R Curtis Ellison

Boston University, Boston, Massachusetts, United States

Are you R Curtis Ellison?

Claim your profile

Publications (85)525.02 Total impact

  • Source
    R. Curtis Ellison
    Addiction 08/2014; 109(8). · 4.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and Aims Eggs are a ubiquitous and important source of dietary cholesterol and nutrients, yet their relationship to coronary heart disease (CHD) remains unclear. While some data have suggested a positive association between egg consumption and CHD, especially among diabetic subjects, limited data exist on the influence of egg consumption on subclinical disease. Thus, we sought to examine whether egg consumption is associated with calcified atherosclerotic plaques in the coronary arteries. Methods In a cross-sectional design, we studied 1848 participants of the NHLBI Family Heart Study without known CHD. Egg consumption was assessed by a semi-quantitative food frequency questionnaire and coronary-artery calcium (CAC) was measured by cardiac CT. We defined prevalent CAC using an Agatston score of at least 100 and fitted generalized estimating equations to calculate prevalence odds ratios of CAC. Results Mean age was 56.5 years and 41% were male. Median consumption of eggs was 1/week. There was no association between frequency of egg consumption and prevalent CAC. Odds ratios (95% CI) for CAC were 1.0 (reference), 0.95 (0.66-1.38), 0.94 (0.63-1.40), and 0.90 (0.57-1.42) for egg consumption of almost never, 1-3 times per month, once per week, and 2+ times per week, respectively (p for trend 0.66), adjusting for age, sex, BMI, smoking, alcohol, physical activity, income, field center, total calories, and bacon. Additional control for hypertension and diabetes mellitus, or restricting the analysis to subjects with diabetes mellitus or fasting glucose >126 mg/dL did not alter the findings. Conclusions These data do not provide evidence for an association between egg consumption and prevalent CAC in adult men and women.
    e-SPEN Journal. 06/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND & AIMS: Metabolic syndrome (MetS), characterized by abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, and insulin resistance is a major public health concern in the United States. Omega-3 fatty acids have been relatively well studied in relation to many individual cardiovascular risk factors; however, their effects on MetS are not well established. METHODS: We conducted a cross-sectional study consisting of 4941 participants from the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study to assess the relation of dietary omega-3 fatty acids with the prevalence of MetS. Omega-3 intake was assessed using a food frequency questionnaire and we used generalized estimating equations to estimate adjusted odds ratios for prevalent MetS. RESULTS: Our study population had a mean age (SD) of 52.1 (13.9) years and 45.9% were men. The mean (SD) of dietary omega-3 fatty acids was 0.25 g/day (0.27). From the lowest to the highest quintile of dietary omega-3 fatty acids, multivariable adjusted ORs (95% CI) for MetS were 1.00 (ref), 0.90 (0.72-1.13), 1.03 (0.82-1.28), 0.94 (0.74-1.18), and 0.99 (0.77-1.25), respectively. In a secondary analysis, neither fish consumption nor dietary alpha-linolenic acid was associated with MetS. CONCLUSIONS: Our findings do not support an association between dietary omega-3 fatty acids and MetS in a large US population.
    Clinical nutrition (Edinburgh, Scotland) 05/2013; · 3.27 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Apolipoprotein E allele 4 (apo ɛ4) and smoking each have been associated with an unfavorable lipid profile. We used data collected on 1,472 subjects in the National Heart, Lung, and Blood Institute Family Heart Study to assess whether smoking interacts with apo ɛ4 to influence the levels of plasma lipids. We dichotomized smoking and apo ɛ4 and used analysis of covariance to estimate the means of lipids. Smokers had lower body mass index, were younger, and consumed less fruits and vegetables. Among individuals without apo ɛ4, comparing nonsmokers with smokers, mean low density lipoprotein cholesterol (LDL) was 129.3 and 134.4 mg/dL, respectively, for women and 126.1 and 127.6 mg/dL, respectively, for men. Among subjects with an apo ɛ4 allele, corresponding means were 132.0, and 152.9 mg/dL, respectively, for women and 131.3 and 137.3 mg/dL, respectively, for men (P for interaction <0.001 for women and 0.11 for men). A similar interaction was observed for total cholesterol among women (P=0.02). This study shows a statistically significant effect modification of the relation of apo ɛ4 to LDL and total cholesterol by smoking among women. Smoking may enhance genetic susceptibility to an unfavorable lipid profile among subjects with apo ɛ4.
    Lipids 04/2012; 35(8):827-831. · 2.56 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We sought to examine whether ε4 carrier status modifies the relation between body mass index (BMI) and HDL. The National Heart, Lung, and Blood Institute Family Heart Study included 657 families with high family risk scores for coronary heart disease and 588 randomly selected families of probands in the Framingham, Atherosclerosis Risk in Communities, and Utah Family Health Tree studies. We selected 1402 subjects who had ε4 carrier status available. We used generalized estimating equations to examine the interaction between BMI and ε4 allele carrier status on HDL after adjusting for age, gender, smoking, alcohol intake, mono- and poly-unsaturated fat intake, exercise, comorbidities, LDL, and family cluster. The mean (standard deviation) age of included subjects was 56.4(11.0) years and 47% were male. Adjusted means of HDL for normal, overweight, and obese BMI categories were 51.2(± 0.97), 45.0(± 0.75), and 41.6(± 0.93), respectively, among 397 ε4 carriers (p for trend < 0.0001) and 53.6(± 0.62), 51.3(± 0.49), and 45.0(± 0.62), respectively, among 1005 non-carriers of the ε4 allele (p-value for trend < 0.0001). There was no evidence for an interaction between BMI and ε4 status on HDL(p-value 0.39). Our findings do not support an interaction between ε4 allele status and BMI on HDL.
    Lipids in Health and Disease 09/2011; 10:167. · 2.31 Impact Factor
  • R. Curtis Ellison
    [Show abstract] [Hide abstract]
    ABSTRACT: The recognition by scientists and the public of potential health effects of moderate drinking increased approximately two decades ago from reports of the so-called ‘French Paradox’: high levels of risk factors among the French but very low rates of coronary heart disease (CHD). Literally thousands of publications since then have confirmed that moderate drinking, especially of wine, is associated with a lower risk of many of the diseases of ageing. Further, a large number of mechanisms have been identified, including effects of drinking on blood lipids, endothelial function, coagulation, inflammation, glucose metabolism, and gene expression. When a national television program in the US in 1991 informed the public that moderate wine consumption may lower the risk of CHD, it was the first time that a reliable major news source had even suggested that there may be beneficial, rather than just harmful, effects of a beverage containing alcohol. This information immediately led a number of ‘scientists’ and ‘experts’ to attempt to explain the reported lower rates of CHD among the French by factors other than wine intake: the French do not know how to diagnose CHD; heart disease rates in France are no lower than in many other parts of the world (usually citing developing countries); the French do not consume a high-fat diet; even if there is less CHD, many more people die of alcohol abuse and we cannot encourage drinking. These criticisms have not stood the test of time. It is clear from an immense, and amazingly consistent, amount of research that moderate drinkers, especially of wine, have considerably lower rates of many diseases and live longer. For most middle-aged and older adults, unless there are contraindications to alcohol, moderate drinking can be considered as one component of a ‘healthy lifestyle’.
    Journal of Wine Research 07/2011; 22(2):105-108.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Epidemiologic studies have suggested beneficial effects of flavonoids on cardiovascular disease. Cocoa and particularly dark chocolate are rich in flavonoids and recent studies have demonstrated blood pressure lowering effects of dark chocolate. However, limited data are available on the association of chocolate consumption and the risk of coronary heart disease (CHD). We sought to examine the association between chocolate consumption and prevalent CHD. We studied in a cross-sectional design 4970 participants aged 25-93 years who participated in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. Chocolate intake was assessed through a semi-quantitative food frequency questionnaire. We used generalized estimating equations to estimate adjusted odds ratios. Compared to subjects who did not report any chocolate intake, odds ratios (95% CI) for CHD were 1.01 (0.76-1.37), 0.74 (0.56-0.98), and 0.43 (0.28-0.67) for subjects consuming 1-3 times/month, 1-4 times/week, and 5+ times/week, respectively (p for trend <0.0001) adjusting for age, sex, family CHD risk group, energy intake, education, non-chocolate candy intake, linolenic acid intake, smoking, alcohol intake, exercise, and fruit and vegetables. Consumption of non-chocolate candy was associated with a 49% higher prevalence of CHD comparing 5+/week vs. 0/week [OR = 1.49 (0.96-2.32)]. These data suggest that consumption of chocolate is inversely related with prevalent CHD in a general United States population.
    Clinical nutrition (Edinburgh, Scotland) 04/2011; 30(2):182-7. · 3.27 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: While a diet rich in anti-oxidant has been favorably associated with coronary disease and hypertension, limited data have evaluated the influence of such diet on subclinical disease. Thus, we sought to examine whether chocolate consumption is associated with calcified atherosclerotic plaque in the coronary arteries (CAC). In a cross-sectional design, we studied 2217 participants of the NHLBI Family Heart Study. Chocolate consumption was assessed by a semi-quantitative food frequency questionnaire and CAC was measured by cardiac CT. We defined prevalent CAC using an Agatston score of at least 100 and fitted generalized estimating equations to calculate prevalence odds ratios of CAC. There was an inverse association between frequency of chocolate consumption and prevalent CAC. Odds ratios (95% CI) for CAC were 1.0 (reference), 0.94 (0.66-1.35), 0.78 (0.53-1.13), and 0.68 (0.48-0.97) for chocolate consumption of 0, 1-3 times per month, once per week, and 2+ times per week, respectively (p for trend 0.022), adjusting for age, sex, energy intake, waist-hip ratio, education, smoking, alcohol consumption, ratio of total-to-HDL-cholesterol, non-chocolate candy, and diabetes mellitus. Controlling for additional confounders did not alter the findings. Exclusion of subjects with coronary heart disease or diabetes mellitus did not materially change the odds ratio estimates but did modestly decrease the overall significance (p = 0.07). These data suggest that chocolate consumption might be inversely associated with prevalent CAC.
    Clinical nutrition (Edinburgh, Scotland) 02/2011; 30(1):38-43. · 3.27 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: urate may have effects on vascular remodeling and atherosclerosis. We had shown an association between serum uric acid (SUA) and carotid atherosclerotic plaques. Inflammation and vascular remodeling in atherosclerosis promote coronary artery calcification (CAC), a preclinical marker for atherosclerosis. Here, we examined whether SUA is associated with CAC, using the same study sample and methods as for our previous carotid atherosclerosis study. the national Heart, Lung, and Blood Institute Family Heart Study is a multicenter study designed to assess risk factors for heart disease. Participants were recruited from population-based cohorts in the US states of Massachusetts, North Carolina, Minnesota, Utah, and Alabama. CAC was assessed with helical computed tomography (CT). We conducted sex-specific and family-cluster analyses, as well as additional analyses among persons without risk factors related to both cardiovascular disease and hyperuricemia, adjusting for potential confounders as we had in the previous study of carotid atherosclerosis. for the CAC study, 2412 subjects had both SUA and helical CT results available (55% women, age 58 ± 13 yrs, body mass index 27.6 ± 5.3). We found no association of SUA with CAC in men or women [OR in men: 1.0, 1.11, 0.86, 0.90; women: 1.0, 0.83, 1.00, 0.87 for increasing categories of SUA: < 5 (referent group), 5 to < 6, 6 to < 6.8, ≥ 6.8 mg/dl, respectively], nor in subgroup analyses. replicating the methods used to demonstrate an association of SUA with carotid atherosclerosis did not reveal any association between SUA and CAC, suggesting that SUA likely does not contribute to atherosclerosis through effects on arterial calcification. The possibility that urate has divergent pathophysiologic effects on atherosclerosis and artery calcification merits further study.
    The Journal of Rheumatology 10/2010; 38(1):111-7. · 3.26 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Both anxiety and elevated heart rate (HR) have been implicated in the development of hypertension. The HyperGen cohort, consisting of siblings with severe and mild hypertension, an age-matched random sample of persons from the same base populations, and unmedicated adult offspring of the hypertensive siblings (N = 1,002 men and 987 women), was analyzed for an association of the angiotenisinogen AGTM235T genotype (TT, MT, MM) with an endophenotype, heart rate (HR) in high and low anxious groups. The interaction of AGTM genotype with anxiety, which has been independently associated with hypertension, was investigated adjusting for age, hypertension status, smoking, alcohol consumption, beta blocker medication, body mass index, physical activity and hours of television viewing (sedentary life style). Although there was no main effect of genotype on HR in men or women, high anxious men with the TT genotype had high HR, whereas high anxious men with the MM genotype had low HR. In women, HR was inversely associated with anxiety but there was no interaction with genotype. The results suggest that high anxiety in men with the TT genotype may increase risk for hypertension whereas the MM genotype may be protective in high anxious men. This type of gene x environment interaction may be one reason why genome wide association studies sometimes fail to replicate. The locus may be important only in combination with certain environmental factors.
    PLoS ONE 01/2010; 5(10):e13353. · 3.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To determine whether alcohol consumption is associated with cardiovascular disease (CVD) among HIV-infected veterans. Using established thresholds for alcohol consumption, we analyzed cross-sectional data from 4743 men (51% HIV infected) from the Veterans Aging Cohort Study, a prospective cohort of HIV-infected veterans and demographically similar HIV-uninfected veterans. Using logistic regression, we estimated the odds ratio (OR) for the association between alcohol consumption and prevalent CVD. Among HIV-infected and HIV-uninfected men, respectively, hazardous drinking (33.2% vs. 30.9%,), alcohol abuse and dependence (20.9% vs. 26.2%), and CVD (14.6% vs. 19.8%) were common. Among HIV-infected men, hazardous drinking [OR = 1.43, 95% confidence interval (CI) = 1.05 to 1.94] and alcohol abuse and dependence (OR = 1.55, 95% CI = 1.07 to 2.23) were associated with a higher prevalence of CVD compared with infrequent and moderate drinking. Among HIV-uninfected men, past drinkers had a higher prevalence of CVD (OR = 1.30, 95% CI = 1.01 to 1.67). For HIV-infected and HIV-uninfected men, traditional risk factors and kidney disease were associated with CVD. Among HIV-infected men, hazardous drinking and alcohol abuse and dependence were associated with a higher prevalence of CVD compared with infrequent and moderate drinking even after adjusting for traditional CVD risk factors, antiretroviral therapy, and CD4 count.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 12/2009; 53(2):247-53. · 4.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this study was to assess the relationship between lifestyle factors and abdominal subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) in a community-based setting. Cross-sectional associations between lifestyle factors (dietary quality, physical activity, smoking, and alcohol consumption) and SAT and VAT volumes were examined in 2,926 Framingham Heart Study participants (48.6% women, aged 50 +/- 10 years). Diets consistent with the 2005 Dietary Guidelines Adherence Index and greater physical activity were inversely associated with SAT and VAT (P < 0.0001-0.002). In men, former smoking was associated with higher SAT (2,743 +/- 56 cm(3)) compared with current smokers (2,629 +/- 88 cm(3)) or those who never smoked (2,538 +/- 44 cm(3); P = 0.02). Both former and current smoking was associated with higher VAT (P = 0.03 [women]; P = 0.005 [men]). Women with high amounts of alcohol intake (>7 drinks/week) had lower SAT (2,869 +/- 106 cm(3)) than those who consumed less alcohol (3,184 +/- 44 cm(3), P = 0.006); significant differences in VAT were not observed (P = 0.18). In men, high amounts of alcohol intake (>14 drinks/week) were associated with higher VAT (2,272 +/- 59 cm(3)) compared with intake of <or=14 drinks/week (2,139 +/- 25 cm(3), P = 0.04), whereas SAT did not differ (P = 0.91). An increasing number of healthy lifestyle factors were associated with lower SAT and VAT volumes (all P < 0.003). Adherence to recommended dietary guidelines and physical activity are associated with lower SAT and VAT volumes. However, both smoking and high alcohol intake are differentially associated with VAT volumes. Further research to uncover the putative mechanisms is warranted.
    Diabetes care 12/2008; 32(3):505-10. · 7.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To examine the association of serum uric acid (SUA) with a marker of preclinical cardiovascular disease (CVD), carotid atherosclerotic plaques (PLQ), where early evidence of risk may be evident, focusing on individuals without CV risk factors. The National Heart, Lung, and Blood Institute Family Heart Study is a multicenter study designed to assess risk factors for heart disease. PLQ were assessed with carotid ultrasound. We conducted sex-specific logistic regression to assess the association of SUA with presence of PLQ, including analyses among persons without risk factors related to both CVD and hyperuricemia. In total, 4,866 participants had both SUA and carotid ultrasound assessed (54% women, mean age 52 yrs, mean body mass index 27.6). The association of SUA with PLQ increased with increasing SUA levels, demonstrating a dose-response relation for men [OR 1.0, 1.29, 1.61, 1.75, for SUA categories < 5 (reference), 5 to < 6, 6 to < 6.8, >or= 6.8 mg/dl, respectively; p = 0.002]. Similar associations were found in men without CV risk factors. We found no relation of SUA with PLQ in women. In this large study, SUA was associated with carotid atherosclerotic plaques in men. Results were similar in the absence of CV risk factors. These results suggest that SUA may have a pathophysiologic role in atherosclerosis in men.
    The Journal of Rheumatology 11/2008; 36(2):378-84. · 3.26 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of obesity and metabolic syndrome (MetS). Alanine aminotransferase (ALT) levels are used to detect NAFLD and have also been associated with increased risk for MetS, diabetes mellitus, and cardiovascular disease (CVD). We studied the relationship between ALT levels and these disorders in a long-term follow-up study. Framingham Offspring Heart Study participants (n = 2812; mean age, 44 years; 56% women) were followed for the development of MetS, diabetes, CVD, and all-cause mortality using logistic regression (MetS, diabetes) or Cox proportional hazards models (CVD, all-cause mortality). Among individuals at baseline, per 1 standard deviation increase in log ALT level, there were increased odds of the development of MetS (odds ratio [OR] 1.21, P < .001) and diabetes (OR, 1.48; P < .0001) over 20 years of follow-up. These findings also applied to participants with ALT levels within the normal range (MetS OR, 1.17; P = .006; diabetes OR, 1.34; P =.002). There was an increased risk of CVD in age/gender-adjusted models (hazard ratio, 1.23; P < .0001), but this was attenuated in multivariable-adjusted models (hazard ratio 1.05; P = .27); no association was observed for all-cause mortality. Aspartate aminotransferase levels were found to be associated with an increased risk of only diabetes. Both normal and increased levels of ALT are associated with long-term development of multiple metabolic disorders. These results indicate the potential for ALT values as biomarkers for the risk of metabolic disease.
    Gastroenterology 09/2008; 135(6):1935-44, 1944.e1. · 12.82 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Population trends in patterns of alcohol use are important data for policymakers but are generally based on repeated cross-sectional surveys. We used self-reported alcohol consumption data collected repeatedly over 50 years (1948-2003) among 8600 Framingham Heart Study participants to determine patterns of alcohol use and disorders according to sex, age, and birth cohorts. Among drinkers, there was a decrease across succeeding birth cohorts in average alcohol intake: among individuals between ages 30 and 59 years, age-adjusted mean intake was 30.6, 25.5, and 21.0 g/day for those born in 1900-1919, 1920-1939, and 1940-1959, respectively, in men (P<.001), and 14.2, 12.3, and 10.4 g/day, respectively, in women (P<.001). In all birth cohorts, proportion of abstinence increased and average consumption among drinkers decreased with age. Furthermore, proportion of moderate use was higher but heavy use was lower in the younger birth cohorts than in the older cohorts. The proportion of alcohol from beer decreased and that from wine increased with age for all cohorts. Among the 2 earlier birth cohorts, the cumulative incidence of an alcohol use disorder from age 40 to 79 years was much higher in men (12.8%) than in women (3.8%); it tended to be slightly higher among subjects born after 1920 than among those born 1900-1919. We found a decrease in average intake and more wine consumption over the more than 50 years of follow-up. The cumulative incidence of alcohol use disorders, however, did not show a decrease.
    The American journal of medicine 08/2008; 121(8):695-701. · 5.30 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is an important correlate of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. We sought to examine the relations between parental obesity and the serum ALT and AST levels among offspring in a community-based sample. Participants (n = 1732) of the Framingham Offspring Study (50% women; mean age, 42 years) who had serum ALT and AST measurements and both parents in the original Framingham cohort were studied. Study participants were grouped into early-onset parental obesity (n = 193) (at least one parent obese), later-onset parental obesity (n = 460), and no parental obesity (n = 1079) subgroups. The association between elevated ALT or AST levels and parental obesity was tested using generalized estimating equations to account for familial correlations. In multivariable analysis including adjustment for offspring obesity, significantly higher ALT levels were observed among individuals with paternal early-onset obesity as compared with those without paternal obesity (P = .02). Offspring with early-onset paternal obesity were more likely to have elevated ALT levels compared with those without paternal obesity (odds ratio, 1.75; 95% confidence interval, 1.06-2.89; P = .03). There was no association with elevated ALT levels among offspring with maternal early-onset obesity (odds ratio, 1.10; 95% confidence interval, 0.76-1.59; P = .61). There was no association between parental obesity and serum AST levels. Early-onset paternal obesity, but not maternal obesity, increases the odds of elevated serum ALT levels in offspring, suggesting a predisposition to developing elevated serum ALT levels that may be mediated through familial early-onset obesity.
    Gastroenterology 04/2008; 134(4):953-9. · 12.82 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Previous studies have suggested a positive association between phenotypes of fucosyltransferase 3 (FUT3) gene (also known as Lewis gene) and coronary heart disease. We used data on 1735 unrelated subjects in the Framingham Offspring Study to assess whether 3 functional single-nucleotide polymorphisms (SNPs) of the FUT3 gene (T59G, T1067A, and T202C) were associated with prevalent atherothrombotic disease. Contrary to T1067A and T202C SNPs, there was evidence for an association between T59G SNP and atherothrombotic disease prevalence. In a multivariable model controlling for age, sex, alcohol intake, pack-years of smoking, ratio of total to high-density lipoprotein cholesterol, and diabetes mellitus, ORs (95% CI) for prevalent atherothrombotic disease were 1.0 (reference), 0.80 (0.46-1.41), and 6.70 (1.95-23.01) for TT, TG, and GG genotypes of the T59G SNP, respectively. Minor alleles of T202C and T1067A SNPs showed a modest and nonsignificant association with atherothrombotic disease. Overall, FUT3 polymorphism that influences the enzyme activity (GG genotype for T59G or > or = 1 minor allele of T202C or T1067A) was associated with increased atherothrombotic disease prevalence (OR 1.57, 1.05-2.34), and this association was stronger among abstainers (2-fold increased odds) than among current drinkers (P for interaction .11). Our data suggest that functional mutations of the FUT3 gene may be associated with an increased atherothrombotic disease prevalence, especially among abstainers. Additional studies are warranted to confirm these findings.
    American heart journal 05/2007; 153(4):636-9. · 4.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Use of anti-hyperlipidemic medications compromises genetic analysis because of altered lipid profiles. We propose an empirical method to adjust lipid levels for medication effects so that the adjusted lipid values substitute the unmedicated lipid values in the genetic analysis. Published clinical trials were reviewed for HMG-CoA reductase inhibitors and fibric acid derivatives as mono-drug therapy. HMG-CoA reductase inhibitors showed similar effects in African Americans (AA) and non-African Americans (non-AA) for lowering total cholesterol (TC, -50.7 mg/dl), LDL cholesterol (LDL-C, -48.1 mg/dl), and triglycerides (TG, -19.7 mg/dl). Their effect on increasing HDL cholesterol (HDL-C) in AA (+0.4 mg/dl) was lower than in Non-AA (+2.3 mg/dl). The effects of fibric acid derivatives were estimated as -46.1 mg/dl for TC, -40.1 mg/dl for LDL-C, and +5.9 mg/dl for HDL-C in non-AA. The corresponding effects in AA were less extreme (-20.1 mg/dl, -11.4 mg/dl, and +3.1 mg/dl). Similar effect for TG (59.0 mg/dl) was shown in AA and non-AA. The above estimated effects were applied to a multipoint variance components linkage analysis on the lipid levels in 2,403 Whites and 2,214 AA in the HyperGEN study. The familial effects did vary depending on whether the lipids were adjusted for medication use. For example, the heritabilities increased after medication adjustment for TC and LDL-C, but did not change significantly for HDL-C and TG. Ethnicity-specific medication adjustments using our empirical method can be employed in epidemiological and genetic analysis of lipids.
    BMC Genetics 02/2007; 8:60. · 2.81 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    The American Journal of Cardiology 09/2006; 98(5):628-32. · 3.21 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    Hypertension 09/2006; 48(2):335-41. · 6.87 Impact Factor

Publication Stats

3k Citations
525.02 Total Impact Points

Institutions

  • 2000–2014
    • Boston University
      • • Section of Preventive Medicine and Epidemiology
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 1991–2014
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States
  • 2013
    • Sarawak General Hospital
      Seriki, Sarawak, Malaysia
  • 1997–2012
    • University of Massachusetts Boston
      • Clinical Epidemiology Research and Training Unit
      Boston, Massachusetts, United States
  • 2011
    • Partners HealthCare
      Boston, Massachusetts, United States
  • 2006–2011
    • Brigham and Women's Hospital
      • • Division of Aging
      • • Department of Medicine
      Boston, MA, United States
  • 2010
    • West Virginia University
      Morgantown, West Virginia, United States
  • 2008
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
    • University Medical Center Utrecht
      • Julius Center for Health Sciences and Primary Care
      Utrecht, Provincie Utrecht, Netherlands
  • 2004–2008
    • National Institutes of Health
      • • Branch of Liver Diseases Branch (LDB)
      • • Division of Epidemiology, Statistics and Prevention Research (DESPR)
      Bethesda, MD, United States
  • 2003–2006
    • University of Utah
      • Division of Cardiovascular Genetics
      Salt Lake City, UT, United States
  • 2005
    • University of Alabama at Birmingham
      • Department of Epidemiology
      Birmingham, AL, United States
    • Boston Medical Center
      Boston, Massachusetts, United States
    • University of Minnesota Duluth
      • Laboratory Medicine and Pathology
      Duluth, Minnesota, United States