Biomedical subjects

Michael A Province

Publications and source records attributed to Michael A Province.

At least 19 recordsLinked to original sources

PubMed2007

Genotype-by-sex interaction on fasting insulin concentration: the HyperGEN study.

Recent studies have demonstrated the importance of sex effects on the underlying genetic architecture of insulin-related traits. To explore sex-specific genetic effects on fasting insulin, we tested for genotype-by-sex interaction and conducted linkage analysis of fasting insulin in Hypertension Genetic Epidemiology Network families. Hypertensive siblings and their first-degree relatives were recruited from five field centers. We performed a genome scan for quantitative trait loci influencing fasting insulin among 1,505 European Americans and 1,616 African Americans without diabetes. Sex-stratified linear regression models, adjusted for race, center, and age, were explored. The Mammalian Genotyping Service typed 391 microsatellite markers, spaced roughly 9 cM. Variance component linkage analysis was performed in SOLAR using ethnic-specific marker allele frequencies and multipoint IBDs calculated in MERLIN. We detected a quantitative trait locus influencing fasting insulin in female subjects (logarithm of odds [LOD] = 3.4) on chromosome 2 at 95 cM (between GATA69E12 and GATA71G04) but not in male subjects (LOD = 0.0, P for interaction = 0.007). This sex-specific signal at 2p13.2 was detected in both European-American (LOD = 2.1) and African-American (LOD = 1.2) female subjects. Our findings overlap with several other linkage reports of insulin-related traits and demonstrate the importance of considering complex context-dependent interactions in the search for insulin-related genes.

Alcohol Drinking↗

PubMed2006

Longitudinal and age trends of metabolic syndrome and its risk factors: the Family Heart Study.

BACKGROUND: We report longitudinal changes in the metabolic syndrome (MetS) in 2,458 participants from 480 families in the Family Heart Study. Participants were examined between 1994-96 (FHS-T1) and 2002-03 (FHS-T2), about 7.4 years apart. Additionally, the impact of medication on estimates of MetS prevalence, and associations of MetS with prevalent coronary heart disease (CHD) and type 2 diabetes (T2D) were studied. METHODS: Three definitions for MetS prevalence were considered. One represented the original (o) National Cholesterol Education Program (NCEP) MetS criteria. Two others considered the confounding of medications effects, respectively (m) lipid medications constituted a categorical diagnostic criterion for lipids variables, and (c) lipids and blood pressure variables were corrected with average clinical trials medications effects. Logistic regression of MetS on CHD and T2D, as well as the trend analysis of MetS by age, were performed. RESULTS: MetS increased from 17.1% in FHS-T1(o) to 28.8% in FHS-T2(o); from 19.7% in FHS-T1(m) to 42.5% in FHS-T2(m); and from 18.4% in FHS-T1(c) to 33.6% in FHS-T2(c). While we observed adverse changes in all risk factors, the greatest increase was for waist circumference (25%). The percentages of MetS were about 2 to almost 3 times higher in ages 50 years and older than in younger ages. The odds of having prevalent CHD were about 2.5 times higher in the subjects classified with MetS than without. CONCLUSION: MetS percentages increased noticeably longitudinally and cross-sectionally with older age. These conclusions were reached with and without considering medication use, but correcting risk factors for medications use affects the MetS prevalence estimates. As found in other studies, MetS was associated with increased odds for prevalent CHD.

Journal Article↗

PubMed2006

Alcohol consumption and plasma atrial natriuretic peptide (from the HyperGEN study).

Although moderate alcohol consumption has been associated with a lower risk of cardiovascular disease, underlying physiologic mechanisms are not fully understood. Data relating alcohol intake to atrial natriuretic peptide (ANP) have been inconsistent. We evaluated whether alcohol consumption was associated with plasma ANP in 1,345 participants from the Hypertension Genetic Epidemiology Network (HyperGEN) study. We used random effect models to estimate the adjusted means of logarithmic transformed ANP. The mean age was 35.8 +/- 8.6 years, 91% were normotensive, 46% were men, and 40% and 60% were African-Americans and whites, respectively. In a model adjusting for age, body mass index, field center, education, gender, race, and serum albumin, alcohol consumption was positively associated with ANP in men (p < 0.0001 for trend) and women (p = 0.0014) and in African-Americans (p = 0.006) and whites (p < 0.0001). The adjusted mean of log-transformed ANP was 3.68, 3.67, 3.77, 3.76, 3.86, and 3.91 pg/ml in lifetime abstainers, former drinkers, and current drinkers of 1 to 6, 7 to 12, 13 to 24, and > 24 g/d, respectively. Controlling for additional factors, including left atrial size, ejection fraction, left ventricular mass, end-diastolic volume, systolic blood pressure, smoking, lipids, and serum creatinine did not change the results. Restriction to normotensive subjects yielded similar results. Alcohol intake was associated positively with systolic and diastolic blood pressure (p < 0.0001 each for trend). In conclusion, our data have shown a positive and linear association between alcohol consumption and ANP in men and women, irrespective of race.

Adolescent↗

PubMed2006

Influence of saturated fat and linolenic acid on the association between intake of dairy products and blood pressure.

Data on the association between dairy consumption and blood pressure have been inconsistent. We sought to examine the relation between dairy consumption and prevalent hypertension (HTN) among 4797 participants of the National Heart, Lung, and Blood Institute Family Heart Study. We used generalized estimating equations to estimate prevalence odds ratios of HTN across categories of dairy consumption. From the lowest to the highest sex-, age-, and energy-adjusted quartile of dairy consumption, there was an inverse association between dairy intake and prevalent HTN: odds ratios (95% CIs) were 1.0 (reference), 0.82 (0.64 to 1.05), 0.68 (0.53 to 0.89), and 0.62 (0.45 to 0.84), respectively, in a model adjusting for age, sex, energy intake, field center, body mass index, dietary linolenic acid, saturated and monounsaturated fat, sodium intake, potassium, caffeine, fiber, and fruits and vegetables (P for trend = 0.002). This association was independent of calcium intake and was mainly observed among subjects consuming fewer calories from saturated fat (P for interaction = 0.014). Dairy consumption was inversely associated with systolic (P for trend = 0.003) but not diastolic (P for trend = 0.09) blood pressure. Although subjects consuming > or = 2 servings per day of dairy products and higher total linolenic acid had the lowest prevalence odds of HTN, there was no evidence for interaction between linolenic acid and dairy consumption on HTN (P for interaction = 0.65). In conclusion, our data indicate an inverse association between dairy consumption and prevalent HTN that was independent of dietary calcium, mainly among individuals consuming less saturated fat. This suggests that consumption of low-fat dairy products might be more beneficial for preventing HTN.

Adult↗

PubMed2006

Association study of CRP gene polymorphisms with serum CRP level and cardiovascular risk in the NHLBI Family Heart Study.

Recent epidemiological studies have indicated that baseline C-reactive protein (CRP) levels may have value in prediction of cardiovascular risk. Using six tag single-nucleotide polymorphisms (SNPs) selected from our complete list of SNPs on the CRP gene, we investigated the association of CRP genotypes with plasma CRP levels and cardiovascular risk in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study cohort (1,296 Caucasians, 48.5% male, 54.7 +/- 12.8 yr old). There was a significant trend toward association of CRP haplotypes with CRP levels (P = 0.045). SNP analysis indicated a highly significant association of SNP -757 (rs3093059, P = 0.0004) and SNP -286 (rs3091244, P = 0.0065) and a borderline association of SNP -7180 (rs1341665, P = 0.06) with CRP levels. Neither CRP haplotypes nor individual SNP genotypes were associated with intima-media thickness of the common carotid or internal carotid artery or the bifurcation of the carotid arteries. These results indicated a strong impact of local SNPs of the CRP gene on plasma CRP levels, but there was no direct evidence that these genetically controlled CRP elevations by local CRP SNPs contributed to cardiovascular disease phenotypes.

Adult↗

PubMed2006

Identification of candidate alkylator-induced cancer susceptibility genes by whole genome scanning in mice.

Secondary malignancies are a serious adverse consequence of alkylator chemotherapy. The risk of developing an alkylator-associated malignancy is influenced by genetic background, although the relevant genetic factors are poorly understood. To screen for novel susceptibility factors, we established a mouse model of alkylator-induced malignancy. We exposed mice from 20 inbred strains to the prototypical alkylating agent, N-nitroso-N-ethylurea (ENU). ENU was a potent carcinogen in many of the strains tested, inducing 140 tumors in 240 ENU-treated mice (66% incidence of at least one tumor in evaluable mice), compared with a background incidence of 8% spontaneous tumors in 240 strain-, age-, and sex-matched control mice (relative risk, 8.4; P < 0.0001). A wide variety of tumor histologies were noted, including epithelial carcinomas, soft tissue sarcomas, and hematopoietic tumors. Cancer susceptibility was a heritable trait for the most common tumor types, lung adenocarcinoma (H(2) = 0.25), T cell lymphoma (H(2) = 0.19), and myeloid malignancies (H(2) = 0.10). Quantitative trait locus mapping identified regions on chromosomes 3, 6, 9, and 15 containing candidate genes associated with lung adenoma, lung carcinoma, and lymphoma susceptibility. This novel mouse model recapitulates many features of human alkylator-associated cancer and supports the hypothesis that susceptibility to this syndrome is influenced by inherited polymorphisms that could be used to make informed clinical treatment decisions.

Alkylating Agents↗

PubMed2006

Association of coronary artery calcified plaque with clinical coronary heart disease in the National Heart, Lung, and Blood Institute's Family Heart Study.

The presence of calcified coronary artery plaque has shown variable association with clinical coronary heart disease (CHD), particularly after adjustment for other risk factors. From 2002 to 2004, as part of the National Heart, Lung, and Blood Institute's Family Heart Study, coronary artery calcium (CAC) scans by 4-slice multidetector computed tomography were performed in 3,359 subjects, including 389 with clinically diagnosed CHD. Among these was a cohort of 2,254 patients who had been asymptomatic at an initial examination 7 to 9 years previously (1994 to 1996), with 111 who had developed newly diagnosed, nonfatal CHD since the initial examination. In cross-sectional analyses, we examined associations between CAC and CHD in the entire group and in the subgroup seen at the initial examination. In the 2 sets of analyses, odds ratios for CHD ranged from approximately 4 in those with CAC scores of 100 to 199 (p <0.01) to >20 in those with CAC scores >/=1,000 (p <0.0001) compared with those with no measurable CAC. This steep gradient of risk persisted after adjustment for risk factors. A quantitative CHD family history score was significantly associated with CHD even after adjusting for all standard risk factors and including CAC in the model. In conclusion, CAC was strongly associated with CHD even after adjustment for standard risk factors and family history contributed independently to CHD risk.

Adult↗

PubMed2006

Racial differences in the association of coronary calcified plaque with left ventricular hypertrophy: the National Heart, Lung, and Blood Institute Family Heart Study and Hypertension Genetic Epidemiology Network.

Studies have reported a lower burden of calcified atherosclerotic plaque in coronary arteries in African-Americans than in whites. Findings from autopsy studies of sudden cardiac death have suggested a link between left ventricular hypertrophy and severity of coronary atherosclerosis. Echocardiograms and cardiac computed tomograms were analyzed in 334 African-American (84% hypertensive) and 196 white (66% hypertensive) adults with no history of coronary heart disease or revascularization procedures at study entry. The relation of coronary artery calcium (CAC) score to left ventricular mass and left ventricular mass indexed to body surface area was assessed by Spearman's correlations and mixed linear models. Covariates included age, gender, field center, weight, height, systolic blood pressure, number of antihypertensive medications, diabetes, total and high-density lipoprotein cholesterol levels, and current smoking and alcohol consumption. In African-Americans, a significant and independent association between CAC score and left ventricular mass or left ventricular mass indexed to body surface area was present with the 2 analytic strategies. Spearman's correlation coefficients for CAC score with left ventricular mass and left ventricular mass indexed to body surface area were 0.14 (p = 0.015) and 0.13 (p = 0.025), respectively, after multivariable adjustment. In whites, the associations of CAC score with measurements of left ventricular mass were weaker and only marginally significant in mixed linear models. In conclusion, these findings suggest that CAC reflects a different risk burden between African-Americans and whites, and future studies examining the prognostic implications of CAC in African-Americans should consider the potential association between CAC and left ventricular hypertrophy.

Aged↗

PubMed2006

Evidence of QTL on 15q21 for high-density lipoprotein cholesterol: the National Heart, Lung, and Blood Institute Family Heart Study (NHLBI FHS).

A genome-wide linkage scan was conducted to identify regions potentially having quantitative trait loci (QTLs) influencing high-density lipoprotein (HDL) cholesterol. We found suggestive evidence of a QTL (lod score (LOD)=1.75, p=0.00224, and q=0.07649) influencing the variation of plasma levels of age- and sex-adjusted HDL-cholesterol on chromosome 15q21 at marker D15S659 in the NHLBI FHS data. Owing to the perturbations to lipid profiles associated with diabetes, the analysis was repeated excluding diabetic subjects from the sample. The lod score increased from 1.75 to 2.71 (p=0.00021, q=0.05392) at the same chromosome 15 location, despite the reduction in sample size. This finding indicates that the inclusion of diabetic subjects in the analysis may confound the presence of a QTL for HDL-cholesterol on 15q21. Because of the known effects of important covariates such as metabolic variables and lifestyle habits that may interact with a putative QTL, we also analyzed HDL-cholesterol with a progressive adjustment. When body mass index, smoking, and habitual alcohol intake were added to age- and sex-adjustment, we found strong evidence for linkage in the complete sample (LOD=4.77, p=0.0000013, and q=0.00016) as well as in the non-diabetic sub-sample (LOD=4.52, p=0.0000025, and q=0.00026) on chromosome 15q21 (between D15S659 and D15S195 markers). These results suggest that there are multiple pathways and factors involving genetic and environmental effects influencing HDL-cholesterol levels, and by taking some of these known factors into account, we obtained strong evidence of a QTL influencing HDL-cholesterol levels. While this putative QTL may also have an effect in diabetes, our data suggest a more pronounced role in non-diabetics. A prominent candidate gene residing within the linkage region on 15q21 is hepatic lipase (HL), which has a major role in lipoprotein metabolism.

Adult↗

PubMed2006

Meta-analysis of genome-wide scans for blood pressure in African American and Nigerian samples. The National Heart, Lung, and Blood Institute GeneLink Project.

BACKGROUND: In many genetic studies of complex traits, sample sizes are often too small to detect linkages of low-to-moderate effects. However, the combined linkage evidence across several studies can be synthesized using meta-analysis with the aim of providing more definitive support of linkage. METHODS: In the current study using the National Heart, Lung, and Blood Institute (NHLBI) GeneLink Project, a meta-analysis based on a modification of Fisher's method of pooling P values was used to investigate linkage for systolic blood pressure (SBP) and diastolic blood pressure (DBP) values across three studies involving African American and Nigerian families (HyperGEN, Health, Risk Factors, Exercise Training and Genetics [HERITAGE], and Genetics of Hypertension in Blacks). RESULTS: The meta results suggest two regions (2p and 7p) provide enhanced linkage evidence compared with the individual study results. The maximal meta Lod score of 2.9 on 2p14-p13.1 (64-78 cM) represented approximately 1-Lod unit increase over the respective individual study scores. This general region has been implicated previously involving primarily families of white ethnicity and provides confirmatory evidence that this QTL is common across ethnic groups. The second finding at 7p21.3-p15.3 (8-25 cM) provided a meta Lod of 3.5. Although region was implicated primarily in the Nigerian subjects the low-level but consistent support involving the African American families (individual Lod score of 1.0) suggests a novel QTL with respect to BP variation in individuals of black ethnicity. CONCLUSIONS: Follow-up studies involving positional cloning efforts of the combined families showing linkage evidence in these regions (particularly 2p) may be warranted to verify these findings and identify the genes and causative variants.

Adolescent↗

PubMed2006

Dietary linolenic acid and fasting glucose and insulin: the National Heart, Lung, and Blood Institute Family Heart Study.

OBJECTIVE: To assess whether dietary linolenic acid is associated with fasting insulin and glucose. RESEARCH METHODS AND PROCEDURES: In a cross-sectional design, we studied 3993 non-diabetic participants of the National Heart, Lung, and Blood Institute Family Heart Study 25 to 93 years of age. Linolenic acid was assessed through a food frequency questionnaire, and laboratory data were obtained after at least a 12-hour fast. We used generalized linear models to calculate adjusted means of insulin and glucose across quartiles of dietary linolenic acid. RESULTS: From the lowest to the highest sex-specific quartile of dietary linolenic acid, means +/- standard error for logarithmic transformed fasting insulin were 4.06 +/- 0.02 (reference), 4.09 +/- 0.02, 4.13 +/- 0.02, and 4.17 +/- 0.02 pM, respectively (trend, p < 0.0001), after adjustment for age, sex, energy intake, waist-to-hip ratio, smoking, and high-density lipoprotein-cholesterol. When dietary linolenic acid was used as a continuous variable, the multivariable adjusted regression coefficient was 0.42 +/- 0.08. There was no association between dietary linolenic acid and fasting glucose (trend p = 0.82). DISCUSSION: Our data suggest that higher consumption of dietary linolenic acid is associated with higher plasma insulin, but not glucose levels, in non-diabetic subjects. Additional studies are needed to assess whether higher intake of linolenic acid results in an increased insulin secretion and improved glucose use in vivo.

Adult↗

PubMed2006

The impact of data quality on the identification of complex disease genes: experience from the Family Blood Pressure Program.

The application of genome-wide linkage scans to uncover susceptibility loci for complex diseases offers great promise for the risk assessment, treatment, and understanding of these diseases. However, for most published studies, linkage signals are typically modest and vary considerably from one study to another. The multicenter Family Blood Pressure Program has analyzed genome-wide linkage scans of over 12 000 individuals. Based on this experience, we developed a protocol for large linkage studies that reduces two sources of data error: pedigree structure and marker genotyping errors. We then used the linkage signals, before and after data cleaning, to illustrate the impact of missing and erroneous data. A comprehensive error-checking protocol is an important part of complex disease linkage studies and enhances gene mapping. The lack of significant and reproducible linkage findings across studies is, in part, due to data quality.

Blood Pressure↗

PubMed2006

Familial clustering for features of the metabolic syndrome: the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study.

OBJECTIVE: Metabolic syndrome-related traits (obesity, glucose intolerance/insulin resistance, dyslipidemia, and hypertension) have been shown to be genetically correlated. It is less clear, however, if the genetic correlation extends to novel risk factors associated with inflammation, impaired fibrinolytic activity, and hyperuricemia. We present a bivariate genetic analysis of MetS-related traits including both traditional and novel risk factors. RESEARCH DESIGN AND METHODS: Genetic correlations were estimated using a variance components procedure in 1,940 nondiabetic white individuals from 445 families in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. Twelve MetS-related traits, including BMI, waist circumference, blood pressure, white blood cell count, fasting serum triglycerides, HDL cholesterol, insulin, glucose, plasminogen activator inhibitor-1 antigen, uric acid, and C-reactive protein, were measured and adjusted for covariates, including lifestyle variables. RESULTS: Significant genetic correlations were detected among BMI, waist circumference, HDL cholesterol, triglycerides, insulin, and plasminogen activator inhibitor-1 antigen and between uric acid and all of the above variables except insulin. C-reactive protein and white blood cell count were genetically correlated with each other, and both showed significant genetic correlations with waist circumference and insulin. Fasting glucose was not significantly genetically correlated with any of the other traits. CONCLUSIONS: These results suggest that pleiotropic effects of genes or shared family environment contribute to the familial clustering of MetS-related traits.

Adult↗

PubMed2005

Microsatellite linkage analysis, single-nucleotide polymorphisms, and haplotype associations with ECB21 in the COGA data.

This study, part of the Genetic Analysis Workshop 14 (GAW14), explored real Collaborative Study on the Genetics of Alcoholism data for linkage and association mapping between genetic polymorphisms (microsatellite and single-nucleotide polymorphisms (SNPs)) and beta (16.5-20 Hz) oscillations of the brain rhythms (ecb21). The ecb21 phenotype underwent the statistical adjustments for the age of participants, and for attaining a normal distribution. A total of 1,000 subjects' available phenotypes were included in linkage analysis with microsatellite markers. Linkage analysis was performed only for chromosome 4 where a quantitative trait locus with 5.01 LOD score had been previously reported. Previous findings related this location with the gamma-aminobutyric acid type A (GABAA) receptor. At the same location, our analysis showed a LOD score of 2.2. This decrease in the LOD score is the result of a drastic reduction (one-third) of the available GAW14 phenotypic data. We performed SNP and haplotype association analyses with the same phenotypic data under the linkage peak region on chromosome 4. Seven Affymetrix and two Illumina SNPs showed significant associations with ecb21 phenotype. A haplotype, a combination of SNPs TSC0044171 and TSC0551006 (the latter almost under the region of GABAA genes), showed a significant association with ecb21 (p = 0.015) and a relatively high frequency in the sample studied. Our results affirmed that the GABA region has potential of harboring genes that contribute quantitatively to the beta oscillation of the brain rhythms. The inclusion of the remaining 614 subjects, which in the GAW14 had missing data for the ecb21, can improve the strength of the associations as they have already shown that they contribute quite important information in the linkage analysis.

Alcoholism↗

PubMed2005

Two major QTLs and several others relate to factors of metabolic syndrome in the family blood pressure program.

Genome-wide variance components linkage analysis was performed on 4 latent factors underlying metabolic syndrome derived from 10 risk factors. The latent factors represent obesity and insulin, blood pressure, lipids and insulin, and central obesity. The metabolic syndrome factor scores were derived in 4 ethnic groups recruited in 3 Networks of the Family Blood Pressure Program: GENOA (blacks, Hispanics, and whites), HyperGEN (blacks and whites), SAPPHIRe (Asians). Heritabilities of metabolic syndrome factors ranged from 66% for obesity and insulin to 11% for blood pressure factor. We observed higher heritabilities for obesity and insulin, and lipids and insulin, whereas those for blood pressure and central obesity were smaller. Linkage analysis detected two major quantitative trait loci. One of them linked to the obesity and insulin factor with a lod score of 3.94 (P=0.00001, marker GATA11A06, D18S53, 41.24 cM) at marker positions linkage (lod 4.71, at 46.84 cM at 1-cM-apart distances linkage), located on chromosome 18p11.21 in GENOA black. The other linked to the blood pressure factor with a lod score of 3.22 (P=0.000059, marker GATA49C09, D17S1290, 82 cM) at marker positions linkage (lod 3.56, at 84.63 cM for 1 cM apart distances linkage) located on chromosome 17q23.1 in Hispanics. These quantitative trait loci, together with 4 additional ones with lod scores >2.5, and 30 additional ones with lod score >1.7, offer hope for dissecting the genetic architecture of metabolic syndrome with beneficial implications for molecular diagnosis, prognosis, and in potential medical intervention.

Asian People↗

PubMed2005

An evaluation of the metabolic syndrome in a large multi-ethnic study: the Family Blood Pressure Program.

BACKGROUND: The Family Blood Pressure Program is an ongoing, NHLBI-sponsored, multi-center program to study the genetic determinants of high blood pressure. The goal of this particular study was to study patterns of metabolic syndrome (MetS) in four ethnic groups: African Americans, Caucasians, Hispanics, and Asians. METHODS: A major part of participants in three networks GENOA, HyperGEN and SAPPHIRe were recruited mainly through hypertensive probands. MetS was defined as a categorical trait following the National Cholesterol Education Program definition (c-MetS). MetS was also characterized quantitatively through multivariate factor analyses (FA) of 10 risk variables (q-MetS). Logistic regression and frequency tables were used for studying associations among traits. RESULTS: Using the NCEP definition, the Hispanic sample, which by design was enriched for type 2 diabetes (T2D), had a very high prevalence of MetS (73%). In contrast, its prevalence in Chinese was the lowest (17%). In African Americans and Hispanics, c-MetS was more prevalent in women than in men. Association of c-MetS with type 2 diabetes (T2D) was prominent in the Hispanics and African Americans, less pronounced in the Whites and Japanese, (although still significant), and weakest in the Chinese sample. Using FA without rotation, we found that the main factor loaded obesity (OBS) and blood pressure (BP) in African Americans; OBS and insulin (INS) in Hispanics, in Japanese, and in Whites; and OBS alone in Chinese. In Hispanics, Whites, and Japanese, BP loaded as a separate factor. Lipids in combination with INS also loaded in a separate factor. Using FA with Varimax rotation, 4 independent factors were identified: "Obesity-INS," "Blood pressure," "Lipids-INS," and "Central obesity." They explained about 60% of the variance present in the original risk variables. CONCLUSION: MetS ethnic differences were identified. Ascertaining for hypertension or T2D increased the MetS prevalence in networks compared with the one in the US general population. Obesity was the most prominent risk factor contributing to both c-MetS and q-MetS. INS contributed in two important factors (obesity and lipids). The information imbedded into c-MetS trait /q-MetS factors scores can contribute in future research of the MetS, especially its utilization in the genetic analysis.

Journal Article↗

PubMed2005

Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study.

BACKGROUND: High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis. METHODS AND RESULTS: To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results. CONCLUSIONS: Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women.

Adult↗

PubMed2005

Dietary linolenic acid and adjusted QT and JT intervals in the National Heart, Lung, and Blood Institute Family Heart study.

OBJECTIVES: The goal of this study was to examine whether higher consumption of total linolenic acid was associated with rate-adjusted QT and JT intervals (QTrr and JTrr, respectively). BACKGROUND: Higher intake of fish omega-3 fatty acids and plant omega-3 such as alpha-linolenic acid is associated with lower risk of myocardial infarction. While long-chain omega-3 can inhibit ventricular arrhythmia, it is not known whether alpha-linolenic acid influences ventricular repolarization. METHODS: We studied 3,642 subjects from the National Heart, Lung, and Blood Institute Family Heart study who were free of myocardial infarction, left ventricular hypertrophy, pacemaker, and with QRS <120 ms. We used the 95th percentile of the gender-specific distribution of QTrr and JTrr to define abnormally prolonged repolarization. Within each gender, we created age- and energy-adjusted tertiles of linolenic acid and used regression models for analyses. RESULTS: Mean age was 50 years, and average intake of total linolenic acid was 0.74 g/day. There was an inverse association between consumption of linolenic acid and QTrr and JTrr (p for trend 0.001 and 0.0005, respectively). From the lowest (reference) to the highest gender-, age-, and energy-adjusted tertile of linolenic acid, multivariable adjusted odds ratios for prolonged QTrr were 1.0, 0.74 (95% confidence interval [CI] 0.57 to 0.96), and 0.59 (95% CI 0.44 to 0.77), respectively (p for trend 0.0003). Corresponding values for JTrr were 1.0, 0.73 (95% CI 0.52 to 1.03), and 0.59 (95% CI 0.40 to 0.87), respectively (p for trend 0.009). Exclusion of subjects taking drugs known to influence QT did not influence this association. CONCLUSIONS: Higher intake of dietary linolenic acid might be associated with a reduced risk of abnormally prolonged repolarization in men and women.

Adult↗