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Curhan, Gary

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Curhan

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Gary

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Curhan, Gary
Author's Publications: search.filters.isAuthorOfPublication.da96f932-d292-44c8-bddd-3de890b595c8

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    Genetic Predisposition to High Blood Pressure Associates With Cardiovascular Complications Among Patients With Type 2 Diabetes: Two Independent Studies
    (American Diabetes Association, 2012) Qi, Qibin; Forman, John; Jensen, Majken; Flint, Alan; Curhan, Gary; Rimm, Eric; Hu, Frank; Qi, Lu
    Hypertension and type 2 diabetes (T2D) commonly coexist, and both conditions are major risk factors for cardiovascular disease (CVD). We aimed to examine the association between genetic predisposition to high blood pressure and risk of CVD in individuals with T2D. The current study included 1,005 men and 1,299 women with T2D from the Health Professionals Follow-up Study and Nurses’ Health Study, of whom 732 developed CVD. A genetic predisposition score was calculated on the basis of 29 established blood pressure–associated variants. The genetic predisposition score showed consistent associations with risk of CVD in men and women. In the combined results, each additional blood pressure–increasing allele was associated with a 6% increased risk of CVD (odds ratio [OR] 1.06 [95% CI 1.03–1.10]). The OR was 1.62 (1.22–2.14) for risk of CVD comparing the extreme quartiles of the genetic predisposition score. The genetic association for CVD risk was significantly stronger in patients with T2D than that estimated in the general populations by a meta-analysis (OR per SD of genetic score 1.22 [95% CI 1.10–1.35] vs. 1.10 [1.08–1.12]; I2 = 71%). Our data indicate that genetic predisposition to high blood pressure is associated with an increased risk of CVD in individuals with T2D.
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    Shorter length dialysis sessions are associated with increased mortality, independent of body weight
    (2012) Flythe, Jennifer E.; Curhan, Gary; Brunelli, Steven M.
    Hemodialysis patients have high rates of mortality that may be related to aspects of the dialytic procedure. In prior studies, shorter length dialysis sessions have been associated with decreased survival, but these studies may have been confounded by body size differences. Here we tested whether in-center thrice-weekly hemodialysis patients with adequate urea clearances but shorter dialysis session length is associated with mortality independent of body size. Data were taken from a large national cohort of patients from a large dialysis organization undergoing thrice-weekly, in-center hemodialysis. In the primary analysis, patients with prescribed dialysis sessions greater and less than 240 minutes were pair-matched on post-dialysis weight as well as on age, gender, and vascular access type. Compared to prescribed longer dialysis sessions, session lengths less than 240 minutes were significantly associated with increased all-cause mortality (adjusted hazard ratio 1.26). The association was consistent across strata of age, gender, and dialysis post-weight. Secondary analyses found a dose-response between prescribed session length and survival. Thus, among patients with adequate urea clearance, shorter dialysis session lengths are associated with increased mortality independent of body weight.
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    Psoriasis and risk of type 2 diabetes among women and men in the United States: a population-based cohort study
    (2011) Li, Wenqing; Han, Jiali; Hu, Frank; Curhan, Gary; Qureshi, Abrar A.
    Type 2 diabetes (T2D) shares some common risk factors with psoriasis. We evaluated the association between psoriasis and risk of incident T2D among women and men in the United States in a mixed retrospective-prospective cohort study. 184,395 participants were included from an older cohort of women (the Nurses’ Health Study, NHS) (1996–2008), a younger cohort of women (NHS II) (1991–2007) and an older cohort of men (Health Professionals’ Follow-Up Study, HPFS) (1986–2006). During 2,700,958 person-years of follow-up, 9,938 incident T2D cases were confirmed. We found a significantly increased risk of T2D associated with psoriasis only among younger women (NHS II); multivariate-adjusted relative risk (RR) (95% confidence interval (CI)) was 1.25 1.05–1.49). When only including those younger than 60 years during follow-up (NHS and HPFS), we observed a non-significant trend toward increased risk for T2D. In a pooled-analysis of the three cohorts, psoriatics younger than 60 years were at a higher risk of T2D; RR 1.26 (1.08–1.48) for women, and 1.26 (1.08–1.46) for both sexes combined. Further, the risk of T2D was much higher for those developing psoriasis at an early age. In conclusion, we found an association between psoriasis and risk of T2D among individuals younger than 60 years.
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    Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies
    (BMJ Publishing Group Ltd., 2014) Qi, Qibin; Chu, Audrey Yu-lei; Kang, Jae Hee; Huang, Jinyan; Rose, Lynda M; Jensen, Majken; Liang, Liming; Curhan, Gary; Pasquale, Louis; Wiggs, Janey; De Vivo, Immaculata; Chan, Andrew; Choi, Hyon K; Tamimi, Rulla; Ridker, Paul; Hunter, David; Willett, Walter; Rimm, Eric; Chasman, Daniel; Hu, Frank; Qi, Lu
    Objective: To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity. Design: Prospective cohort study. Setting: Health professionals in the United States. Participants: 9623 women from the Nurses’ Health Study, 6379 men from the Health Professionals Follow-up Study, and a replication cohort of 21 421 women from the Women’s Genome Health Study. Main outcome measure Repeated measurement of BMI over follow-up. Results: There was an interaction between fried food consumption and a genetic risk score based on 32 BMI-associated variants on BMI in both the Nurses’ Health Study and Health Professionals Follow-up Study (P≤0.001 for interaction). Among participants in the highest third of the genetic risk score, the differences in BMI between individuals who consumed fried foods four or more times a week and those who consumed fried foods less than once a week amounted to 1.0 (SE 0.2) in women and 0.7 (SE 0.2) in men, whereas the corresponding differences were 0.5 (SE 0.2) and 0.4 (SE 0.2) in the lowest third of the genetic risk score. The gene-diet interaction was replicated in the Women’s Genome Health Study (P<0.001 for interaction). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.1 (SE 0.2), 1.6 (SE 0.3), and 2.2 (SE 0.6) for fried food consumption less than once, one to three times, and four or more times a week (P<0.001 for interaction); and the odds ratios (95% confidence intervals) for obesity per 10 risk alleles were 1.61 (1.40 to 1.87), 2.12 (1.73 to 2.59), and 2.72 (2.12 to 3.48) across the three categories of consumption (P=0.002 for interaction). In addition, the variants in or near genes highly expressed or known to act in the central nervous system showed significant interactions with fried food consumption, with the FTO (fat mass and obesity associated) variant showing the strongest result (P<0.001 for interaction). Conclusion: Our findings suggest that consumption of fried food could interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity.
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    Gene × Physical Activity Interactions in Obesity: Combined Analysis of 111,421 Individuals of European Ancestry
    (Public Library of Science, 2013) Ahmad, Shafqat; Rukh, Gull; Varga, Tibor V.; Ali, Ashfaq; Kurbasic, Azra; Shungin, Dmitry; Ericson, Ulrika; Koivula, Robert W.; Chu, Audrey Yu-lei; Rose, Lynda M.; Ganna, Andrea; Qi, Qibin; Stančáková, Alena; Sandholt, Camilla H.; Elks, Cathy E.; Curhan, Gary; Jensen, Majken; Tamimi, Rulla; Allin, Kristine H.; Jørgensen, Torben; Brage, Soren; Langenberg, Claudia; Aadahl, Mette; Grarup, Niels; Linneberg, Allan; Paré, Guillaume; Magnusson, Patrik K. E.; Pedersen, Nancy L.; Boehnke, Michael; Hamsten, Anders; Mohlke, Karen L.; Pasquale, Louis; Pedersen, Oluf; Scott, Robert A.; Ridker, Paul; Ingelsson, Erik; Laakso, Markku; Hansen, Torben; Qi, Lu; Wareham, Nicholas J.; Chasman, Daniel; Hallmans, Göran; Hu, Frank; Renström, Frida; Orho-Melander, Marju; Franks, Paul W.
    Numerous obesity loci have been identified using genome-wide association studies. A UK study indicated that physical activity may attenuate the cumulative effect of 12 of these loci, but replication studies are lacking. Therefore, we tested whether the aggregate effect of these loci is diminished in adults of European ancestry reporting high levels of physical activity. Twelve obesity-susceptibility loci were genotyped or imputed in 111,421 participants. A genetic risk score (GRS) was calculated by summing the BMI-associated alleles of each genetic variant. Physical activity was assessed using self-administered questionnaires. Multiplicative interactions between the GRS and physical activity on BMI were tested in linear and logistic regression models in each cohort, with adjustment for age, age2, sex, study center (for multicenter studies), and the marginal terms for physical activity and the GRS. These results were combined using meta-analysis weighted by cohort sample size. The meta-analysis yielded a statistically significant GRS × physical activity interaction effect estimate (Pinteraction = 0.015). However, a statistically significant interaction effect was only apparent in North American cohorts (n = 39,810, Pinteraction = 0.014 vs. n = 71,611, Pinteraction = 0.275 for Europeans). In secondary analyses, both the FTO rs1121980 (Pinteraction = 0.003) and the SEC16B rs10913469 (Pinteraction = 0.025) variants showed evidence of SNP × physical activity interactions. This meta-analysis of 111,421 individuals provides further support for an interaction between physical activity and a GRS in obesity disposition, although these findings hinge on the inclusion of cohorts from North America, indicating that these results are either population-specific or non-causal.
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    A Large Cohort Study of Hypothyroidism and Hyperthyroidism in Relation to Gynecologic Cancers
    (Hindawi Publishing Corporation, 2013) Kang, Jae H.; Kueck, Angela S.; Stevens, Richard; Curhan, Gary; De Vivo, Immaculata; Rosner, Bernard; Alexander, Erik; Tworoger, Shelley
    Background:. Thyroid status may influence tumorigenesis of gynecologic cancers, yet epidemiologic studies of this relationship are limited and inconsistent. Methods:. We evaluated the association of self-reported history of physician-diagnosed hypothyroidism and hyperthyroidism with medical-record confirmed endometrial (EC; all invasive adenocarcinomas) and ovarian cancer (OC; epithelial ovarian or peritoneal cancers) in Nurses' Health Study (NHS) from 1976 to 2010 and NHSII from 1989 to 2011. Cox proportional hazard models were used to estimate multivariable rate ratios (RRs) and 95% confidence intervals based on pooled cohort data. Results:. We confirmed 1314 incident cases of EC and 1150 cases of OC. Neither a history of hypothyroidism nor hyperthyroidism was significantly associated with risk of EC or OC. However, having a history of hypothyroidism for 8+ years (median) was nonsignificantly inversely associated with EC (RR = 0.81; 95% CI = 0.63–1.04; P-trend with history duration = 0.11) and OC (RR = 0.87, 95% CI = 0.66–1.15; P-trend = 0.13). Having a history of hyperthyroidism for 6+ years (median) was non-significantly positively associated with EC (RR = 1.69; 95% CI = 0.86–3.30; P-trend = 0.12) but not OC (RR = 1.12; 95% CI = 0.46–2.72; P-trend = 0.95). Conclusions:. A history of hypothyroidism or hyperthyroidism was not significantly associated with risk of EC or OC.
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    Birth weight and later life adherence to unhealthy lifestyles in predicting type 2 diabetes: prospective cohort study
    (BMJ Publishing Group Ltd., 2015) Li, Yanping; Ley, Sylvia; Tobias, Deirdre; Chiuve, Stephanie; VanderWeele, Tyler; Rich-Edwards, Janet; Curhan, Gary; Willett, Walter; Manson, JoAnn; Hu, Frank; Qi, Lu
    Objectives To prospectively assess the joint association of birth weight and established lifestyle risk factors in adulthood with incident type 2 diabetes and to quantitatively decompose the attributing effects to birth weight only, to adulthood lifestyle only, and to their interaction. Design: Prospective cohort study. Setting: Health Professionals Follow-up Study (1986-2010), Nurses’ Health Study (1980-2010), and Nurses’ Health Study II (1991-2011). Participants: 149 794 men and women without diabetes, cardiovascular disease, or cancer at baseline. Main outcome measure Incident cases of type 2 diabetes, identified through self report and validated by a supplementary questionnaire. Unhealthy lifestyle was defined on the basis of body mass index, smoking, physical activity, alcohol consumption, and the alternate healthy eating index. Results: During 20-30 years of follow-up, 11 709 new cases of type 2 diabetes were documented. The multivariate adjusted relative risk of type 2 diabetes was 1.45 (95% confidence interval 1.32 to 1.59) per kg lower birth weight and 2.10 (1.71 to 2.58) per unhealthy lifestyle factor. The relative risk of type 2 diabetes associated with a combination of per kg lower birth weight and per unhealthy lifestyle factor was 2.86 (2.26 to 3.63), which was more than the addition of the risk associated with each individual factor, indicating a significant interaction on an additive scale (P for interaction<0.001). The attributable proportions of joint effect were 22% (95% confidence interval 18.3% to 26.4%) to lower birth weight alone, 59% (57.1% to 61.5%) to unhealthy lifestyle alone, and 18% (13.9% to 21.3%) to their interaction. Conclusion: Most cases of type 2 diabetes could be prevented by the adoption of a healthier lifestyle, but simultaneous improvement of both prenatal and postnatal factors could further prevent additional cases.
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    Obesity susceptibility loci and uncontrolled eating, emotional eating and cognitive restraint behaviors in men and women
    (2013) Cornelis, Marilyn; Rimm, Eric; Curhan, Gary; Kraft, Phillip; Hunter, David; Hu, Frank; Van Dam, Rob
    Objective: Many confirmed genetic loci for obesity are expressed in regions of the brain that regulate energy intake and reward-seeking behavior. Whether these loci contribute to the development of specific eating behaviors has not been investigated. We examined the relationship between a genetic susceptibility to obesity and cognitive restraint, uncontrolled and emotional eating. Design and Methods Eating behavior and body mass index (BMI) were determined by questionnaires for 1471 men and 2381 women from two U.S cohorts. Genotypes were extracted from genome-wide scans and a genetic-risk score (GRS) derived from 32 obesity-loci was calculated. Results: The GRS was positively associated with emotional and uncontrolled eating(P<0.002). In exploratory analysis, BMI-increasing variants of MTCH2, TNNI3K and ZC3H4 were positively associated with emotional eating and those of TNNI3K and ZC3H4 were positively associated with uncontrolled eating. The BMI-increasing variant of FTO was positively and those of LRP1B and TFAP2B were inversely associated with cognitive restraint. These associations for single SNPs were independent of BMI but were not significant after multiple-testing correction. Conclusions: An overall genetic susceptibility to obesity may also extend to eating behaviors. The link between specific loci and obesity may be mediated by eating behavior but larger studies are warranted to confirm these results.
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    1000 Genomes-based meta-analysis identifies 10 novel loci for kidney function
    (Nature Publishing Group, 2017) Gorski, Mathias; van der Most, Peter J.; Teumer, Alexander; Chu, Audrey Y.; Li, Man; Mijatovic, Vladan; Nolte, Ilja M.; Cocca, Massimiliano; Taliun, Daniel; Gomez, Felicia; Li, Yong; Tayo, Bamidele; Tin, Adrienne; Feitosa, Mary F.; Aspelund, Thor; Attia, John; Biffar, Reiner; Bochud, Murielle; Boerwinkle, Eric; Borecki, Ingrid; Bottinger, Erwin P.; Chen, Ming-Huei; Chouraki, Vincent; Ciullo, Marina; Coresh, Josef; Cornelis, Marilyn C.; Curhan, Gary; d’Adamo, Adamo Pio; Dehghan, Abbas; Dengler, Laura; Ding, Jingzhong; Eiriksdottir, Gudny; Endlich, Karlhans; Enroth, Stefan; Esko, Tõnu; Franco, Oscar H.; Gasparini, Paolo; Gieger, Christian; Girotto, Giorgia; Gottesman, Omri; Gudnason, Vilmundur; Gyllensten, Ulf; Hancock, Stephen J.; Harris, Tamara B.; Helmer, Catherine; Höllerer, Simon; Hofer, Edith; Hofman, Albert; Holliday, Elizabeth G.; Homuth, Georg; Hu, Frank; Huth, Cornelia; Hutri-Kähönen, Nina; Hwang, Shih-Jen; Imboden, Medea; Johansson, Åsa; Kähönen, Mika; König, Wolfgang; Kramer, Holly; Krämer, Bernhard K.; Kumar, Ashish; Kutalik, Zoltan; Lambert, Jean-Charles; Launer, Lenore J.; Lehtimäki, Terho; de Borst, Martin; Navis, Gerjan; Swertz, Morris; Liu, Yongmei; Lohman, Kurt; Loos, Ruth J. F.; Lu, Yingchang; Lyytikäinen, Leo-Pekka; McEvoy, Mark A.; Meisinger, Christa; Meitinger, Thomas; Metspalu, Andres; Metzger, Marie; Mihailov, Evelin; Mitchell, Paul; Nauck, Matthias; Oldehinkel, Albertine J.; Olden, Matthias; WJH Penninx, Brenda; Pistis, Giorgio; Pramstaller, Peter P.; Probst-Hensch, Nicole; Raitakari, Olli T.; Rettig, Rainer; Ridker, Paul; Rivadeneira, Fernando; Robino, Antonietta; Rosas, Sylvia; Ruderfer, Douglas; Ruggiero, Daniela; Saba, Yasaman; Sala, Cinzia; Schmidt, Helena; Schmidt, Reinhold; Scott, Rodney J.; Sedaghat, Sanaz; Smith, Albert V.; Sorice, Rossella; Stengel, Benedicte; Stracke, Sylvia; Strauch, Konstantin; Toniolo, Daniela; Uitterlinden, Andre G.; Ulivi, Sheila; Viikari, Jorma S.; Völker, Uwe; Vollenweider, Peter; Völzke, Henry; Vuckovic, Dragana; Waldenberger, Melanie; Jin Wang, Jie; Yang, Qiong; Chasman, Daniel; Tromp, Gerard; Snieder, Harold; Heid, Iris M.; Fox, Caroline S.; Köttgen, Anna; Pattaro, Cristian; Böger, Carsten A.; Fuchsberger, Christian
    HapMap imputed genome-wide association studies (GWAS) have revealed >50 loci at which common variants with minor allele frequency >5% are associated with kidney function. GWAS using more complete reference sets for imputation, such as those from The 1000 Genomes project, promise to identify novel loci that have been missed by previous efforts. To investigate the value of such a more complete variant catalog, we conducted a GWAS meta-analysis of kidney function based on the estimated glomerular filtration rate (eGFR) in 110,517 European ancestry participants using 1000 Genomes imputed data. We identified 10 novel loci with p-value < 5 × 10−8 previously missed by HapMap-based GWAS. Six of these loci (HOXD8, ARL15, PIK3R1, EYA4, ASTN2, and EPB41L3) are tagged by common SNPs unique to the 1000 Genomes reference panel. Using pathway analysis, we identified 39 significant (FDR < 0.05) genes and 127 significantly (FDR < 0.05) enriched gene sets, which were missed by our previous analyses. Among those, the 10 identified novel genes are part of pathways of kidney development, carbohydrate metabolism, cardiac septum development and glucose metabolism. These results highlight the utility of re-imputing from denser reference panels, until whole-genome sequencing becomes feasible in large samples.
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    A comprehensive survey of genetic variation in 20,691 subjects from four large cohorts
    (Public Library of Science, 2017) Lindström, Sara; Loomis, Stephanie; Turman, Constance; Huang, Hongyan; Huang, Jinyan; Aschard, Hugues; Chan, Andrew; Choi, Hyon; Cornelis, Marilyn; Curhan, Gary; De Vivo, Immaculata; Eliassen, A; Fuchs, Charles; Gaziano, Michael; Hankinson, Susan; Hu, Frank; Jensen, Majken; Kang, Jae Hee; Kabrhel, Christopher; Liang, Liming; Pasquale, Louis; Rimm, Eric; Stampfer, Meir; Tamimi, Rulla; Tworoger, Shelley; Wiggs, Janey; Hunter, David; Kraft, Phillip
    The Nurses’ Health Study (NHS), Nurses’ Health Study II (NHSII), Health Professionals Follow Up Study (HPFS) and the Physicians Health Study (PHS) have collected detailed longitudinal data on multiple exposures and traits for approximately 310,000 study participants over the last 35 years. Over 160,000 study participants across the cohorts have donated a DNA sample and to date, 20,691 subjects have been genotyped as part of genome-wide association studies (GWAS) of twelve primary outcomes. However, these studies utilized six different GWAS arrays making it difficult to conduct analyses of secondary phenotypes or share controls across studies. To allow for secondary analyses of these data, we have created three new datasets merged by platform family and performed imputation using a common reference panel, the 1,000 Genomes Phase I release. Here, we describe the methodology behind the data merging and imputation and present imputation quality statistics and association results from two GWAS of secondary phenotypes (body mass index (BMI) and venous thromboembolism (VTE)). We observed the strongest BMI association for the FTO SNP rs55872725 (β = 0.45, p = 3.48x10-22), and using a significance level of p = 0.05, we replicated 19 out of 32 known BMI SNPs. For VTE, we observed the strongest association for the rs2040445 SNP (OR = 2.17, 95% CI: 1.79–2.63, p = 2.70x10-15), located downstream of F5 and also observed significant associations for the known ABO and F11 regions. This pooled resource can be used to maximize power in GWAS of phenotypes collected across the cohorts and for studying gene-environment interactions as well as rare phenotypes and genotypes.