Association of plasma phospholipid polyunsaturated and trans fatty acids with body mass index: results from the Multi-Ethnic Study of Atherosclerosis.

BACKGROUND/OBJECTIVE: Previous research has focused on associations between dietary fat and body mass index (BMI), but the contributions of different types of fat to BMI remain unclear. The purpose of this study is to estimate whether plasma phospholipid omega-3 (n-3), omega-6 (n-6) or trans fatty acids are associated with BMI at baseline and with subsequent BMI changes over time; and whether total phospholipid n-6 or trans fatty acids modify any association between phospholipid n-3 and BMI. METHODS: Cross-sectional and longitudinal linear mixed models include 6243 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort. Participants were 45-84 years old, had no history of cardiovascular disease at baseline (2000-2002) and were followed for up to 10 years. Plasma phospholipid fatty acids were measured using fasting plasma samples at baseline. Fully adjusted models include demographics, health behaviors and other fatty acids (n-3, n-6 and trans) as appropriate. RESULTS: In fully adjusted models, phospholipid n-3 fatty acid levels were inversely associated with baseline BMI (Ptrend <0.001). Baseline BMI was 1.14 (95% confidence interval (CI): 0.71, 1.57) kg m-2 lower among participants with total n-3 values in the highest vs the lowest quartiles, but was not associated with changes in BMI. Total phospholipid n-6 was positively associated with baseline BMI in partially adjusted but not fully adjusted models. No overall association was observed between fatty acid levels and changes in BMI. No clear association was observed between trans fatty acids and baseline BMI or BMI change. No effect modification in the association between phospholipid n-3 and baseline BMI or BMI change was observed by either phospholipid n-6 or trans fatty acids. CONCLUSIONS: Phospholipid total and specific n-3 fatty acid levels were inversely associated with BMI at baseline, whereas associations tended to be positive for total n-6 fatty acids. Significant associations between fatty acid levels and BMI changes were not observed.

Cognitive function in a middle aged cohort is related to higher quality dietary pattern 5 and 25 years earlier: the CARDIA study.

BACKGROUND: Preserving cognitive function is an important public health issue. We investigated whether dietary pattern associates with cognitive function in middle-age. METHODS: We studied 2435 participants in the community-based Coronary Artery Risk Development in Young Adults (CARDIA) study of black and white men and women aged 18-30 in 1985-86 (year 0, Y0). We hypothesized that a higher A Priori Diet Quality Score, measured at Y0 and Y20, is associated with better cognitive function measured at Y25. The diet score incorporated 46 food groups (each in servings/day) as the sum of quintile ranks of food groups rated beneficial, 0 for food groups rated neutral, and reversed quintile ranks for food groups rated adverse; higher score indicated better diet quality. Y25 cognitive testing included verbal memory (Rey Auditory-Verbal Learning Test (RAVLT)), psychomotor speed (Digit Symbol Substitution Test (DSST)) and executive function (Stroop). RESULTS: Per 10-unit higher diet score at Y20, the RAVLT was 0.32 words recalled higher, the DSST was 1.76 digits higher, and the Stroop was 1.00 seconds+errors lower (better performance) after adjusting for race, sex, age, clinic, and energy intake. Further adjustment for physical activity, smoking, education, and body mass index attenuated the association slightly. Diet score at Y0 and increase in diet score over 20 years were also positively associated with each cognitive test. CONCLUSIONS: A higher quality dietary pattern was associated with better cognitive function 5 years and even 25 years later in apparently healthy middle-aged adults.

Diet quality and markers of endothelial function: the CARDIA study.

BACKGROUND AND AIM: Dietary patterns are associated cross-sectionally with cellular adhesion molecules (CAMs). We studied prospective associations of three dietary patterns with CAMs. METHODS AND RESULTS: In the Coronary Artery Risk Development in Young Adults (CARDIA) study, diet was assessed at years 0 (1985-86) and 7 (1992-93) examinations. Four circulating CAMs (E-selectin, P-selectin, soluble intercellular adhesion molecule 1 (sICAM-1), and vascular cellular adhesion molecule (VCAM)) were assayed at years 7 and 15 (2000-01). We created one index score "A Priori Diet Quality Score" and derived dietary patterns using principal components analysis (PCA). Multivariable linear regression models predicted year 15 CAMs from averaged (year 0/7) dietary patterns. The A Priori Diet Quality Score rated 46 food groups beneficial, neutral or adverse based on hypothesized health effects. We derived two PCA dietary patterns: "fruit and vegetables (FV)" (high intakes of fruit, vegetables, and whole grains) and "meat" (high intakes of red meat, refined grain, and butter). All dietary patterns were related to E-selectin and sICAM-1. P-selectin was not related to the FV dietary pattern. VCAM was only related to the A Priori Diet Quality Score. Strongest associations were for the meat dietary pattern with E-selectin (effect size 28% of an SD (+3.9/13.7 ng/mL)) and P-selectin (effect size 37% of an SD (+4.1/11.2 ng/mL)) and the A Priori Diet Quality Score with sICAM-1 (effect size 34% of an SD (-15.1/44.7 ng/mL)) and VCAM (effect size of 26% of an SD (-45.1/170.3 ng/mL)). CONCLUSION: This prospective analysis suggests that dietary patterns are associated with CAMs.

Ethnicity, plasma phospholipid fatty acid composition and inflammatory/endothelial activation biomarkers in the Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND/OBJECTIVES: It has been recognized that certain long-chain polyunsaturated fatty acids (LC-PUFAs) are involved in inflammation and its resolution. It has also been shown that ethnicity may be a factor in affecting systemic inflammation, and limited evidence suggests it may influence plasma LC-PUFA composition. Given the links among these three factors, we aim to determine ethnicity-based differences in plasma LC-PUFA composition among White, Black, Hispanic and Chinese participants, and whether such differences contribute to variations in markers of inflammation and endothelial activation in a sub-cohort of the Multi-Ethnic Study of Atherosclerosis (MESA). SUBJECTS/METHODS: Plasma phospholipid LC-PUFAs levels (%) were determined in 2848 MESA participants using gas chromatography-flame ionization detection. Enzyme immunoassays determined inflammatory markers levels for high-sensitivity C-reactive protein (n=2848), interleukin-6 (n=2796), soluble tumor necrosis factor-α receptor type 1 (n=998), and endothelial activation markers soluble intercellular adhesion molecule-1 (n=1192) and soluble E-selectin (n=998). The modifying influence of ethnicity was tested by linear regression analysis. RESULTS: Chinese adults were found to have the highest mean levels of plasma eicosapentaenoic acid (EPA, 1.24%) and docosahexaenoic acid (DHA, 4.95%), and the lowest mean levels of γ-linolenic (0.10%), dihomo-γ-linolenic (DGLA, 2.96%) and arachidonic (10.72%) acids compared with the other ethnicities (all P ≤ 0.01). In contrast, Hispanics had the lowest mean levels of plasma EPA (0.70%) and DHA (3.49%), and the highest levels of DGLA (3.59%; all P ≤ 0.01). Significant differences in EPA and DHA among ethnicities were attenuated following adjustment for dietary non-fried fish and fish oil supplementation. Ethnicity did not modify the associations of LC-PUFAs with markers of inflammation or endothelial activation (all P (interaction)>0.05). CONCLUSIONS: The absence of a modifying effect of ethnicity indicates that the putative benefits of LC-PUFAs with respect to inflammation are pan-ethnic. Future longitudinal studies may elucidate the origin(s) of ethnicity-based differences in LC-PUFA composition and whether certain patterns, that is, high plasma levels of DGLA and low levels of EPA/DHA, contribute to inflammation-associated health outcomes.

Obesity modifies the association between plasma phospholipid polyunsaturated fatty acids and markers of inflammation: the Multi-Ethnic Study of Atherosclerosis.

BACKGROUND AND OBJECTIVE: Systemic inflammation is a well-known risk factor for diseases such as atherosclerosis and is augmented by the presence of obesity. In addition, it has been shown that inflammation may be negatively influenced by certain macronutrients, specifically the omega-3 and omega-6 fatty acids. The primary aim of this study is to determine whether obesity modifies the association between plasma phospholipid polyunsaturated fatty acids (PUFAs) and markers of inflammation and endothelial activation in Multi-Ethnic Study of Atherosclerosis (MESA) participants. SUBJECTS: A sample of 2848 adults (25% African American, Chinese, Hispanic, and White) randomly selected from the MESA cohort. MEASUREMENTS: Relative plasma PUFA concentrations were determined using gas chromatography-flame ionization detection. Levels of three inflammatory markers (high-sensitivity C-reactive protein, interleukin (IL)-6 and tumor necrosis factor-receptor 1) and two endothelial activation markers (soluble intercellular adhesion molecule-1 (sICAM-1) and E-selectin) were determined with enzyme immunoassays. Linear regression analysis was used to evaluate the relationship between these markers and plasma PUFAs. RESULTS: Obesity modified the associations of linoleic acid (P(int)=0.01), dihomo-γ-linolenic (P(int)=0.07) and eicosapentaenoic acid (EPA) (P(int)=0.04) with sICAM-1 concentrations; in addition, obesity modified the association of IL-6 with dihomo-γ-linolenic (P(int)=0.01). In obese individuals, sICAM-1 was inversely related to EPA levels (P=0.02), but directly related to linoleic acid levels (P<0.001). Conversely, sICAM-1 was inversely related to linoleic acid levels in normal weight individuals (P=0.04). IL-6 concentrations were significantly and directly related to dihomo-γ-linolenic acid (DGLA) in normal weight (P=0.01) and obese participants (P<0.001), but the scale of increase across tertiles was greater in obese adults. Main effects of fatty acid and inflammatory marker associations are also reported. CONCLUSION: The modifying effect of obesity on the association of plasma PUFAs with IL-6 and sICAM-1 suggests differences in fatty acid metabolism and may also have implications in dietary fatty acid intake for obese individuals, particularly for linoleic and EPAs. Further study is warranted to confirm and explain the strong associations of DGLA with inflammatory and endothelial activation markers.

Dairy intake and changes in blood pressure over 9 years: the ARIC study.

Dairy product intake could contribute to preventing hypertension, but information linking intake of these foods with changes in blood pressure over long periods of time, particularly in non-whites, is scarce. We analyzed the Atherosclerosis Risk in Communities study, a prospective cohort in the United States, to assess whether different types of dairy products were associated with changes in blood pressure over time. The analysis included 6912 white and 1296 African-American nonhypertensive men and women, aged 45-64 at baseline. After 9 years of follow-up, systolic blood pressure of whites consuming three or more daily servings of low-fat milk increased 2.7 mm Hg less than in those consuming less than one serving per week (P for trend=0.01). Among African Americans, dairy products intake was not associated with changes in blood pressure over time. In conclusion, higher low-fat milk intake was associated with lower increases in blood pressure in whites but not in African Americans.

Metabolic syndrome and risk of venous thromboembolism: Longitudinal Investigation of Thromboembolism Etiology.

SUMMARY BACKGROUND: In a recent case-control study, the odds of metabolic syndrome (MetSyn) among deep vein thrombosis cases were almost twice those among controls. We tested the hypothesis that the incidence of non-cancer-related venous thromboembolism (VTE) is higher among adults with MetSyn and further, that associations are stronger for idiopathic than secondary VTE. METHODS: A total of 20 374 middle-aged and elderly adults were followed for over 12 years for incident VTE in the Longitudinal Investigation of Thromboembolism Etiology (LITE). All hospitalizations were identified and VTEs validated by chart review. Baseline MetSyn was defined using ATP III guidelines, including >or=3 of the following components: abdominal obesity, elevated blood pressure, low HDL-cholesterol, high triglycerides and high glucose. Because sex modified the relation between MetSyn and VTE (p(interaction) = 0.001), proportional hazards regression analyses were stratified by sex to assess the associations of MetSyn and its components with risk of incident non-cancer-related VTE, adjusting for potential confounders. RESULTS: Incident VTE (n = 358) included 196 idiopathic events. Baseline MetSyn was associated with risk of total VTE (hazard ratio (HR) = 1.84, 95% CI = 1.30, 2.59) and idiopathic VTE (HR = 1.59, 95% CI = 1.02, 2.47) among men, but not women. The association was largely attributable to abdominal obesity (HR of VTE = 2.10, 95% CI = 1.51, 2.93, in men; HR of VTE = 1.70, 95% CI = 1.24, 2.34, in women), with no additional contribution by the other MetSyn components. CONCLUSION: Although abdominal obesity was associated with increased risk of VTE in both men and women, MetSyn and its other components do not seem important in VTE etiology.

Serum phospholipid and cholesteryl ester fatty acids and estimated desaturase activities are related to overweight and cardiovascular risk factors in adolescents.

AIM/HYPOTHESIS: The objective of this study was to describe the relation of serum fatty acids and desaturase activity (DA) to overweight, insulin sensitivity and cardiovascular disease (CVD) risk factors in adolescents. METHODS: The relations of % serum phospholipid (PL) and cholesteryl ester (CE) fatty acids and estimated DA with CVD risk factors were examined in 264 adolescents (average age 15 years). Fatty acids were determined by gas liquid chromotography. Surrogate measures of DA were expressed as ratios of serum fatty acids: Delta9 DA=16:0/16:1; Delta6 DA=20:3,n6/18:2,n6 (PL) or 18:3,n6/18:2,n6 (CE); and Delta5 DA=20:4,n6/20:3,n6. Spearman partial correlations of fatty acids (%) and DA ratios with CVD risk factors were reported, adjusting for age, sex, race, Tanner stage, energy intake and physical activity. RESULTS: Overweight adolescents compared to normal weight had more adverse levels of CVD risk factors, composition of PL and CE fatty acids in serum, and Delta6 DA and Delta5 DA ratios. Linoleic acid was inversely related to body mass index (BMI), waist circumference and triglycerides (P

Heritability and genetic correlations of insulin sensitivity measured by the euglycaemic clamp.

AIMS: Studies investigating genetic factors influencing insulin sensitivity/insulin resistance have measured this phenotype using a variety of methods. In this study, genetic correlations and heritability of insulin sensitivity measured using the euglycaemic hyperinsulinaemic clamp and related phenotypes were examined. METHODS: The study population included 818 non-diabetic individuals from 297 nuclear families. Genetic correlations and heritability estimates were calculated using variance components methods. RESULTS: Homeostasis model of insulin resistance (HOMA-IR) and fasting insulin were very highly phenotypically and genetically correlated (r = 0.99 and r = 0.99). HOMA-IR and insulin sensitivity measured with the euglycaemic clamp were only moderately genetically correlated (r = -0.53), suggesting that the two traits may be influenced, at least in part, by different genes. Heritabilities for fasting insulin (h2 = 0.36) and HOMA-IR (h2 = 0.38) were consistent with the published literature, but heritability for insulin sensitivity measured by the euglycaemic clamp was slightly lower than other published estimates (h(2) = 0.24). CONCLUSIONS: Because HOMA-IR (or fasting insulin) and insulin sensitivity measured with the euglycaemic clamp are not highly genetically correlated, they should not be used interchangeably in genetic studies. Given the very high correlations between fasting insulin and HOMA-IR, HOMA-IR does not offer any advantage over fasting insulin in analyses of insulin sensitivity in this population.

Plasma hemostatic factors and endothelial markers in four racial/ethnic groups: the MESA study.

BACKGROUND: Hemostatic factors and endothelial markers may play some role in racial/ethnic differences in cardiovascular disease (CVD) rates. However, little information exists on hemostatic factors and endothelial markers across racial/ethnic groups. OBJECTIVES: To describe, in four American racial/ethnic groups (Caucasian, Black, Hispanic, and Chinese), mean levels of selected hemostatic factors and endothelial markers. PATIENTS AND METHODS: Multi-ethnic Study of Atherosclerosis baseline data were used (participant age: 45-84 years). Sex-specific analysis of covariance models, and t-tests for pairwise comparisons, were used to compare means of factors and markers. Adjustments were made for demographics and traditional CVD risk factors. Differences were significant at P < 0.05. RESULTS: Blacks had the highest levels of factor VIII, D-Dimer, plasmin-antiplasmin (PAP), and von Willebrand factor, among the highest levels of fibrinogen and E-selectin (women only), but among the lowest levels of intercellular adhesion molecule 1 (ICAM-1), and, in men, the lowest levels of plasminogen activator inhibitor-1 (PAI-1). Whites and Hispanics tended to have intermediate levels of factors and markers, although they had the highest levels of ICAM-1, and Hispanics had the highest mean levels of fibrinogen and E-selectin (women only). Chinese participants had among the highest levels of PAI-1, but the lowest, or among the lowest, of all other factors and markers. No soluble thrombomodulin differences were observed. CONCLUSIONS: In this large cohort, hemostatic factor and endothelial marker mean levels varied by race/ethnicity, even after adjustment for traditional CVD risk factors.