J Michael Gaziano

Harvard Medical School, Boston, Massachusetts, United States

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Publications (463)4090.65 Total impact

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    ABSTRACT: We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 × 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 × 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 × 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 × 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 × 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 × 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.
    Nature genetics. 08/2014;
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    ABSTRACT: Genome-wide association studies (GWAS) have mapped risk alleles for at least ten distinct cancers to a small region of 63,000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (ASSET) across six distinct cancers in 34,248 cases and 45,036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single nucleotide polymorphisms (SNPs): five in the TERT gene (region 1: rs7726159, P=2.10x10-39; region 3: rs2853677, P=3.30x10-36 and PConditional=2.36x10-8; region 4: rs2736098, P=3.87x10-12 and PConditional=5.19x10-6, region 5: rs13172201, P=0.041 and PConditional=2.04x10-6; and region 6: rs10069690, P=7.49x10-15 and PConditional=5.35x10-7) and one in the neighboring CLPTM1L gene (region 2: rs451360; P=1.90x10-18 and PConditional=7.06x10-16). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele specific effects on DNA methylation were seen for a subset of risk loci indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.
    Human Molecular Genetics 07/2014; · 7.69 Impact Factor
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    ABSTRACT: Recent posttrial analysis of a completed randomized trial found an increased risk of prostate cancer among healthy men taking high-dose vitamin E supplements. Trials that examined the effect of vitamin C supplements on cancer risk are few.OBJECTIVE: We examined whether vitamin E or vitamin C supplementation affects the risk of cancer events during posttrial follow-up of the Physicians' Health Study II.DESIGN: Beginning in 1997, a total of 14,641 US male physicians aged ≥50 y were randomly assigned to receive 400 IU of vitamin E every other day, 500 mg of vitamin C daily, or their respective placebos. The vitamin E and vitamin C treatment ended in 2007, and observational follow-up continued through June 2011.RESULTS: This study included an additional 356 cases of incident prostate cancer and 771 total cancers that developed during a mean (maximum) of 2.8 (3.8) y of posttrial observation. During an overall mean of 10.3 (13.8) y, there were a total of 1373 incident prostate cancers and 2669 total cancers documented. In comparison with placebo, vitamin E supplementation had no effect on the incidence of prostate cancer (HR: 0.99; 95% CI: 0.89, 1.10) or total cancers (HR: 1.02; 95% CI: 0.95, 1.10). There was also no effect of vitamin C supplementation on total cancers (HR: 1.02; 95% CI: 0.94, 1.10) or incident prostate cancer (HR: 1.03; 95% CI: 0.93, 1.15). Neither vitamin E nor vitamin C supplementation had effects on other site-specific cancers overall. Stratification by known cancer risk factors, history of cancer, other randomized treatment, and follow-up time showed no significant interactions.Conclusion: In this large-scale randomized trial in men, vitamin E and C supplementation had no immediate or long-term effects on the risk of total cancers, prostate cancer, or other site-specific cancers. This trial was registered at clinicaltrials.gov as NCT00270647.
    American Journal of Clinical Nutrition 07/2014; · 6.50 Impact Factor
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    ABSTRACT: Background: The prevalence of class III obesity (body mass index [BMI]$40 kg/m 2) has increased dramatically in several countries and currently affects 6% of adults in the US, with uncertain impact on the risks of illness and death. Using data from a large pooled study, we evaluated the risk of death, overall and due to a wide range of causes, and years of life expectancy lost associated with class III obesity.
    PLoS Medicine 07/2014; 16(21). · 15.25 Impact Factor
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    ABSTRACT: The Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed higher prostate cancer incidence in men supplemented with high-dose α-tocopherol. We therefore examined whether pre-supplementation plasma α-tocopherol or γ-tocopherol was associated with overall or high-grade prostate cancer. A stratified case-cohort sample that included 1,746 incident prostate cancer cases diagnosed through June, 2009 and a subcohort of 3,211 men was derived from the SELECT trial of 35,533 men. Plasma was collected at entry in 2001-2004, and median follow-up was 5.5 years (range, 0 - 7.9 years). Incidence of prostate cancer as a function of plasma α-tocopherol, γ-tocopherol, and supplementation with α-tocopherol or selenomethionine was estimated by the hazard ratio (HR). Plasma γ-tocopherol was not associated with prostate cancer. Men with higher α-tocopherol concentrations appeared to have risk similar to that of men with lower concentrations [overall HR for fifth (Q5) vs. first quintile (Q1), 1.21 (95% confidence interval (CI), 0.88-1.66, P-trend=0.24; in the trial placebo arm, Q5 HR, 0.85, 95% CI, 0.44-1.62, P-trend=0.66]. We found a strong positive plasma α-tocopherol association among men receiving the trial selenomethionine supplement [Q5 HR, 2.04, 95% CI, 1.29-3.22; P-trend=0.005]. A positive plasma α-tocopherol-prostate cancer association also appeared limited to high-grade disease (Gleason grade 7-10, overall Q5 HR, 1.59, 95% CI, 1.13-2.24, P-trend=0.001; among men receiving selenomethionine, HR, 2.12, 95% CI, 1.32-3.40; P-trend=0.0002). Our findings indicate that higher plasma α-tocopherol concentrations may interact with selenomethionine supplements to increase high-grade prostate cancer risk, suggesting a biological interaction between α-tocopherol and selenium itself or selenomethionine.
    Cancer prevention research (Philadelphia, Pa.). 06/2014;
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    ABSTRACT: Multiple myeloma (MM) is a rare but highly fatal malignancy. High body weight is associated with this cancer, but several questions remain regarding the aetiological relevance of timing and location of body weight. To address these questions, we conducted a pooled analysis of MM mortality using 1·5 million participants (including 1388 MM deaths) from 20 prospective cohorts in the National Cancer Institute Cohort Consortium. Proportional hazards regression was used to calculate pooled multivariate hazard ratios (HRs) and 95% confidence intervals (CIs). Associations with elevated MM mortality were observed for higher early-adult body mass index (BMI; HR = 1·22, 95% CI: 1·09-1·35 per 5 kg/m(2) ) and for higher cohort-entry BMI (HR 1·09, 95% CI: 1·03-1·16 per 5 kg/m(2) ) and waist circumference (HR = 1·06, 95% CI: 1·02-1·10 per 5 cm). Women who were the heaviest, both in early adulthood (BMI 25+) and at cohort entry (BMI 30+) were at greater risk compared to those with BMI 18·5 ≤ 25 at both time points (HR = 1·95, 95% CI: 1·33-2·86). Waist-to-hip ratio and height were not associated with MM mortality. These observations suggest that overall, and possibly also central, obesity influence myeloma mortality, and women have the highest risk of death from this cancer if they remain heavy throughout adulthood.
    British Journal of Haematology 05/2014; · 4.94 Impact Factor
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    ABSTRACT: The insulin-like growth factor (IGF) signaling pathway has been implicated in prostate cancer (PCa) initiation, but its role in progression remains unknown. Among 5887 PCa patients (704 PCa deaths) of European ancestry from seven cohorts in the National Cancer Institute Breast and Prostate Cancer Cohort Consortium, we conducted Cox kernel machine pathway analysis to evaluate whether 530 tagging single nucleotide polymorphisms (SNPs) in 26 IGF pathway-related genes were collectively associated with PCa mortality. We also conducted SNP-specific analysis using stratified Cox models adjusting for multiple testing. In 2424 patients (313 PCa deaths), we evaluated the association of prediagnostic circulating IGF1 and IGFBP3 levels and PCa mortality. All statistical tests were two-sided. The IGF signaling pathway was associated with PCa mortality (P = .03), and IGF2-AS and SSTR2 were the main contributors (both P = .04). In SNP-specific analysis, 36 SNPs were associated with PCa mortality with P trend less than .05, but only three SNPs in the IGF2-AS remained statistically significant after gene-based corrections. Two were in linkage disequilibrium (r (2) = 1 for rs1004446 and rs3741211), whereas the third, rs4366464, was independent (r (2) = 0.03). The hazard ratios (HRs) per each additional risk allele were 1.19 (95% confidence interval [CI] = 1.06 to 1.34; P trend = .003) for rs3741211 and 1.44 (95% CI = 1.20 to 1.73; P trend < .001) for rs4366464. rs4366464 remained statistically significant after correction for all SNPs (P trend.corr = .04). Prediagnostic IGF1 (HRhighest vs lowest quartile = 0.71; 95% CI = 0.48 to 1.04) and IGFBP3 (HR = 0.93; 95% CI = 0.65 to 1.34) levels were not associated with PCa mortality. The IGF signaling pathway, primarily IGF2-AS and SSTR2 genes, may be important in PCa survival.
    CancerSpectrum Knowledge Environment 05/2014; · 14.07 Impact Factor
  • AHA EPI/NPAM Scientific Sessions 2014; 03/2014
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    ABSTRACT: Over the last 2 decades, observational evidence largely supports an association between light to moderate alcohol consumption (up to 1 drink per day in women and up to 2 drinks per day in men) and a lower risk of cardiovascular disease (CVD), largely driven by a reduction in coronary heart disease. Most studies suggest a nadir in risk in the light to moderate range of alcohol intake, which is then countered by an increase in cardiomyopathy, sudden death, and hemorrhagic stroke at higher drinking levels that offsets potential benefits. The mechanisms of cardioprotective effects of alcohol are complex and there are multiple pathways by which moderate alcohol consumption reduces the risk of CVD. Recent evidence continues to emerge on the physiologic and genetic mechanisms through which alcohol may reduce the risk of developing CVD. Ongoing debate also lingers whether there are important differences in cardiovascular effects according to alcoholic beverage type (beer vs red wine vs liquor). Another emerging area of interest is the role of alcohol consumption on the development of intermediate cardiovascular endpoints such as hypertension and diabetes that lead to the development of CVD as well as other important cardiovascular sequelae. Alcohol consumption has also been shown to impact the risk of other CVD endpoints including congestive heart failure, alcoholic cardiomyopathy, atrial fibrillation, and peripheral artery disease. Overall, alcohol still carries significant public health implications given its plausible benefits on CVD along with its well-documented adverse effects, warranting continued caution and a discussion with one's primary care provider regarding intake.
    Journal of cardiopulmonary rehabilitation and prevention 03/2014; · 1.59 Impact Factor
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    ABSTRACT: The Randomized Endo-vein Graft Prospective (REGROUP) trial (ClinicalTrials.gov NCT01850082) is a randomized, intent-to-treat, 2-arm, parallel-design, multicenter study funded by the Cooperative Studies Program (CSP No. 588) of the US Department of Veterans Affairs. Cardiac surgeons at 16 Veterans Affairs (VA) medical centers with technical expertise in performing both endoscopic vein harvesting (EVH) and open vein harvesting (OVH) were recruited as the REGROUP surgeon participants. Subjects requiring elective or urgent coronary artery bypass grafting using cardiopulmonary bypass with use of ≥1 saphenous vein graft will be screened for enrollment using pre-established inclusion/exclusion criteria. Enrolled subjects (planned N = 1150) will be randomized to 1 of the 2 arms (EVH or OVH) after an experienced vein harvester has been assigned. The primary outcomes measure is the rate of major adverse cardiac events (MACE), including death, myocardial infarction, or revascularization. Subject assessments will be performed at multiple times, including at baseline, intraoperatively, postoperatively, and at discharge (or 30 days after surgery, if still hospitalized). Assessment of leg-wound complications will be completed at 6 weeks after surgery. Telephone follow-ups will occur at 3-month intervals after surgery until the participating sites are decommissioned after the trial's completion (approximately 4.5 years after the full study startup). To assess long-term outcomes, centralized follow-up of MACE for 2 additional years will be centrally performed using VA and non-VA clinical and administrative databases. The primary MACE outcome will be compared between the 2 arms, EVH and OVH, at the end of the trial duration.
    Clinical Cardiology 03/2014; · 1.83 Impact Factor
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    ABSTRACT: The etiology of male breast cancer is poorly understood, partly because of its relative rarity. Although genetic factors are involved, less is known regarding the role of anthropometric and hormonally related risk factors. In the Male Breast Cancer Pooling Project, a consortium of 11 case-control and 10 cohort investigations involving 2405 case patients (n = 1190 from case-control and n = 1215 from cohort studies) and 52013 control subjects, individual participant data were harmonized and pooled. Unconditional logistic regression generated study design-specific (case-control/cohort) odds ratios (ORs) and 95% confidence intervals (CIs), with exposure estimates combined using fixed effects meta-analysis. All statistical tests were two-sided. Risk was statistically significantly associated with weight (highest/lowest tertile: OR = 1.36; 95% CI = 1.18 to 1.57), height (OR = 1.18; 95% CI = 1.01 to 1.38), and body mass index (BMI; OR = 1.30; 95% CI = 1.12 to 1.51), with evidence that recent rather than distant BMI was the strongest predictor. Klinefelter syndrome (OR = 24.7; 95% CI = 8.94 to 68.4) and gynecomastia (OR = 9.78; 95% CI = 7.52 to 12.7) were also statistically significantly associated with risk, relations that were independent of BMI. Diabetes also emerged as an independent risk factor (OR = 1.19; 95% CI = 1.04 to 1.37). There were also suggestive relations with cryptorchidism (OR = 2.18; 95% CI = 0.96 to 4.94) and orchitis (OR = 1.43; 95% CI = 1.02 to 1.99). Although age at onset of puberty and histories of infertility were unrelated to risk, never having had children was statistically significantly related (OR = 1.29; 95% CI = 1.01 to 1.66). Among individuals diagnosed at older ages, a history of fractures was statistically significantly related (OR = 1.41; 95% CI = 1.07 to 1.86). Consistent findings across case-control and cohort investigations, complemented by pooled analyses, indicated important roles for anthropometric and hormonal risk factors in the etiology of male breast cancer. Further investigation should focus on potential roles of endogenous hormones.
    CancerSpectrum Knowledge Environment 02/2014; · 14.07 Impact Factor
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    ABSTRACT: Objectives. We investigated the association between body mass index (BMI) and mortality among Asian Americans. Methods. We pooled data from prospective cohort studies with 20 672 Asian American adults with no baseline cancer or heart disease history. We estimated hazard ratios and 95% confidence intervals (CIs) with Cox proportional hazards models. Results. A high, but not low, BMI was associated with increased risk of total mortality among individuals aged 35 to 69 years. The BMI was not related to total mortality among individuals aged 70 years and older. With a BMI 22.5 to < 25 as the reference category among never-smokers aged 35 to 69 years, the hazard ratios for total mortality were 0.83 (95% CI = 0.47, 1.47) for BMI 15 to < 18.5; 0.91 (95% CI = 0.62, 1.32) for BMI 18.5 to < 20; 1.08 (95% CI = 0.86, 1.36) for BMI 20 to < 22.5; 1.14 (95% CI = 0.90, 1.44) for BMI 25 to < 27.5; 1.13 (95% CI = 0.79, 1.62) for BMI 27.5 to < 30; 1.82 (95% CI = 1.25, 2.64) for BMI 30 to < 35; and 2.09 (95% CI = 1.06, 4.11) for BMI 35 to 50. Higher BMI was also related to increased cardiovascular disease and cancer mortality. Conclusions. High BMI is associated with increased mortality risk among Asian Americans. (Am J Public Health. Published online ahead of print January 16, 2014: e1-e6. doi:10.2105/AJPH.2013.301573).
    American Journal of Public Health 01/2014; · 3.93 Impact Factor
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    ABSTRACT: Studies have previously examined the relation between a single measure of plasma fatty acids and risk of heart failure. However, it is unclear whether the use of repeated measures of fatty acids over time is required for the assessment of omega-3 fatty acids heart failure relation. Using a nested case-control design, this ancillary study used 421 cases and 421 matched controls from the Physicians' Health Study to assess the variability of plasma phospholipid fatty acids over time and compare the results of omega-3 fatty acids heart failure associations using a single versus repeated measurements of plasma phospholipid fatty acids. Plasma omega-3 fatty acids were measured at baseline (1982) and approximately 15 years later using gas chromatography. Spearman's correlation coefficients between baseline and follow-up measures of α-linolenic acid (ALA), EPA, DPA, and DHA were 0.20, 0.45, 0.28, and 0.50, respectively, in the control series. Multivariable adjusted odds ratios for heart failure per standard deviation higher plasma ALA were 0.98 (95 % CI 0.85-1.13) when using baseline ALA and 0.86 (95 % CI 0.74-1.01) when using the average of baseline and follow-up ALA measurements. Corresponding odds ratios for total long chain omega-3 FAs (EPA + DHA + DPA) were 0.87 (0.73-1.03) and 0.88 (0.75-1.04). Our data demonstrate modest correlation between measurements of plasma phospholipid fatty acids spaced by 15 years. A single measurement of plasma phospholipid fatty acids appears reasonable to estimate the risk of heart failure over long-term follow-up.
    European Journal of Nutrition 01/2014; · 3.13 Impact Factor
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    ABSTRACT: Screening and diagnosis of prostate cancer (PCa) is hampered by an inability to predict who has the potential to develop fatal disease and who has indolent cancer. Studies have identified multiple genetic risk loci for PCa incidence, but it is unknown whether they could be used as biomarkers for PCa-specific mortality (PCSM). To examine the association of 47 established PCa risk single-nucleotide polymorphisms (SNPs) with PCSM. We included 10 487 men who had PCa and 11 024 controls, with a median follow-up of 8.3 yr, during which 1053 PCa deaths occurred. The main outcome was PCSM. The risk allele was defined as the allele associated with an increased risk for PCa in the literature. We used Cox proportional hazards regression to calculate the hazard ratios of each SNP with time to progression to PCSM after diagnosis. We also used logistic regression to calculate odds ratios for each risk SNP, comparing fatal PCa cases to controls. Among the cases, we found that 8 of the 47 SNPs were significantly associated (p<0.05) with time to PCSM. The risk allele of rs11672691 (intergenic) was associated with an increased risk for PCSM, while 7 SNPs had risk alleles inversely associated (rs13385191 [C2orf43], rs17021918 [PDLIM5], rs10486567 [JAZF1], rs6465657 [LMTK2], rs7127900 (intergenic), rs2735839 [KLK3], rs10993994 [MSMB], rs13385191 [C2orf43]). In the case-control analysis, 22 SNPs were associated (p<0.05) with the risk of fatal PCa, but most did not differentiate between fatal and nonfatal PCa. Rs11672691 and rs10993994 were associated with both fatal and nonfatal PCa, while rs6465657, rs7127900, rs2735839, and rs13385191 were associated with nonfatal PCa only. Eight established risk loci were associated with progression to PCSM after diagnosis. Twenty-two SNPs were associated with fatal PCa incidence, but most did not differentiate between fatal and nonfatal PCa. The relatively small magnitudes of the associations do not translate well into risk prediction, but these findings merit further follow-up, because they may yield important clues about the complex biology of fatal PCa. In this report, we assessed whether established PCa risk variants could predict PCSM. We found eight risk variants associated with PCSM: One predicted an increased risk of PCSM, while seven were associated with decreased risk. Larger studies that focus on fatal PCa are needed to identify more markers that could aid prediction.
    European Urology 01/2014; · 10.48 Impact Factor
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    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. 01/2014;
  • Andrew B. Petrone, J. Michael Gaziano, Luc Djoussé
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    ABSTRACT: The 5-year risk of death following onset of heart failure (HF) is about 50%. While previous studies have shown beneficial effects of light-to-moderate alcohol consumption and risk of cardiovascular diseases and mortality, it is unclear whether moderate alcohol consumption is associated with a lower risk of death in HF subjects. We investigated whether alcohol consumption and type of alcohol preference are associated with risk of total mortality in 449 US male physicians with prevalent HF. Alcohol consumption was assessed via food frequency questionnaire, and mortality was ascertained via annual follow up questionnaires and adjudicated by an Endpoint Committee. The mean age of subjects was 75.7 ± 8.2 years with an average follow up of 7 years. We found evidence of a J-shaped relation between alcohol consumption and mortality [HR (95% CI): 1.00 (ref), 0.85 (0.61-1.20), 0.60 (0.40-0.88), and 0.71 (0.42-1.21), for alcohol intake of none, <1/day, 1-2/day, and 3+/day respectively (p for quadratic trend: 0.058)]. There was no relation between beverage preference (beer, wine, or liquor) and mortality. In conclusion, our data showed a J-shaped association between alcohol intake and mortality in patients with HF.
    The American Journal of Cardiology. 01/2014;
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    ABSTRACT: Inflammatory processes have been associated with an increased risk of atrial fibrillation (AF), potentially allowing for preventive therapy by anti-inflammatory agents such as aspirin. However, the effect of chronic aspirin on the incidence of AF has not been evaluated in a prospective cohort followed for an extended period.
    Journal of the American Heart Association. 01/2014; 3(4).
  • Eric D Peterson, J Michael Gaziano, Philip Greenland
    JAMA The Journal of the American Medical Association 12/2013; · 29.98 Impact Factor
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    ABSTRACT: -Adult height has been hypothesized to be inversely associated with coronary heart disease but studies have produced conflicting results. We sought to examine the relationship between adult height and the prevalence of coronary artery calcium (CAC), a direct measure of subclinical atherosclerosis and surrogate marker of CHD. Method and Results-We evaluated the relationship between adult height and CAC in 2,703 participants from the NHLBI Family Heart Study who underwent cardiac computed tomography. We used generalized estimating equations to calculate the prevalence odds ratios for the presence of CAC (CAC>0) across sex-specific quartiles of height. The mean age of the sample was 54.8 years and 60.2% were female. There was an inverse association between adult height and CAC. After adjusting for age, race, field center, waist circumference, smoking, alcohol, physical activity, systolic blood pressure, antihypertensive medications, diabetes, diabetic medications, LDL cholesterol, HDL cholesterol, lipid-lowering medications, and income, individuals in the tallest quartile had 30% lower odds of having prevalent CAC. The odds ratios (95% CI) for the presence of CAC across consecutive sex-specific quartiles of height were 1.0 (reference), 1.15 (0.86-1.53), 0.95(0.73-1.22), and 0.70 (0.53-0.93), p for trend <0.01. There was no evidence of effect modification for the relationship between adult height and CAC by age or socioeconomic status. -The results of our study suggest an inverse, independent association between adult height and CAC.
    Circulation Cardiovascular Imaging 12/2013; · 5.80 Impact Factor
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    ABSTRACT: We sought to test the hypothesis that plasma galectin 3 (Gal-3) is positively associated with the risk of heart failure (HF) in male subjects. While Gal-3 has been reported as prognostic factor in HF patients, limited data are available on the role of Gal-3 in the development of HF. We used a prospective nested-case control study (n = 462 cases and 462 controls) within the Physicians' Health Study for current analyses. For each case of HF, we randomly selected one control among subjects that were alive and free of HF at the time of index case occurrence and matched on age, race, and time of blood collection. Gal-3 was measured using ELISA and we used conditional logistic regression to compute adjusted odds ratios. Mean age at baseline was 58.3 y and median log-Gal-3 was 1.50 (IQR: 1.20-1.73) ng/ml. Cubic splines suggested a non-linear relation between Gal-3 and HF. Odds ratios (95% CI) for HF were 1.0 (ref), 0.89 (0.58-1.38), 1.08 (0.71-1.67), and 1.57 (1.03-2.39) across consecutive quartiles of Gal-3 after adjustment for body mass index, diabetes, atrial fibrillation, hypertension, C-reactive protein, alcohol, smoking, and exercise. The Gal-3-HF relation was seen for HF with and without antecedent coronary heart disease. Our data are consistent with a positive non-linear association between Gal-3 and HF risk in male subjects.
    European Journal of Heart Failure 12/2013; · 5.25 Impact Factor

Publication Stats

20k Citations
4,090.65 Total Impact Points

Institutions

  • 1991–2014
    • Harvard Medical School
      • • Department of Medicine
      • • Division of Nutrition
      Boston, Massachusetts, United States
    • Brigham and Women's Hospital
      • • Division of Preventive Medicine
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 2013
    • University of Minnesota Duluth
      • Laboratory Medicine and Pathology
      Duluth, Minnesota, United States
  • 2010–2013
    • Imperial College London
      • • Department of Epidemiology and Biostatistics
      • • Department of Primary Care and Public Health
      London, ENG, United Kingdom
    • Dana-Farber Cancer Institute
      • Department of Medical Oncology
      Boston, MA, United States
    • Mayo Clinic - Rochester
      • Department of Health Science Research
      Rochester, MN, United States
  • 2012
    • University of Iowa
      Iowa City, Iowa, United States
    • University of Ioannina
      • Department of Hygiene and Epidemiology
      Yannina, Epirus, Greece
    • University of Texas MD Anderson Cancer Center
      Houston, Texas, United States
  • 2011–2012
    • Dartmouth–Hitchcock Medical Center
      Lebanon, New Hampshire, United States
    • Brown University
      • Department of Epidemiology
      Providence, Rhode Island, United States
    • Boston University
      Boston, Massachusetts, United States
  • 2009–2012
    • National Cancer Institute (USA)
      • • Division of Cancer Epidemiology and Genetics
      • • Laboratory of Experimental Immunology
      Bethesda, MD, United States
    • Medical College of Wisconsin
      • Department of Medicine
      Milwaukee, WI, United States
  • 2005–2012
    • Cornell University
      • • Division of Nutritional Sciences (DNS)
      • • Department of Nutritional Sciences
      Ithaca, NY, United States
  • 1994–2012
    • Harvard University
      • • Department of Epidemiology
      • • Department of Nutrition
      Boston, MA, United States
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States
  • 2007–2011
    • University of Southern California
      • Department of Preventive Medicine
      Los Angeles, CA, United States
    • Rutgers New Jersey Medical School
      • Department of Epidemiology
      Newark, NJ, United States
    • Columbia University
      • Division of General Medicine
      New York City, NY, United States
    • Stanford University
      • Department of Medicine
      Stanford, CA, United States
  • 2005–2011
    • Overton Brooks VA Medical Center
      Shreveport, Louisiana, United States
  • 2002–2011
    • Beth Israel Deaconess Medical Center
      • Department of Medicine
      Boston, Massachusetts, United States
    • Partners HealthCare
      Boston, Massachusetts, United States
    • University of Zurich
      • Internal Medicine Unit
      Zürich, ZH, Switzerland
    • University of California, San Francisco
      • Department of Epidemiology and Biostatistics
      San Francisco, CA, United States
  • 2008–2010
    • University of California, Los Angeles
      • Department of Epidemiology
      Los Angeles, CA, United States
    • Providence Portland Medical Center
      Portland, Oregon, United States
  • 2006–2009
    • U.S. Department of Veterans Affairs
      • Office of Research and Development (ORD)
      Washington, D. C., DC, United States
  • 2004–2007
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
    • Walter Reed National Military Medical Center
      Washington, Washington, D.C., United States
    • University of Missouri
      Columbia, Missouri, United States
    • Saint Vincent Hospital
      Worcester, Massachusetts, United States
  • 2003
    • Northwestern University
      • Department of Preventive Medicine
      Evanston, IL, United States
  • 1999
    • University of Massachusetts Medical School
      • Meyers Primary Care Institute
      Worcester, MA, United States
  • 1996
    • Whitaker Wellness Institute
      Newport Beach, California, United States
    • Wageningen University
      Wageningen, Gelderland, Netherlands