Biomedical subjects

Jose M Ordovas

Publications and source records attributed to Jose M Ordovas.

At least 19 recordsLinked to original sources

PubMed2007

APOA5 gene variation modulates the effects of dietary fat intake on body mass index and obesity risk in the Framingham Heart Study.

Diet is an important environmental factor interacting with our genes to modulate the likelihood of developing lipid disorders and, consequently, cardiovascular disease risk. Our objective was to study whether dietary intake modulates the association between APOA5 gene variation and body weight in a large population-based study. Specifically, we have examined the interaction between the APOA5-1131T>C and 56C>G (S19W) polymorphisms and the macronutrient intake (total fat, carbohydrate, and protein) in their relation to the body mass index (BMI) and obesity risk in 1,073 men and 1,207 women participating in the Framingham Offspring Study. We found a consistent and statistically significant interaction between the -1131T>C single-nucleotide polymorphism (SNP; but not the 56C>G) and total fat intake for BMI. This interaction was dose-dependent, and no statistically significant heterogeneity by gender was detected. In subjects homozygous for the -1131T major allele, BMI increased as total fat intake increased. Conversely, this increase was not present in carriers of the -1131C minor allele. Accordingly, we found significant interactions in determining obesity and overweight risks. APOA5-1131C minor allele carriers had a lower obesity risk (OR, 0.61, 95%; CI, 0.39-0.98; P = 0.032) and overweight risk (OR, 0.63, 95%; CI, 0.41-0.96; P = 0.031) compared with TT subjects in the high fat intake group (>or=30% of energy ) but not when fat intake was low (OR, 1.16, 95%; CI, 0.77-1.74; P = 0.47 and OR = 1.15, 95%; CI, 0.77-1.71; P = 0.48) for obesity and overweight, respectively). When specific fatty acid groups were analyzed, monounsaturated fatty acids showed the highest statistical significance for these interactions. In conclusion, the APOA5-1131T>C SNP, which is present in approximately 13% of this population, modulates the effect of fat intake on BMI and obesity risk in both men and women.

Apolipoprotein A-V↗

PubMed2007

Informative-transmission disequilibrium test (i-TDT): combined linkage and association mapping that includes unaffected offspring as well as affected offspring.

To date, there is no test valid for the composite null hypothesis of no linkage or no association that utilizes transmission information from heterozygous parents to their unaffected offspring as well as the affected offspring from ascertained nuclear families. Since the unaffected siblings also provide information about linkage and association, we introduce a new strategy called the informative-transmission disequilibrium test (i-TDT), which uses transmission information from heterozygous parents to all of the affected and unaffected offspring in ascertained nuclear families and provides a valid chi-square test for both linkage and association. The i-TDT can be used in various study designs and can accommodate all types of independent nuclear families with at least one affected offspring. We show that the transmission/disequilibrium test (TDT) (Spielman et al. [1993] Am. J. Hum. Genet. 52:506-516) is a special case of the i-TDT, if the study sample contains only case-parent trios. If the sample contains only affected and unaffected offspring without parental genotypes, the i-TDT is equivalent to the sibship disequilibrium test (SDT) (Horvath and Laird [1998] Am. J. Hum. Genet. 63:1886-1897. In addition, the test statistic of i-TDT is simple, explicit and can be implemented easily without intensive computing. Through computer simulations, we demonstrate that power of the i-TDT can be higher in many circumstances compared to a method that uses affected offspring only. Applying the i-TDT to the Framingham Heart Study data, we found that the apolipoprotein E (APOE) gene is significantly linked and associated with cross-sectional measures and longitudinal changes in total cholesterol.

Apolipoproteins E↗

PubMed2006

Candidate genes affecting Drosophila life span identified by integrating microarray gene expression analysis and QTL mapping.

The current increase in life expectancy observed in industrialized societies underscores the need to achieve a better understanding of the aging process that could help the development of effective strategies to achieve healthy aging. This will require not only identifying genes involved in the aging process, but also understanding how their effects are modulated by environmental factors, such as dietary intake and life style. Although the human genome has been sequenced, it may be impractical to study humans or other long-lived organisms to gain a mechanistic understanding about the aging process. Thus, short-lived animal models are essential to identifying the mechanisms and genes that affect the rate and quality of aging as a first step towards identifying genetic variants in humans. In this study, we investigated gene expression changes between two strains of Drosophila (Oregon and 2b) for which quantitative trait loci (QTLs) affecting life span were identified previously. We collected males and females from both strains at young and old ages, and assessed whole genome variation in transcript abundance using Affymetrix GeneChips. We observed 8217 probe sets with detectable transcripts. A total of 2371 probe sets, representing 2220 genes, exhibited significant changes in transcript abundance with age; and 839 probe sets were differentially expressed between Oregon and 2b. We focused on the 359 probe sets (representing 354 genes) that exhibited significant changes in gene expression both with age and between strains. We used these genes to integrate the analysis of microarray gene expression data, bioinformatics, and the results of genetic mapping studies reported previously, to identify 49 candidate genes and four pathways that could potentially be responsible for regulating life span and involved in the process of aging in Drosophila and humans.

Aging↗

PubMed2006

A direct assessment of genetic contribution to the incidence of coronary infarct in the general population Greek EPIC cohort.

To estimate the fraction of the incidence of coronary infarct attributable to the combined action of common genetic polymorphisms likely to be related to this condition, we conducted a case-control study nested within the Greek component of the European Prospective Investigation into Cancer and Nutrition. A total of 202 cases with a new, medically confirmed coronary infarct and 197 controls who had not developed an infarct by the time the corresponding case was diagnosed, were identified. A simple a priori score, relying on a total of 11 genetic polymorphisms was developed. Each polymorphism contributed 1 unit if the subject was homozygous for the high-risk allele, 0.5 units if the subject was heterozygous and 0 units if the subject was homozygous for the low-risk allele. Cases were over-represented in the presumed high genetic risk score values (chi square for trend = 10.18; p = 0.0014). The odds ratio to develop coronary infarct was 1.55 (95% confidence interval: 1.02-2.37) for score > or = 3.0, and 2.02 (1.31-3.11) for score > or = 3.5. In both instances the population fraction of the disease attributable to genetic predisposition exceeded 22%. Assuming a prior probability of at least 0.10 for the score to be predictive of coronary infarct risk, our findings are more likely than not to be truly positive. Our results, based on a simple score integrating the additive impact of 11 genetic polymorphisms, indicate that genetic predisposition accounts for a considerable fraction of the incidence of coronary infarct in the community.

Adult↗

PubMed2006

Codon 54 polymorphism of the fatty acid binding protein (FABP) 2 gene is associated with increased cardiovascular risk in the dyslipidemic diabetic participants of the Veterans Affairs HDL intervention trial (VA-HIT).

The threonine (Thr) for alanine (Ala) codon 54 polymorphism of the fatty acid binding protein (FABP) 2 gene, when compared to the wild type, is associated with dyslipidemia. Since dyslipidemia is common in diabetes and is associated with increased cardiovascular risk, we tested the hypothesis that Thr-54 is associated with increased cardiovascular risk in patients with diabetes. The secondary prevention veterans affairs HDL intervention trial (VA-HIT) was carried out in patients with dyslipidemia. The DNA of trial participants (n=776) was screened for the Thr-54 polymorphism and cardiovascular endpoints were monitored. The polymorphism was detected in 370 (47.7%). For first occurrence of the primary endpoint [myocardial infarction (MI) or coronary heart disease (CHD) death] the hazard ratio (HR) and confidence intervals (Cox proportional hazards model) was 2.5 (1.2, 5.3) p=.02 in diabetic carriers of Thr-54 versus carriers without diabetes or fasting glucose >7 mmol/L. For the expanded endpoint (stroke, MI or CHD death), the corresponding HR was 3.0 (1.4, 5.4) p=.0003 and for the stroke alone the corresponding HR was 3.5 (1.4-8.9) p=.01. The higher cumulative incidence of the expanded endpoint in diabetic participants carrying the FABP2 polymorphism versus non-diabetic carriers was consistently present throughout the 5 years of the study (p=.0002). We conclude that based on the VA-HIT data, the Thr-54 polymorphism of the FABP2 gene is associated with a 2-3.5-fold increase in cardiovascular risk in dyslipidemic men with diabetes compared to their non-diabetic counterparts.

Aged↗

PubMed2006

Association of a 31 bp VNTR in the CBS gene with postload homocysteine concentrations in the Framingham Offspring Study.

Elevated total plasma homocysteine concentrations (tHcy), both fasting and post-methionine load, have been established as risk factors for vascular disease. Recently, we described the association of a 31 bp variable number of tandem repeats (VNTR) in the cystathionine beta-synthase (CBS) gene with both CBS enzyme activity and tHcy concentrations. In the present study, we determined the 31 bp VNTR genotypes in 2598 individuals of the Framingham Offspring Study and studied the association between this genotype and fasting, 2-h post-methionine load and delta (ie increase upon methionine loading) tHcy concentrations in 1416 subjects. We observed a positive association between the number of repeat units of the CBS 31 bp VNTR and both postload and delta tHcy concentrations. Adjustment for possible effect modifying factors like age, sex and vitamin (B6, B12 and folate) status did not change this observation. We hereby confirm the results of our earlier study, in which we found that this 31 bp VNTR is a genetic determinant of post-methionine load tHcy concentrations. Since also post-methionine load tHcy concentrations are found to be associated with an increased risk for cardiovascular disease (CVD), this 31 bp VNTR may be considered a risk factor for CVD.

Aged↗

PubMed2006

The Val279Phe variant of the lipoprotein-associated phospholipase A2 gene is associated with catalytic activities and cardiovascular disease in Korean men.

CONTEXT AND OBJECTIVE: It is unclear whether lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) exerts a pro- or antiatherogenic effect on cardiovascular disease (CVD). We investigated the association between Lp-PLA(2) variant (V279F and A379V) and CVD in Korean men. DESIGN: CVD patients (n = 532) and healthy controls (n = 670) were genotyped for the Lp-PLA(2) polymorphism (V279F and A379V). MAIN OUTCOME MEASURES: We calculated odds ratio (OR) on CVD risk and measured anthropometries, lipid profiles, low-density lipoprotein (LDL) particle size, oxidized LDL, lipid peroxides, and Lp-PLA(2) activity. RESULTS: The presence of the 279F allele was associated with a lower risk of CVD [OR 0.646 (95% confidence interval 0.490-0.850), P = 0.002], and the association still remained after adjustments for age, body mass index, waist circumference, waist to hip ratio, cigarette smoking, and alcohol consumption [OR 0.683 (95% confidence interval 0.512-0.911), P = 0.009]. Lp-PLA(2) activity was lower in CVD patients taking a lipid-lowering drug (31%), those not taking a lipid-lowering drug (26%), and control subjects (23%) with the V/F genotype, compared with those with the V/V genotype. Subjects with the F/F genotype in controls and two CVD patients groups showed no appreciable enzymatic activity. Control subjects with the V/F genotype had larger LDL particle size than those with the V/V genotype. In addition, control subjects carrying the F allele showed lower malondialdehyde concentrations. On the other hand, we found no significant relationship between A379V genotype and CVD risk. CONCLUSIONS: The association of the F279 loss of function variant with the reduced risk of CVD supports the concept that Lp-PLA(2) plays a proatherogenic and causative role in CVD.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed2006

Dietary intake of n-6 fatty acids modulates effect of apolipoprotein A5 gene on plasma fasting triglycerides, remnant lipoprotein concentrations, and lipoprotein particle size: the Framingham Heart Study.

BACKGROUND: Apolipoprotein A5 gene (APOA5) variation is associated with plasma triglycerides (TGs). However, little is known about whether dietary fat modulates this association. METHODS AND RESULTS: We investigated the interaction between APOA5 gene variation and dietary fat in determining plasma fasting TGs, remnant-like particle (RLP) concentrations, and lipoprotein particle size in 1001 men and 1147 women who were Framingham Heart Study participants. Polymorphisms -1131T>C and 56C>G, representing 2 independent haplotypes, were analyzed. Significant gene-diet interactions between the -1131T>C polymorphism and polyunsaturated fatty acid (PUFA) intake were found (P<0.001) in determining fasting TGs, RLP concentrations, and particle size, but these interactions were not found for the 56C>G polymorphism. The -1131C allele was associated with higher fasting TGs and RLP concentrations (P<0.01) in only the subjects consuming a high-PUFA diet (>6% of total energy). No heterogeneity by sex was found. These interactions showed a dose-response effect when PUFA intake was considered as a continuous variable (P<0.01). Similar interactions were found for the sizes of VLDL and LDL particles. Only in carriers of the -1131C allele did the size of these particles increase (VLDL) or decrease (LDL) as PUFA intake increased (P<0.01). We further analyzed the effects of n-6 and n-3 fatty acids and found that the PUFA-APOA5 interactions were specific for dietary n-6 fatty acids. CONCLUSIONS: Higher n-6 (but not n-3) PUFA intake increased fasting TGs, RLP concentrations, and VLDL size and decreased LDL size in APOA5 -1131C carriers, suggesting that n-6 PUFA-rich diets are related to a more atherogenic lipid profile in these subjects.

Adult↗

PubMed2006

Variants at the APOA5 locus, association with carotid atherosclerosis, and modification by obesity: the Framingham Study.

Genetic variation at the apolipoprotein A5 gene (APOA5) is associated with increased triglyceride concentrations, a risk factor for atherosclerosis. Carotid intimal medial thickness (IMT) is a surrogate measure of atherosclerosis burden. We sought to determine the association of common APOA5 genetic variants with carotid IMT and stenosis. A total of 2,273 Framingham Offspring Study participants underwent carotid ultrasound and had data on at least one of the five APOA5 variants (-1131T>C, -3A>G, 56C>G, IVS3+476G >A, and 1259T>C). Although none of the individual variants was significantly associated with carotid measures, the haplotype defined by the presence of the rare allele of the 56C>G variant was associated with a higher common carotid artery (CCA) IMT compared with the wild-type haplotype (0.75 vs. 0.73 mm; P < 0.05). The rare allele of each of the -1131T >C, -3A>G, IVS3+476G>A, and 1259T>C variants and the haplotype defined by the presence of the rare alleles in these four variants were each significantly associated with CCA IMT in obese participants. These associations remained significant even after adjustment for triglycerides. APOA5 variants were associated with CCA IMT, particularly in obese participants. The mechanism of these associations and the effect modification by obesity are independent of fasting triglyceride levels.

Apolipoprotein A-V↗

PubMed2006

Association between well-characterized lipoprotein-related genetic variants and carotid intimal medial thickness and stenosis: The Framingham Heart Study.

OBJECTIVE: To determine the association of well-characterized lipoprotein-related genetic variants with carotid intimal medial thickness (IMT) and stenosis. METHODS: 3380 men and women from the Framingham Offspring Study underwent carotid ultrasound to determine carotid IMT and stenosis>/=25%. We genotyped 12 variants in 10 lipoprotein-related genes known to be associated with significant differences in lipoprotein levels. RESULTS: For most of the variants, there was no association with carotid IMT. In multivariable, sex-specific analyses, the rare allele of the cholesterol ester transfer protein (CETP) TaqIB variant was associated with lower ICA IMT in men. Hypertension was associated with higher ICA IMT only in male carriers of the rare allele of the APOCIII Sst-1 variant (p for the interaction=0.041). In analyses of carotid stenosis in male, carriers of the lipoprotein lipase (LPL) N291S rare variant showed a higher risk of carotid stenosis (OR=2.59, 95% confidence interval: 1.11-6.02, p=0.028) compared to NN genotype. CONCLUSIONS: While there is no evidence for a significant association of several common lipoprotein-related genetic variants with carotid IMT, our results are consistent with the previously reported role of CETP and LPL genetic variants in cardiovascular risk and the possible modulation of the association between hypertension and carotid IMT by APOCIII Sst-1 variant.

Adolescent↗

PubMed2006

The Nutrition, Aging, and Memory in Elders (NAME) study: design and methods for a study of micronutrients and cognitive function in a homebound elderly population.

BACKGROUND: Micronutrient status can affect cognitive function in the elderly; however, there is much to learn about the precise effects. Understanding mediating factors by which micronutrient status affects cognitive function would contribute to elders' quality of life and their ability to remain in the home. OBJECTIVES: The Nutrition, Aging, and Memory in Elders (NAME) Study is designed to advance the current level of knowledge by investigating potential mediating factors by which micronutrient status contributes to cognitive impairment and central nervous system abnormalities in the elderly. NAME targets homebound elders because they are understudied and particularly at risk for poor nutritional status. METHODS: Subjects are community-based elders aged 60 and older, recruited through area Aging Services Access Points. The NAME core data include demographics; neuropsychological testing and activities of daily living measures; food frequency, health and behavioral questionnaires; anthropometrics; gene status; plasma micronutrients, homocysteine, and other blood determinants. A neurological examination, psychiatric examination, and brain MRI and volumetric measurements are obtained from a sub-sample. RESULTS: Preliminary data from first 300 subjects are reported. These data show that the NAME protocol is feasible and that the enrolled subjects are racially diverse, at-risk, and had similar basic demographics to the population from which they were drawn. CONCLUSION: The goal of the NAME study is to evaluate novel relationships between nutritional factors and cognitive impairment. These data may provide important information on potential new therapeutic strategies and supplementation standards for the elderly to maintain cognitive function and potentially reduce the public health costs of dementia.

Activities of Daily Living↗

PubMed2006

Nutrigenetics, plasma lipids, and cardiovascular risk.

Cardiovascular disease (CVD) results from complex interactions between genetic and environmental factors. The evidence supports that gene-environment interactions modulate plasma lipid concentrations and potentially CVD risk. Several genes (eg, apolipoprotein A-I and A-IV, apolipoprotein E, and hepatic lipase) are providing proof-of-concept for the application of genetics in the context of personalized nutrition for CVD prevention. The spectrum of candidate genes has been expanding to incorporate those involved in intracellular lipid metabolism and especially those transcription factors (ie, peroxisome proliferator activator receptors) that act as sensors of nutrients in the cell (eg, polyunsaturated fatty acids) to trigger metabolic responses through activation of specific sets of genes. However, current knowledge is still very limited and so is the potential benefit of its application to clinical practice. Thinking needs to evolve from simple scenarios (eg, one single dietary component, a single nucleotide polymorphism and risk factor) to more realistic situations involving multiple interactions. One of the first situations where personalized nutrition is likely to be beneficial is in patients with dyslipidemia who require special intervention with dietary treatment. This process could be more efficient if the recommendations were carried out based on genetic and molecular knowledge. Moreover, adherence to dietary advice may increase when it is supported with information based on nutritional genomics, and a patient believes the advice is personalized. However, a number of important changes in the provision of health care are needed to achieve the potential benefits associated with this concept, including a teamwork approach with greater integration among physicians, food and nutrition professionals, and genetic counselors.

Cardiovascular Diseases↗

PubMed2006

The SNP276G>T polymorphism in the adiponectin (ACDC) gene is more strongly associated with insulin resistance and cardiovascular disease risk than SNP45T>G in nonobese/nondiabetic Korean men independent of abdominal adiposity and circulating plasma adiponectin.

This study aimed to determine whether polymorphisms of the adiponectin (ACDC) gene independently contribute to insulin resistance (IR) and other cardiovascular disease (CVD) risk factors in nonobese, nondiabetic Korean men after adjusting for major environmental factors that influence IR. Among the 7 ACDC single-nucleotide polymorphisms (SNPs;C-11377G, T45G, G276T, H241P, Y111H, G90S, and R221S) prescreened in 48 subjects, we genotyped 333 subjects for SNP45 and SNP276, both of which showed an allele frequency of more than 2%. In Pearson correlation and multiple stepwise regression analyses, we found that waist circumference was the most important influencing factor (beta = .369, P < .001) in homeostasis model assessment (HOMA)-IR, whereas plasma adiponectin was the second most important (beta = -.217, P = .023). At position 276, T/T subjects showed significantly lower glucose concentrations (P = .043) and higher low-density lipoprotein particle sizes (P = .033) than the G/G and G/T subjects. The subjects also had lower serum triglycerides and HOMA-IR; however, these results were not statistically significant. After adjusting for waist circumference and plasma adiponectin, T/T subjects showed a significantly lower HOMA-IR than G/G or G/T subjects (P = .048). On the other hand, at position 45, only glucose concentrations were significantly lower in G carriers (P = .005). In the SNP45-SNP276 haplotype test, TT/TT subjects (having T/T at both SNP45 and SNP276) showed significantly lower IR before and after adjusting for waist circumference and adiponectin levels than did other carriers. In conclusion, we suggest that SNP276G>T, rather than SNP45T>G, is more strongly associated (both directly and indirectly) than with several components of metabolic syndrome and CVD risk, including IR, triglyceride concentration, and low-density lipoprotein particle size, in nonobese, nondiabetic men.

Abdomen↗

PubMed2006

Uncoupling protein 2 promoter polymorphism -866G/A, central adiposity, and metabolic syndrome in Asians.

A polymorphism in the promoter region of uncoupling protein 2 gene -866G/A has been associated with its expression levels in adipose tissue, the risk of obesity, and metabolic abnormalities. Our purpose was to examine the associations of -866G/A with body fat and the risk of metabolic syndrome in a random sample of 4018 Asians (1858 men and 2160 women) from three ethnic groups (Chinese, Malay, and Indian). The minor allele frequency of -866G/A polymorphism in South Asians was similar to that in whites. After adjustment for covariates including age, cigarette smoking, and physical activity, the -866A/A genotype was associated with higher waist-to-hip ratio as compared with the wild-type genotype in Chinese and Indian men (p = 0.018 and p = 0.046, respectively). Moreover, Indian men with -866A/A genotype had a significantly increased risk of metabolic syndrome as compared with those homozygous for the wild-type (odds ratio, 2.66; 95% confidence interval, 1.21 to 5.88; p = 0.015). Such a risk was mainly caused by the excess presence of hypertriglyceridemia and central obesity. Our findings indicate that the uncoupling protein 2 gene -866G/A polymorphism may increase the risks of central obesity and metabolic syndrome, with greater effects on Asian men.

Adiposity↗

PubMed2006

Comparison of low-fat meal and high-fat meal on postprandial lipemic response in non-obese men according to the -1131T>C polymorphism of the apolipoprotein A5 (APOA5) gene (randomized cross-over design).

OBJECTIVE: The purpose of this study was to compare low-fat (LF) meal and high-fat (HF) meal on the postprandial lipemic responses according to the -1131T>C polymorphism of the APOA5 gene in a population usually consuming a LF diet and having a high frequency of the variant allele at the APOA5 -1131T>C SNP. METHODS: This study was conducted using a cross-over design and 49 non-obese healthy men (42.8 +/- 0.7 yrs, 23.9 +/- 0.25 kg/m(2)) participated in the meal tolerance test. They were randomly assigned to consume one of two types of experimental enteral formulae (LF vs HF) with a seven-day interval. Blood samples were collected at 0, 2, 3, 4 and 6h after ingestion and analyzed for total and chylomicron TG, glucose, insulin and free fatty acid. RESULTS: No differences were found in anthropometic parameter, calorie and macronutrient intakes and total energy expenditure between TT (n = 23) and TC + CC (n = 26) men. Fasting total TG were higher in TC + CC men than TT men, but fasting chylomicron TG were not significantly different between TT men and C carriers, TT subjects had no significant differences in postprandial responses of total TG and chylomicron TG and postprandial mean changes of chylomicron TG between LF and HF meal. On the other hand, C carriers had delayed peak time of total TG compared to TT subject and higher postprandial response and mean changes of chylomicron TG at HF meal compared to LF meal. CONCLUSION: The capacity to clear chylomicron-TG or hydrolyze TG might become a rate-limiting factor on HF diet in TC + CC men resulting in higher postprandial triglyceridemia. Therefore, HF diet for C carriers of the APOA5 gene may be one of important CVD risk factors.

Adult↗

PubMed2006

Nutritional risk and the metabolic syndrome in women: opportunities for preventive intervention from the Framingham Nutrition Study.

BACKGROUND: Diet is recognized as a key factor in the cause and management of the metabolic syndrome (MetS). However, policies to guide preventive clinical nutrition interventions of the condition are limited. OBJECTIVES: We examined the relation between dietary quality and incident MetS in adult women and identified foci for preventive nutrition interventions. DESIGN: This was a prospective study of 300 healthy women (aged 30-69 y) in the Framingham Offspring-Spouse study who were free of MetS risk factors at baseline. The development of individual MetS traits and overall MetS status during 12 y of follow-up were compared in women by tertile of nutritional risk, based on intake of 19 nutrients. Multivariate logistic regression models considered age, smoking, physical activity, and menopausal status. RESULTS: Baseline age-adjusted mean nutrient intake and ischemic heart disease risk profiles differed by tertile of nutritional risk. Women with higher nutritional risk profiles consumed more dietary lipids (total, saturated, and monounsaturated fats) and alcohol and less fiber and micronutrients; they had higher cigarette use and waist circumferences. Compared with women with the lowest nutritional risk, those in the highest tertile had a 2- to 3-fold risk of the development of abdominal obesity and overall MetS during 12 y of follow-up [odds ratio: 2.3 (95% CI: 1.2, 4.3) and 3.0 (95% CI: 1.2, 7.6), respectively]. CONCLUSIONS: Higher composite nutritional risk predicts the development of abdominal obesity and MetS during long-term follow-up in healthy women, independent of lifestyle and ischemic heart disease risk factors. Preventive nutrition interventions for obesity and MetS risk reduction should focus on the overall nutritional quality of women's dietary profiles.

Abdominal Fat↗

PubMed2006

The ABCG5 polymorphism contributes to individual responses to dietary cholesterol and carotenoids in eggs.

The ATP binding cassette G5 (ABCG5) polymorphisms have been postulated to play a role in the response to dietary cholesterol. The objective of this study was to examine the contribution of the ABCG5 polymorphism on the plasma response to consumption of cholesterol and carotenoids from eggs. For this purpose, genotyping was conducted for 40 men and 51 premenopausal women who were randomly assigned to consume an egg (EGG, 640 mg/d additional dietary cholesterol and 600 microg lutein+ zeaxanthin) or placebo (SUB, 0 mg/d cholesterol, 0 microg lutein + zeaxanthin) diet for 30 d. The two arms of the dietary intervention were separated by a 3-wk washout period. Plasma concentrations of total cholesterol, LDL cholesterol (LDL-C), and HDL cholesterol were determined. Because eggs are an excellent source of lutein and zeaxanthin, the plasma levels of these carotenoids were also measured in a subset of subjects to determine whether the response to carotenoid intake was similar to that seen for dietary cholesterol and to evaluate the contribution of ABCG5 polymorphism to both responses. Individuals possessing the C/C genotype experienced a greater increase in both LDL-C (P < 0.05) and a trend for lutein (P = 0.08) during the EGG period compared with those individuals with the C/G (heterozygote) or G/G genotypes (homozygotes). These results, although obtained from a small number of subjects, suggest that the ABCG5 polymorphism may play a role in the plasma response to dietary cholesterol and carotenoids.

ATP Binding Cassette Transporter, Subfamily G, Mem↗

PubMed2006

Metagenomics: the role of the microbiome in cardiovascular diseases.

PURPOSE OF REVIEW: The human oral and intestinal microbiota interact with the host through poorly understood metabolic pathways. Investigation of such complex ecosystems and interactions has been difficult. In this paper, we assess the current evidence supporting the role of the microbiota as a significant determinant of cardiovascular disease risk. RECENT FINDINGS: The link between oral disease and cardiovascular disease was established about 15 years ago. The accumulated evidence supports, but does not prove a causal association between periodontal infection and cardiovascular disease and suggests some physiologically obvious connections between these pathologies, namely, inflammatory and immune responses, and hemostasis. Moreover, some studies have observed higher concentrations of total and LDL-cholesterol and triglycerides and lower concentrations of HDL-cholesterol in individuals with periodontitis before periodontal treatment. Likewise, recent reports suggest the influence of the gut microbiome in the risk of common age-related diseases such as cancer and potentially cardiovascular disease through modification of classical risk factors such as obesity, insulin resistance and plasma lipids. SUMMARY: The recognition that microorganisms may play an even more important role in maintaining human health than in generating diseases places metagenomics as one of the most relevant areas of future research. The knowledge of the hundreds of genomes that we host and their interaction with our own genome shall provide a much more complete understanding of the individual nutritional needs and may be an obligated part of future personalized healthcare approaches.

Cardiovascular Diseases↗