Person: Djousse, Luc
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Djousse
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Luc
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Djousse, Luc
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Publication Television Viewing Time, Physical Activity, and Mortality Among African Americans(Centers for Disease Control and Prevention, 2018) Imran, Tasnim F.; Ommerborn, Mark; Clark, Cheryl; Correa, Adolfo; Dubbert, Patricia; Gaziano, John; Djousse, LucBackground: Prolonged television viewing time, a marker of sedentary activity, is independently associated with increased all-cause mortality; however, this association has rarely been studied in African Americans. The objective of our study was to examine the association between television viewing time and mortality among African Americans by using data from the Jackson Heart Study (JHS). Methods: We studied 5,289 participants from the JHS study who reported television viewing time (h/day) in the JHS baseline questionnaire from 2000 through 2004. Using multivariable Cox regression models adjusted for age, sex, smoking, alcohol use, physical activity, nutrition, prevalent coronary heart disease, chronic kidney disease, diabetes, and hypertension, we computed hazard ratios to examine the association between television viewing time (≤2 h/day, 2–4 h/day, and ≥4 h/day) and mortality. Results: Participants had a mean age of 55 years, and 64% were women. After a median follow-up of 9.9 years (interquartile range, 9.0–10.7), 615 deaths occurred (data analysis conducted in 2017). Hazard ratios for mortality were 1.08 (0.86–1.37) for television time of 2 to 4 hours per day and 1.48 (95% CI: 1.19–1.83) for television time of greater than or equal to 4 hours per day when compared with those who watched television less than 2 hours per day (P trend = .002). When we restricted analyses to those who performed leisure-time activities, the hazard ratios for mortality were 1.10 (95% CI, 0.84–1.45) for television viewing of 2 to 4 hours per day and 1.45 (95% CI, 1.13–1.86) for more than 4 hours per day compared with the less than 2 hours per day. Conclusion: Our findings suggest that greater television viewing time, even among those who perform leisure-time physical activities, is associated with increased all-cause mortality among African Americans. Thus, it may serve as an indicator of a sedentary lifestyle with potential for intervention.Publication Association between adiponectin and heart failure risk in the Physicians' Health Study(2012) Djousse, Luc; Wilk, Jemma; Hanson, Naomi Q.; Glynn, Robert; Tsai, Michael Y.; Gaziano, J. MichaelLimited data are available on the association between adiponectin and incident heart failure. In the current ancillary study to the Physicians' Health Study, we used a prospective nested-case control design to examine whether plasma adiponectin concentration was related to the risk of heart failure. We selected 787 incident heart failure cases and 787 matched controls for the current analysis. Each control was selected using a risk set sampling technique at the time of the occurrence of the index case and matched on year of birth, age at blood collection, and race. Adiponectin was measured using ELISA. Heart failure occurrence was self-reported in annual follow-up questionnaire. Validation of self-reported heart failure in this cohort has been published. The mean age was 58.7 years. In a conditional logistic regression adjusting for age, race, time of blood collection, year of birth, hypertension, atrial fibrillation, smoking, alcohol intake, and exercise, estimates of the relative risk (95% confidence interval) were 1.0 (ref), 0.74 (0.53–1.04), 0.67 (0.48–0.94), 0.70 (0.50–0.99), and 0.92 (0.65–1.30) from the lowest to the highest quintile of adiponectin, respectively, p for quadratic trend 0.004. Additional adjustment for potential mediating factors including diabetes, C-reactive protein, and body mass index led to the attenuation of the estimate of effect [1.0 (ref), 0.81 (0.57–1.15), 0.75 (0.53–1.06), 0.83 (0.58–1.18), and 1.26 (0.87–1.81) across consecutive quintiles of adiponectin]. Our data are consistent with a J-shaped association between total adiponectin and the risk of heart failure among US male physicians.Publication Is Plasma Pentadecanoic Acid a Reasonable Biomarker of Dairy Consumption?(Blackwell Publishing Ltd, 2013) Djousse, LucPublication Dietary Magnesium and Genetic Interactions in Diabetes and Related Risk Factors: A Brief Overview of Current Knowledge(MDPI, 2013) Hruby, Adela; McKeown, Nicola M.; Song, Yiqing; Djousse, LucNutritional genomics has exploded in the last decade, yielding insights—both nutrigenomic and nutrigenetic—into the physiology of dietary interactions and our genes. Among these are insights into the regulation of magnesium transport and homeostasis and mechanisms underlying magnesium’s role in insulin and glucose handling. Recent observational evidence has attempted to examine some promising research avenues on interaction between genetics and dietary magnesium in relation to diabetes and diabetes risk factors. This brief review summarizes the recent evidence on dietary magnesium’s role in diabetes and related traits in the presence of underlying genetic risk, and discusses future potential research directions.Publication Plasma Fatty Acid Binding Protein 4 and Risk of Sudden Cardiac Death in Older Adults(Hindawi Publishing Corporation, 2013) Djousse, Luc; Maziarz, Marlena; Biggs, Mary L.; Ix, Joachim H.; Zieman, Susan J.; Kizer, Jorge R.; Lemaitre, Rozenn N.; Mozaffarian, Dariush; Tracy, Russell P.; Mukamal, Kenneth; Siscovick, David S.; Sotoodehnia, NonaAlthough fatty acid binding protein 4 (FABP4) may increase risk of diabetes and exert negative cardiac inotropy, it is unknown whether plasma concentrations of FABP4 are associated with incidence of sudden cardiac death (SCD). We prospectively analyzed data on 4,560 participants of the Cardiovascular Health Study. FABP4 was measured at baseline using ELISA, and SCD events were adjudicated through review of medical records. We used Cox proportional hazards to estimate effect measures. During a median followup of 11.8 years, 146 SCD cases occurred. In a multivariable model adjusting for demographic, lifestyle, and metabolic factors, relative risk of SCD associated with each higher standard deviation (SD) of plasma FABP4 was 1.15 (95% CI: 0.95–1.38), P = 0.15. In a secondary analysis stratified by prevalent diabetes status, FABP4 was associated with higher risk of SCD in nondiabetic participants, (RR per SD higher FABP4: 1.33 (95% CI: 1.07–1.65), P = 0.009) but not in diabetic participants (RR per SD higher FABP4: 0.88 (95% CI: 0.62–1.27), P = 0.50), P for diabetes-FABP4 interaction 0.049. In summary, a single measure of plasma FABP4 obtained later in life was not associated with the risk of SCD in older adults overall. Confirmation of our post-hoc results in nondiabetic people in other studies is warranted.Publication Gene × dietary pattern interactions in obesity: analysis of up to 68 317 adults of European ancestry(Oxford University Press, 2015) Nettleton, Jennifer A.; Follis, Jack L.; Ngwa, Julius S.; Smith, Caren E.; Ahmad, Shafqat; Tanaka, Toshiko; Wojczynski, Mary K.; Voortman, Trudy; Lemaitre, Rozenn N.; Kristiansson, Kati; Nuotio, Marja-Liisa; Houston, Denise K.; Perälä, Mia-Maria; Qi, Qibin; Sonestedt, Emily; Manichaikul, Ani; Kanoni, Stavroula; Ganna, Andrea; Mikkilä, Vera; North, Kari E.; Siscovick, David S.; Harald, Kennet; Mckeown, Nicola M.; Johansson, Ingegerd; Rissanen, Harri; Liu, Yongmei; Lahti, Jari; Hu, Frank; Bandinelli, Stefania; Rukh, Gull; Rich, Stephen; Booij, Lisanne; Dmitriou, Maria; Ax, Erika; Raitakari, Olli; Mukamal, Kenneth; Männistö, Satu; Hallmans, Göran; Jula, Antti; Ericson, Ulrika; Jacobs,, David R.; Van Rooij, Frank J. A.; Deloukas, Panos; Sjögren, Per; Kähönen, Mika; Djousse, Luc; Perola, Markus; Barroso, Inês; Hofman, Albert; Stirrups, Kathleen; Viikari, Jorma; Uitterlinden, André G.; Kalafati, Ioanna P.; Franco, Oscar H.; Mozaffarian, Dariush; Salomaa, Veikko; Borecki, Ingrid B.; Knekt, Paul; Kritchevsky, Stephen B.; Eriksson, Johan G.; Dedoussis, George V.; Qi, Lu; Ferrucci, Luigi; Orho-Melander, Marju; Zillikens, M. Carola; Ingelsson, Erik; Lehtimäki, Terho; Renström, Frida; Cupples, L. Adrienne; Loos, Ruth J. F.; Franks, PaulObesity is highly heritable. Genetic variants showing robust associations with obesity traits have been identified through genome-wide association studies. We investigated whether a composite score representing healthy diet modifies associations of these variants with obesity traits. Totally, 32 body mass index (BMI)- and 14 waist–hip ratio (WHR)-associated single nucleotide polymorphisms were genotyped, and genetic risk scores (GRS) were calculated in 18 cohorts of European ancestry (n = 68 317). Diet score was calculated based on self-reported intakes of whole grains, fish, fruits, vegetables, nuts/seeds (favorable) and red/processed meats, sweets, sugar-sweetened beverages and fried potatoes (unfavorable). Multivariable adjusted, linear regression within each cohort followed by inverse variance-weighted, fixed-effects meta-analysis was used to characterize: (a) associations of each GRS with BMI and BMI-adjusted WHR and (b) diet score modification of genetic associations with BMI and BMI-adjusted WHR. Nominally significant interactions (P = 0.006–0.04) were observed between the diet score and WHR-GRS (but not BMI-GRS), two WHR loci (GRB14 rs10195252; LYPLAL1 rs4846567) and two BMI loci (LRRN6C rs10968576; MTIF3 rs4771122), for the respective BMI-adjusted WHR or BMI outcomes. Although the magnitudes of these select interactions were small, our data indicated that associations between genetic predisposition and obesity traits were stronger with a healthier diet. Our findings generate interesting hypotheses; however, experimental and functional studies are needed to determine their clinical relevance.Publication Genetically Elevated Fetuin-A Levels, Fasting Glucose Levels, and Risk of Type 2 Diabetes: The Cardiovascular Health Study*(American Diabetes Association, 2013) Jensen, Majken; Bartz, Traci M.; Djousse, Luc; Kizer, Jorge R.; Zieman, Susan J.; Rimm, Eric; Siscovick, David S.; Psaty, Bruce M.; Ix, Joachim H.; Mukamal, KennethOBJECTIVE Fetuin-A levels are associated with higher risk of type 2 diabetes, but it is unknown if the association is causal. We investigated common (>5%) genetic variants in the fetuin-A gene (AHSG) fetuin-A levels, fasting glucose, and risk of type 2 diabetes. RESEARCH DESIGN AND METHODS Genetic variation, fetuin-A levels, and fasting glucose were assessed in 2,893 Caucasian and 542 African American community-living individuals 65 years of age or older in 1992–1993. RESULTS Common AHSG variants (rs4917 and rs2248690) were strongly associated with fetuin-A concentrations (P < 0.0001). In analyses of 259 incident cases of type 2 diabetes, the single nucleotide polymorphisms (SNPs) were not associated with diabetes risk during follow-up and similar null associations were observed when 579 prevalent cases were included. As expected, higher fetuin-A levels were associated with higher fasting glucose concentrations (1.9 mg/dL [95% CI, 1.2–2.7] higher per SD in Caucasians), but Mendelian randomization analyses using both SNPs as unbiased proxies for measured fetuin-A did not support an association between genetically predicted fetuin-A levels and fasting glucose (−0.3 mg/dL [95% CI, −1.9 to 1.3] lower per SD in Caucasians). The difference between the associations of fasting glucose with actual and genetically predicted fetuin-A level was statistically significant (P = 0.001). Results among the smaller sample of African Americans trended in similar directions but were statistically insignificant. CONCLUSIONS Common variants in the AHSG gene are strongly associated with plasma fetuin-A concentrations, but not with risk of type 2 diabetes or glucose concentrations, raising the possibility that the association between fetuin-A and type 2 diabetes may not be causal.Publication Plasma Phospholipid Saturated Fatty Acids and Incident Atrial Fibrillation: The Cardiovascular Health Study(Blackwell Publishing Ltd, 2014) Fretts, Amanda M.; Mozaffarian, Dariush; Siscovick, David S.; Djousse, Luc; Heckbert, Susan R.; King, Irena B.; McKnight, Barbara; Sitlani, Colleen; Sacks, Frank; Song, Xiaoling; Sotoodehnia, Nona; Spiegelman, Donna; Wallace, Erin R.; Lemaitre, Rozenn N.Background: Prior studies suggest that circulating fatty acids may influence the risk of atrial fibrillation (AF), but little is known about the associations of circulating saturated fatty acids with risk of AF. Methods and Results: The study population included 2899 participants from the Cardiovascular Health Study, a community‐based longitudinal cohort of adults aged 65 years or older in the United States who were free of prevalent coronary heart disease and AF in 1992. Cox regression was used to assess the association of all the long‐chain saturated fatty acids—palmitic acid (16:0), stearic acid (18:0), arachidic acid (20:0), behenic acid (22:0), and lignoceric acid (24:0)—with incident AF. During a median of 11.2 years of follow‐up, 707 cases of incident AF occurred. After adjustment for other AF risk factors, higher levels of circulating 16:0 were associated with a higher risk of AF (hazard ratio comparing highest and lowest quartiles: 1.48; 95% CI: 1.18, 1.86). In contrast, higher levels of circulating 18:0, 20:0, 22:0, and 24:0 were each associated with a lower risk of AF. The hazard ratios (95% CI) for AF in the top and bottom quartiles were 0.76 (95% CI: 0.61, 0.95) for 18:0; 0.78 (95% CI: 0.63, 0.97) for 20:0; 0.62 (95% CI: 0.50, 0.78) for 22:0; and 0.68 (95% CI: 0.55, 0.85) for 24:0. Conclusions: Results from this prospective cohort study of older adults demonstrate divergent associations of circulating 16:0 versus longer‐chain saturated fatty acids with incident AF, highlighting the need to investigate both determinants of these levels and potential pathways of the observed differential risk.Publication Aspirin Use and Risk of Atrial Fibrillation in the Physicians' Health Study(Blackwell Publishing Ltd, 2014) Ofman, Peter; Petrone, Andrew B.; Peralta, Adelqui; Hoffmeister, Peter; Albert, Christine; Djousse, Luc; Gaziano, John; Rahilly‐Tierney, Catherine R.Background: 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. Methods and Results: This study was comprised of a prospective cohort of 23 480 male participants of the Physicians' Health Study. Aspirin intake and covariates were estimated using self‐reported questionnaires. Incident AF was ascertained through yearly follow‐up questionnaires. Cox's regression, with adjustment for multiple covariates, was used to estimate relative risk of AF. Average age at baseline was 65.1±8.9 years. During a mean follow‐up of 10.0 years, 2820 cases of AF were reported. Age‐standardized incidence rates were 12.6, 11.1, 12.7, 11.3, 15.8, and 13.8/1000 person‐years for people reporting baseline aspirin intake of 0, <14 days per year, 14 to 30 days per year, 30 to 120 days per year, 121 to 180 days per year, and >180 days per year, respectively. Multivariable adjusted hazard ratios (95% confidence interval) for incident AF were 1.00 (reference), 0.88 (0.76 to 1.02), 0.93 (0.76 to 1.14), 0.96 (0.80 to 1.14), 1.07 (0.80 to 1.14), and 1.04 (0.94 to 1.15) across consecutive categories of aspirin intake. Analysis of the data using time‐varying Cox's regression model to update aspirin intake over time showed similar results. Conclusions: In a large cohort of males followed for a long period, we did not find any association between aspirin use and incident AF.Publication Fried Food Consumption and Cardiovascular Health: A Review of Current Evidence(MDPI, 2015) Gadiraju, Taraka V.; Patel, Yash; Gaziano, John; Djousse, LucFried food consumption and its effects on cardiovascular disease are still subjects of debate. The objective of this review was to summarize current evidence on the association between fried food consumption and cardiovascular disease, diabetes, hypertension and obesity and to recommend directions for future research. We used PubMed, Google Scholar and Medline searches to retrieve pertinent publications. Most available data were based on questionnaires as a tool to capture fried food intakes, and study design was limited to case-control and cohort studies. While few studies have reported a positive association between frequencies of fried food intake and risk of coronary artery disease, heart failure, diabetes or hypertension, other investigators have failed to confirm such an association. There is strong evidence suggesting a higher risk of developing chronic disease when fried foods are consumed more frequently (i.e., four or more times per week). Major gaps in the current literature include a lack of detailed information on the type of oils used for frying foods, stratification of the different types of fried food, frying procedure (deep and pan frying), temperature and duration of frying, how often oils were reused and a lack of consideration of overall dietary patterns. Besides addressing these gaps, future research should also develop tools to better define fried food consumption at home versus away from home and to assess their effects on chronic diseases. In summary, the current review provides enough evidence to suggest adverse health effects with higher frequency of fried food consumption. While awaiting confirmation from future studies, it may be advisable to the public to consume fried foods in moderation while emphasizing an overall healthy diet.