes only when they had a high-SFA intake (above the population mean: 29.7 ± 0.7 vs. 28.1 ± 0.5 kg/m²; P = 0.037 in the GOLDN and 33.6. ± 0.8 vs. 31.2 ± 0.4 kg/m²; P = 0.006 in BPRHS). No associations with BMI were found at lower SFA intakes. We found no significant interactions with carbohydrate intake. In conclusion, SFA intake modulates the association between FTO and BMI in American populations.

Background: The US Head Start program serves low-income preschoolers and their caregivers and provides an opportunity for assessment and intervention on obesity. We sought to determine the prevalence of obesity among children and their caregivers and to identify variables that are associated with child body mass index (BMI) z scores and caregiver BMI., Design/setting: Cross-sectional data on diet and BMI from 770 caregiver-child dyads recruited from 57 Head Start centers in Alabama and Texas., Methods: Height and weight of each caregiver and child were measured using standardized protocols. Dietary intakes of caregiver-child dyads were collected using three 24-hour dietary recalls and Block food frequency questionnaires. Data were collected between September 2004 and November 2005. The larger Food Pyramid categories were divided into 17 food consumption groups and tested for their association with child BMI z scores. Analysis of variance was used to test if food groups were significantly associated with child BMI z score., Results: The prevalence of obesity among children was 18.4%, 24.3%, and 37.3% among black, Hispanic, and white children, respectively (P<0.0001), whereas it was 58.3%, 41.4%, and 41.6% among black, Hispanic, and white caregivers, respectively (P<0.0001). Child BMI z scores and caregiver BMIs were correlated (r=0.16, P<0.0001). In multivariable models, children were 1.90 (95% confidence interval 1.31-2.74) times more likely to have BMI ≥95th percentile if their caregiver was obese. Five variables (fruits, unsweetened beverages, low-fat dairy, race, and caregiver's BMI) were significantly associated with child BMI z scores. Fruits were inversely related, whereas unsweetened beverages, low-fat dairy, and caregiver's BMI were positively associated with child BMI z score (P<0.03). Compared to whites, black and Hispanic children had lower BMI z scores (P<0.05)., Conclusions: The high prevalence of obesity in this population together with the observed inverse association between fruit consumption and BMI, if replicated in other studies, suggests that interventions that promote fruit consumption could have beneficial effects on child BMI., (Copyright © 2011 American Dietetic Association. Published by Elsevier Inc. All rights reserved.)

Background: Several genome-wide association studies have identified novel loci (KCTD10, MVK, and MMAB) that are associated with HDL-cholesterol concentrations. Of the environmental factors that determine HDL cholesterol, high-carbohydrate diets have been shown to be associated with low concentrations., Objective: The objective was to evaluate the associations of 8 single nucleotide polymorphisms (SNPs) located within the KCTD10, MVK, and MMAB loci with lipids and their potential interactions with dietary carbohydrates., Design: KCTD10, MVK, and MMAB SNPs were genotyped in 920 subjects (441 men and 479 women) who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study. Biochemical measurements were made by using standard procedures. Dietary intakes were estimated by using a validated questionnaire., Results: For the SNPs KCTD10&#95;i5642G-->C and MVK&#95;S52NG-->A, homozygotes for the major alleles (G) had lower HDL-cholesterol concentrations than did carriers of the minor alleles (P = 0.005 and P = 0.019, respectively). For the SNP 12inter&#95;108466061A-->G, homozygotes for the minor allele (G) had higher total cholesterol and LDL-cholesterol concentrations than did AG subjects (P = 0.030 and P = 0.034, respectively). Conversely, homozygotes for the major allele (G) at MMAB&#95;3U3527G-->C had higher LDL-cholesterol concentrations than did carriers of the minor allele (P = 0.034). Significant gene-diet interactions for HDL cholesterol were found (P < 0.001-0.038), in which GG subjects at SNPs KCTD10&#95;i5642G-->C and MMAB&#95;3U3527G-->C and C allele carriers at SNP KCTD10&#95;V206VT-->C had lower concentrations only if they consumed diets with a high carbohydrate content (P < 0.001-0.011)., Conclusion: These findings suggest that the KCTD10 (V206VT-->C and i5642G-->C) and MMAB&#95;3U3527G-->C variants may contribute to the variation in HDL-cholesterol concentrations, particularly in subjects with high carbohydrate intakes.

The scaffolding protein PDZ domain containing 1 (PDZK1) regulates the HDL receptor scavenger receptor class B type I. However, the effect of PDZK1 genetic variants on lipids and metabolic syndrome (MetS) traits remains unknown. This study evaluated the association of 3 PDZK1 single nucleotide polymorphisms (SNP) (i33968C > T, i15371G > A, and i19738C > T) with lipids and risk of MetS and their potential interactions with diet. PDZK1 SNP were genotyped in 1000 participants (481 men, 519 women) included in the Genetics of Lipid Lowering Drugs and Diet Network study. Lipoprotein subfractions were measured by proton NMR spectroscopy and dietary intake was estimated using a validated questionnaire. The PDZK1&#95;i33968C > T polymorphism was associated with MetS (P = 0.034), mainly driven by the association of the minor T allele with higher plasma triglycerides (P = 0.004) and VLDL (P = 0.021), and lower adiponectin concentrations (P = 0.022) than in participants homozygous for the major allele (C). We found a significant gene x BMI x diet interaction, in which the deleterious association of the i33968T allele with MetS was observed in obese participants with high PUFA and carbohydrate (P-values ranging from 0.004 to 0.020) intakes. Conversely, a there was a protective effect in nonobese participants with high PUFA intake (P < 0.05). These findings suggest that PDZK1&#95;i33968C > T genetic variants may be associated with a higher risk of exhibiting MetS. This gene x BMI x diet interaction offers the potential to identify dietary and other lifestyle changes that may obviate the onset of MetS in individuals with a specific genetic background.

Background: Smoking is associated with increased postprandial hypertriglyceridemia (PPT). Inflammation and insulin resistance are potential "drivers" for this phenomenon. We tested whether inflammatory patterns and/or insulin resistance explain the effect of smoking on PPT., Methods and Results: Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n=1036, age 49+/-16y) were included. Each participant was asked to suspend use of lipid-lowering drugs for 3 weeks and was given a high-fat milkshake (83% fat and 700kcal/m(2)). Triglyceride concentrations at 0, 3.5 and 6h after the fat load were measured. Inflammatory markers were measured at baseline. Principal component analysis was used to derive inflammatory patterns from individual inflammatory markers (hsCRP, IL2 soluble receptor-alpha, IL6, TNF-alpha and MCP1). Insulin resistance (IR) was estimated using the HOMA equation. Repeated measures-ANOVA was used for analyses. Two inflammatory patterns, namely CRP-IL6 pattern and MCP1-TNF-alpha pattern, were derived. We found significant main (smoking and time) and interaction (smokingxtime) effects (P<0.01) for triglycerides. The multivariate-adjusted triglyceride (mg/dL) concentrations (mean+/-S.E.M.) for never, past and current smokers were 127.38+/-1.04, 119.82+/-1.05 and 134.92+/-1.08 at 0h; 229.42+/-1.04, 238.39+/-1.05 and 293.94+/-1.08 at 3.5h; and 194.63+/-1.04, 208.38+/-1.05 and 248.27+/-1.08 at 6h after the fat load, respectively. Smoking remained significant after adjusting for HOMA-IR and/or inflammatory patterns which showed independent associations with PPT (P<0.05)., Conclusions: These data confirm impaired metabolism of fat among smokers and suggest that mechanisms other than inflammation or insulin resistance may explain the observed hypertriglyceridemia among smokers.

The transcription factor 7-like 2 (TCF7L2) has been recently associated with diabetes risk, and it may exert its effect through metabolic syndrome (MetS)-related traits and be subjected to modification by environmental factors. We investigated the effect of single nucleotide polymorphisms (SNP), rs7903146 and rs12255372, within the TCF7L2 locus on postprandial lipemia and other MetS-related traits and their modulation by dietary fat. Data were collected from 1083 European Americans participating in the Genetics of Lipid Lowering Drugs and Diet Network Study. Carriers of the minor T allele at the C/T rs7903146 SNP had higher fasting plasma glucose (P = 0.012), lower homeostasis model assessment of beta cell function (P = 0.041), higher plasma VLDL (P = 0.035), and lower large LDL particle (P = 0.007) concentrations and higher risk of MetS (P = 0.011) than CC individuals. Moreover, we identified significant interactions between this SNP and PUFA intake modulating fasting VLDL particle concentrations (P = 0.016) and postprandial triglycerides (TG) (P = 0.028), chylomicrons (P = 0.025), total VLDL (P = 0.026), and large VLDL (P = 0.018) concentrations. Thus, only T allele carriers with a PUFA intake > or = 7.36% of energy had elevated fasting plasma VLDL concentrations and postprandial TG-rich lipoproteins. These variables did not differ in T allele carriers and noncarriers in the low-PUFA intake group. Moreover, these significant interactions were due exclusively to (n-6) PUFA intake. In summary, high (n-6) PUFA intakes (> or = 6.62% of energy intake) were associated with atherogenic dyslipidemia in carriers of the minor T allele at the TCF7L2 rs7903146 SNP and may predispose them to MetS, diabetes, and cardiovascular disease.

Objectives: To estimate the umbilical cord blood lead levels (BLLs) of Pakistani neonates and to identify determinants for umbilical BLLs., Methods: We conducted a cross-sectional study of mothers and infants at one of the two obstetric units of two tertiary care hospitals in Karachi during January-August 2005. Information from 540 mothers selected randomly from those registered for delivery was obtained about their pregnancy, diet, and current and past lead exposures. We collected umbilical cord blood for lead levels analyzed using graphite furnace atomic absorption spectrophotometry. We computed geometric and arithmetic means. We performed multiple linear regression analysis to identify factors associated with log-transformed umbilical cord BLLs. We also performed logistic regression analysis to identify determinants of high lead cord BLLs (10 microg/dl)., Results: The geometric mean cord BLL of the neonates was 9.6 microg/dl; arithmetic mean (S.D.) was 10.8 microg/dl (5.7) with a median of 9.7 microg/dl and a range of 1.8-48.9 microg/dl. Women who reported intake of less than 58.5mg of elemental iron supplement per day during pregnancy had cord BLL of 10.0 microg/dl; in comparison those women who had higher iron intake had lower cord BLL (8.4 microg/dl). Those who used surma (an eye cosmetic) daily had higher cord BLL (11.5 microg/dl) as compared to those who used it less frequently (9.4 microg/dl). In multivariable linear regression model, higher iron intake, owning a car, and being in 2nd quartile of mid-arm circumference were associated with low lead levels while father's occupation in lead-based industry was associated with significantly higher umbilical cord BLLs. There was interaction of daily surma use and ethnicity. Geometric mean BLLs were varied among surma users by ethnicity., Conclusions: Umbilical cord BLLs are high in Karachi, Pakistan, in comparison to those in developed countries such as United States. Measures are needed to reduce fetal lead exposure to prevent adverse affect on neurocognitive development. Association of low iron (below RDA of 60 mg per day) with high umbilical cord has implications for strengthening iron supplement intake during pregnancy. Umbilical cord BLLs differed among surma users by ethnicity.

Chronic inflammation has been identified as an important component of the metabolic syndrome (MetS). Therefore, environmental and genetic factors contributing to the variation of inflammatory responses could affect individuals' susceptibility to MetS. We investigated the association between common IL1beta genetic polymorphisms, inflammation, and the MetS, and the modulation of diet-related variables (i.e., erythrocyte membrane fatty acid composition) in a white U.S. population. IL1beta single nucleotide polymorphisms (SNP) (-1473G > C, -511G > A, -31T > C, 3966C > T, 6054G > A), clinical and biochemical measurements were characterized in a total of 1120 subjects (540 males and 580 females) participating in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study. The 6054 G > A SNP was significantly associated with plasma C-reactive protein (P = 0.054), adiponectin (P = 0.021), and the prevalence of MetS (P = 0.004). Moreover, there was a significant interaction between the 6054G > A SNP and erythrocyte membrane (n-3) PUFA (P = 0.019). Among subjects with low (n-3) PUFA content (below the median), the 6054 G allele was associated with increased risk of the MetS (OR = 3.29, 95%CI = 1.49-7.26 for GG and OR = 1.95, 95%CI = 0.85-4.46 for GA, P < 0.001) compared with the AA genotype, but there were no significant genotype associations among subjects with high (n-3) PUFA content (above the median). Further analyses supported a significant haplotype global effect on the MetS (P = 0.017) among subjects with low (n-3) PUFA content. These results suggested that IL1beta genetic variants were associated with measures of chronic inflammation and the MetS risk, and that genetic influences were more evident among subjects with low (n-3) PUFA intake.

Purpose: There are no data for factors that could trigger myocardial infarction (MI) in the context of lifestyles in developing countries., Methods: Using a case-crossover design, we assessed the effect of heavy physical exertion, sexual activity, acute respiratory tract infections, and gastroenteritis as triggers for MI in 530 survivors of a first MI from Costa Rica., Results: Relative risks (RRs) for MI in the hour after heavy physical exertion and 2 hours after sexual activity were 4.94 (95% confidence interval [CI], 3.73-6.54) and 5.47 (95% CI, 2.71-11.02). Risk for MI after heavy physical exertion was greater for patients with poor physical fitness or elevated underlying cardiovascular risk (p < 0.0001 and p = 0.06, tests of homogeneity). RRs for acute respiratory tract infection and gastroenteritis were 1.48 (95% CI, 0.92-2.38) and 1.27 (95% CI, 0.95-1.69), respectively. Patients with three or more risk factors had an RR for MI for gastroenteritis of 2.08 (95% CI, 1.31-3.28)., Conclusions: Our results confirm previous studies in developed countries showing that heavy physical exertion and sexual activity are potential triggers for MI, and their effect is modified by physical fitness and underlying cardiovascular risk. Additional studies that explore the biologic effects of gastroenteritis as triggers of MI are warranted.

Background: Moderate alcohol consumption is associated with a lower risk of myocardial infarction (MI). Whether alcohol is truly protective or whether the amount, type, or pattern of intake is the most important is still under debate., Objective: The purpose of this study was to determine whether alcohol intake and drinking patterns are associated with plasma lipids and the risk of MI in Costa Ricans, a population with a low intake of wine., Design: We conducted a study of 2090 cases of a first nonfatal acute MI and 2090 population-based controls matched by age, sex, and residence in Costa Rica, a country with diet and lifestyles different from those of Western countries. Alcohol and dietary intakes were assessed by using validated questionnaires., Results: In a multivariate conditional regression model that controlled for other cardiovascular disease risk factors, the lowest risk of MI [odds ratio (OR) = 0.44; 95% CI: 0.31, 0.61] was observed for those who drank on average 3 drinks/wk (compared with lifelong abstainers). When we looked at the frequency of consumption, we found that the risk of MI among daily drinkers (OR = 0.64; 95% CI: 0.41, 1.01) was not significantly different (P = 0.23) from that of weekend drinkers (OR = 0.76; 95% CI: 0.59, 0.98) regardless of the amount consumed. HDL cholesterol increased with the amount and frequency of alcohol intake. Similar to a few other populations, apparent protection was observed at very low alcohol intakes., Conclusion: Low to moderate consumption of alcohol 1-2 d/wk is independently associated with a reduced risk of MI.

Palm oil and soybean oil are the 2 most widely used cooking oils in the world. Palm oil is consumed mainly in developing countries, where morbidity and mortality due to cardiovascular disease (CVD) are on the rise. Although claims about adverse or protective effects of these oils are commonly made, there are no epidemiologic studies assessing the association between these oils and cardiovascular disease endpoints. We examined whether consumption of palm oil relative to soybean oil and other unsaturated oils (predominantly sunflower) is associated with myocardial infarction (MI) in Costa Rica. The cases (n = 2111) were survivors of a first acute MI and were matched to randomly selected population controls (n = 2111). Dietary intake was assessed with a validated semiquantitative FFQ. Adipose tissue profiles of essential fatty acids were assessed to validate cooking oil intake and found to be consistent with self-reported major oils used for cooking. The data were analyzed using conditional logistic regression. Palm oil users were more likely to have an MI than users of soybean oil [odds ratio (OR) = 1.33; 95% CI: 1.08-1.63] or other cooking oils (OR = 1.23; CI: 0.99-1.52), but they did not differ from users of soybean oil with a high trans-fatty acid content (OR = 1.14; CI: 0.84-1.56). These data suggest that as currently used in Costa Rica, and most likely in many other developing countries, the replacement of palm oil with a polyunsaturated nonhydrogenated vegetable oil would reduce the risk of MI.

Legumes may protect against myocardial infarction (MI). The objective of this study was to determine whether consumption of dried mature beans (referred to as beans), the main legume in Latin America, is associated with MI. The cases (n = 2119) were survivors of a first acute MI and were matched by age, sex, and area of residence to randomly selected population controls (n = 2119) in Costa Rica. Dietary intake was assessed with a validated FFQ. Of the population, 69% consumed > or = 1 serving of beans/d (1 serving = one-third cup of cooked beans, approximately 86 g). Consumption of > or = 1 serving/d was significantly higher (P < 0.001) in rural (81%) than in urban (65%) areas. Individuals who never eat dried beans or whose consumption was < 1 time/mo were classified as nonconsumers. Compared with nonconsumers, intake of 1 serving of beans/d was inversely associated with MI in analyses adjusted for smoking, history of diabetes, history of hypertension, abdominal obesity, physical activity, income, intake of alcohol, total energy, saturated fat, trans fat, polyunsaturated fat, and cholesterol [odds ratio (OR) = 0.62; 95% CI: 0.45-0.88]. No further protection was observed with increased number of servings/d (OR = 0.73; 95% CI: 0.52-1.03 for > 1 serving/d). In summary, we found that consumption of 1 serving of beans/d is associated with a 38% lower risk of MI. No additional protection was observed at intakes > 1 serving/d. These findings are timely given the trend toward increased obesity, cardiovascular disease, and a reduction in the intake of beans in Latin American countries.

Trans-fatty acid intake is associated with coronary heart disease (CHD), but the atherogenic potential of individual trans-fatty acids (FA) from partially hydrogenated oils (18:1 and 18:2) or meat and dairy products (16:1 and 18:1) is unclear. Incident cases (n = 482) of a first nonfatal myocardial infarction (MI) were matched with population controls (n = 482) for age, gender and area of residence, all living in Costa Rica. Trans-FA in adipose tissue samples were assessed by gas chromatography. Odds ratios (OR) and 95% confidence intervals were calculated from conditional logistic regression models. Total adipose tissue trans-fat was positively associated with risk of MI. After adjusting for established risk factors and other confounders, the OR by quintiles of total trans-fat were 1.00, 1.34, 2.05, 2.22 and 2.94 (P-test for trend < 0.01). This association was attributed mainly to 18:2 trans-FA that were abundant in both adipose tissue and in partially hydrogenated soybean oil, margarines and baked products used by this population; OR = 1.00, 0.96, 2.09, 3.51 and 5.05 (P-test for trend < 0.001). Adipose tissue 16:1 trans-FA were also associated with MI; OR = 1.00, 1.57, 1.39, 1.34 and 2.58 (P-test for trend < 0.05). An association with 18:1 trans-FA was not detected. High 18:2 trans-FA in adipose tissue are associated with increased risk of MI. Because the use of hydrogenated oils is increasing worldwide, consumers should be aware of the harmful effects of products containing partially hydrogenated oils.

Background: Biomarkers can provide a more accurate measure of long-term intake than can dietary questionnaires., Objective: The objective was to identify which adipose tissue fatty acids are suitable biomarkers of intake as assessed with a validated food-frequency questionnaire., Design: Costa Rican men with a mean (+/- SD) age of 56 +/- 11 y (n = 367) and women aged 60 +/- 10 y (n = 136) completed a 135-item food-frequency questionnaire and provided an adipose tissue sample. Fifty fatty acids were identified by capillary gas chromatography. Correlation coefficients were calculated after adjustment for age, sex, body mass index, and smoking status., Results: The best adipose tissue marker for total intake of saturated fatty acids was 15:0 + 17:0 (r = 0.18). Both 15:0 and 17:0 were also the best correlates of dairy product intake (r = 0.31 for each). The diet-adipose tissue correlations for n-3 fatty acids were r = 0.34 for 18:3, r = 0.15 for 20:5, and r = 0.18 for 22:6. Fish intake correlated significantly with these adipose tissue n-3 fatty acids. Dietary and adipose tissue n-6 fatty acids were highly correlated: 18:2 (r = 0.58) and 18:3 (r = 0.24). The best indicators of total trans fatty acid intake were ct18:2n-6 and tc18:2n-6 (r = 0.58 for each); total 18:1 trans fatty acid (r = 0.45) and 16:1 trans fatty acid (r = 0.16) were the next best indicators., Conclusions: Adipose tissue is a suitable biomarker of dietary fatty acid intake, particularly for n-3 and n-6 cis polyunsaturated fatty acids and trans fatty acids. Ideally, adipose tissue and dietary questionnaires should complement, rather than substitute for, each other in epidemiologic studies.