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1. Alcohol Intake and Risk of Lethal Prostate Cancer in the Health Professionals Follow-Up Study.

Author

Downer, Mary K, Kenfield, Stacey A, Stampfer, Meir J, Wilson, Kathryn M, Dickerman, Barbra A, Giovannucci, Edward L, Rimm, Eric B, Wang, Molin, Mucci, Lorelei A, Willett, Walter C, Chan, June M, and Van Blarigan, Erin L

Subjects
Humans, Prostatic Neoplasms, Neoplasm Staging, Proportional Hazards Models, Risk, Cohort Studies, Follow-Up Studies, Prospective Studies, Alcohol Drinking, Health Occupations, Adult, Aged, Middle Aged, United States, Male, Prevention, Alcoholism, Alcohol Use and Health, Clinical Research, Substance Misuse, Cancer, Aging, Urologic Diseases, Prostate Cancer, Good Health and Well Being, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeIt is unknown whether alcohol intake is associated with the risk of lethal (metastatic or fatal) prostate cancer. We examine (1) whether alcohol intake among men at risk of prostate cancer is associated with diagnosis of lethal prostate cancer and (2) whether intake among men with nonmetastatic prostate cancer is associated with metastasis or death.MethodsThis prospective cohort study uses the Health Professionals Follow-Up Study (1986 to 2012). Our analysis of alcohol intake among men at risk of prostate cancer included 47,568 cancer-free men. Our analysis of alcohol intake among men with prostate cancer was restricted to 5,182 men diagnosed with nonmetastatic prostate cancer during follow-up. We examine the association of total alcohol, red and white wine, beer, and liquor with lethal prostate cancer and death. Multivariate Cox proportional hazards regression estimated hazard ratios (HRs) and 95% CIs.ResultsAlcohol drinkers had a lower risk of lethal prostate cancer (any v none: HR, 0.84 [95% CI, 0.71 to 0.99]) without a dose-response relationship. Total alcohol intake among patients with prostate cancer was not associated with progression to lethal prostate cancer (any v none: HR, 0.99 [95% CI, 0.57 to 1.72]), whereas moderate red wine intake was associated with a lower risk (any v none: HR, 0.50 [95% CI, 0.29 to 0.86]; P trend = .05). Compared with none, 15 to 30 g/d of total alcohol after prostate cancer diagnosis was associated with a lower risk of death (HR, 0.71 [95% CI, 0.50 to 1.00]), as was red wine (any v none: HR, 0.74 [95% CI, 0.57 to 0.97]; P trend = .007).ConclusionCancer-free men who consumed alcohol had a slightly lower risk of lethal prostate cancer compared with abstainers. Among men with prostate cancer, red wine was associated with a lower risk of progression to lethal disease. These observed associations merit additional study but provide assurance that moderate alcohol consumption is safe for patients with prostate cancer.

Published
2019

2. A prospective study of aspirin use and prostate cancer risk by TMPRSS2:ERG status

Author

Stopsack, Konrad H, Gonzalez-Feliciano, Amparo G, Peisch, Samuel F, Downer, Mary K, Gage, Riley A, Finn, Stephen, Lis, Rosina T, Graff, Rebecca E, Pettersson, Andreas, Pernar, Claire H, Loda, Massimo, Kantoff, Philip W, Ahearn, Thomas U, and Mucci, Lorelei A

Subjects
Biomedical and Clinical Sciences, Health Sciences, Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Prevention, Prostate Cancer, Genetics, Urologic Diseases, Cancer, Aging, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Adult, Aged, Anti-Inflammatory Agents, Non-Steroidal, Aspirin, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Oncogene Proteins, Fusion, Prognosis, Prospective Studies, Prostatic Neoplasms, United States, Transdisciplinary Prostate Cancer Partnership, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract

Background: In a case-control study, aspirin use was associated with a lower risk of a common prostate cancer molecular subtype, the TMPRSS2:ERG gene fusion. We sought to validate this finding in a prospective cohort.Methods: In the Health Professionals Follow-up Study, 49,395 men reported on aspirin use on biennial questionnaires and were followed for prostate cancer incidence over 23 years. TMPRSS2:ERG status was assessed by IHC for presence of ERG on archival tumor specimens for 912 patients with prostate cancer, of whom 48% were ERG-positive.Results: In multivariable models, we found no association between regular use of aspirin and risk of ERG-positive prostate cancer (HR, 1.02; 95% confidence interval, 0.85-1.23), nor any association with duration or frequency of aspirin use. In restricting to cases with either high Gleason grade or advanced stage disease, there remained no association with aspirin use.Conclusions: Data from this prospective study with repeated assessments of aspirin use do not support the hypothesis that aspirin use is associated with a lower risk of ERG-positive prostate cancer.Impact: Aspirin use is unlikely to lower the risk of this common molecular subtype of prostate cancer. However, there is emerging data supporting the role of other lifestyle and genetic factors underlying the development of the TMPRSS2:ERG fusion. Cancer Epidemiol Biomarkers Prev; 27(10); 1231-3. ©2018 AACR.

Published
2018

7. Table S6 from Statin Use Is Associated with Lower Risk of PTEN-Null and Lethal Prostate Cancer

Author

Allott, Emma H., primary, Ebot, Ericka M., primary, Stopsack, Konrad H., primary, Gonzalez-Feliciano, Amparo G., primary, Markt, Sarah C., primary, Wilson, Kathryn M., primary, Ahearn, Thomas U., primary, Gerke, Travis A., primary, Downer, Mary K., primary, Rider, Jennifer R., primary, Freedland, Stephen J., primary, Lotan, Tamara L., primary, Kantoff, Philip W., primary, Platz, Elizabeth A., primary, Loda, Massimo, primary, Stampfer, Meir J., primary, Giovannucci, Edward, primary, Sweeney, Christopher J., primary, Finn, Stephen P., primary, and Mucci, Lorelei A., primary

Published
2023
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8. List of Contributors

Author

Ara, Ignacio, primary, Barbagallo, Mario, additional, Bes-Rastrollo, Maira, additional, Dominguez, Ligia J., additional, Gea, Alfredo, additional, Hershey, María Soledad, additional, Marques-Lopes, Iva, additional, Martínez-Lapiscina, Elena H., additional, Downer, Mary K., additional, Murphy, Karen J., additional, Papadaki, Angeliki, additional, Sánchez-Tainta, Ana, additional, Sánchez-Villegas, Almudena, additional, Toledo, Estefanía, additional, and Zazpe, Itziar, additional

Published
2018
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14. Dietary Intake, FTO Genetic Variants, and Adiposity: A Combined Analysis of Over 16,000 Children and Adolescents

Author

Qi, Qibin, Downer, Mary K., Kilpeläinen, Tuomas O., Taal, H. Rob, Barton, Sheila J., Ntalla, Ioanna, Standl, Marie, Boraska, Vesna, Huikari, Ville, Kiefte-de Jong, Jessica C., Körner, Antje, Lakka, Timo A., Liu, Gaifen, Magnusson, Jessica, Okuda, Masayuki, Raitakari, Olli, Richmond, Rebecca, Scott, Robert A., Bailey, Mark E.S., Scheuermann, Kathrin, Holloway, John W., Inskip, Hazel, Isasi, Carmen R., Mossavar-Rahmani, Yasmin, Jaddoe, Vincent W.V., Laitinen, Jaana, Lindi, Virpi, Melén, Erik, Pitsiladis, Yannis, Pitkänen, Niina, Snieder, Harold, Heinrich, Joachim, Timpson, Nicholas J., Wang, Tao, Yuji, Hinoda, Zeggini, Eleftheria, Dedoussis, George V., Kaplan, Robert C., Wylie-Rosett, Judith, Loos, Ruth J.F., Hu, Frank B., and Qi, Lu

Published
2015
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15. FTO genetic variants, dietary intake and body mass index: insights from 177 330 individuals

Author

Qi, Qibin, Kilpeläinen, Tuomas O., Downer, Mary K., Tanaka, Toshiko, Smith, Caren E., Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y., Renström, Frida, Lin, Xiaochen, Ängquist, Lars H., Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarunveer Singh, Boer, Jolanda M.A., Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H.M., Holloway, John W., Houston, Denise K., Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A., Jääskeläinen, Tiina, Lee, Nanette R., Lehtimäki, Terho, Lemaitre, Rozenn N., Lu, Wei, Luben, Robert N., Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L., Ngwa, Julius S., Perusse, Louis, van Rooij, Frank J.A., Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K, Zhu, Jingwen, Borecki, Ingrid B., Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V., Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G., Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K., Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T., Uitterlinden, André G., Zillikens, M. Carola, Franco, Oscar H., Shyong Tai, E., Ou Shu, Xiao, Siscovick, David S., Toft, Ulla, Verschuren, W.M. Monique, Vollenweider, Peter, Wareham, Nicholas J., Witteman, Jacqueline C.M., Zheng, Wei, Ridker, Paul M., Kang, Jae H., Liang, Liming, Jensen, Majken K., Curhan, Gary C., Pasquale, Louis R., Hunter, David J., Mohlke, Karen L., Uusitupa, Matti, Cupples, L. Adrienne, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I., Franks, Paul W., Sørensen, Thorkild I.A., Hu, Frank B., Loos, Ruth J. F., Nettleton, Jennifer A., and Qi, Lu

Published
2014
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16. Abstract PS7-23: Neoadjuvant and adjuvant therapy (NAT/AT) treatment patterns and clinical characteristics in a real-world cohort of US patients with HR+/HER2− early breast cancer (eBC)

Author

Downer, Mary K, primary, Craggs, Christopher, additional, Dhillon, Preet, additional, Luhn, Patricia, additional, Flores-Avile, Carlos, additional, Tan, Amie, additional, Patre, Monika, additional, Schimmoller, Frauke, additional, and Crnjevic, Tanja Badovinac, additional

Published
2021
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19. Statin Use Is Associated with Lower Risk of PTEN-Null and Lethal Prostate Cancer

Author

Allott, Emma H., primary, Ebot, Ericka M., additional, Stopsack, Konrad H., additional, Gonzalez-Feliciano, Amparo G., additional, Markt, Sarah C., additional, Wilson, Kathryn M., additional, Ahearn, Thomas U., additional, Gerke, Travis A., additional, Downer, Mary K., additional, Rider, Jennifer R., additional, Freedland, Stephen J., additional, Lotan, Tamara L., additional, Kantoff, Philip W., additional, Platz, Elizabeth A., additional, Loda, Massimo, additional, Stampfer, Meir J., additional, Giovannucci, Edward, additional, Sweeney, Christopher J., additional, Finn, Stephen P., additional, and Mucci, Lorelei A., additional

Published
2020
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21. Circulating inflammation markers and prostate cancer

Author

Ugge, Henrik, primary, Downer, Mary K., additional, Carlsson, Jessica, additional, Bowden, Michaela, additional, Davidsson, Sabina, additional, Mucci, Lorelei A., additional, Fall, Katja, additional, Andersson, Sven‐Olof, additional, and Andrén, Ove, additional

Published
2019
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22. Circulating inflammation markers and prostate cancer

Author

Ugge, Henrik, Downer, Mary K., Carlsson, Jessica, Bowden, Michaela, Davidsson, Sabina, Mucci, Lorelei A., Fall, Katja, Andersson, Sven-Olof, Andrén, Ove, Ugge, Henrik, Downer, Mary K., Carlsson, Jessica, Bowden, Michaela, Davidsson, Sabina, Mucci, Lorelei A., Fall, Katja, Andersson, Sven-Olof, and Andrén, Ove

Abstract

BACKGROUND: Chronic inflammation is thought to influence the risk of prostate cancer. The purpose of this population-based case-control study was to evaluate the association of 48 circulating inflammation markers with prostate cancer, to identify candidate markers for further investigation. METHODS: Serum samples collected from 235 prostate cancer patients and 198 population-based controls recruited in Örebro County, Sweden, in 1989-1991, were assessed using a multiplex bead-based immunoassay to determine concentrations of 48 circulating inflammation markers. Logistic regression was first used to evaluate the association between individual markers (highest vs lowest concentration quartile) and prostate cancer in unadjusted and mutually adjusted models. Second, patients with inflammatory conditions, metastatic or advanced prostate cancer, were excluded to address the possible influence of systemic disease on inflammation markers. RESULTS: Individual analyses first identified 21 markers associated with prostate cancer (P < .05), which after mutual adjustment were reduced to seven markers. After the exclusion of men with conditions linked with systemic inflammation, associations between prostate cancer and deviant levels of C-X3-C motif chemokine ligand 1, platelet-derived growth factor subunit B homodimer, interleukin 10, C-C motif chemokine ligand (CCL) 21, and CCL11 remained statistically significant. CONCLUSIONS: In this explorative study, we identified candidate inflammation markers of possible importance for prostate cancer pathophysiology, for further evaluation in prospective studies., Funding Agency:Lions Cancerforskningsfond vid Akademiska sjukhuset i Uppsala. (Part of Lions International)

Published
2019
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23. Abstract A015: Molecular tumor profiling to identify mechanisms linking statin use with lower risk of lethal prostate cancer: Results from the Health Professionals Follow-up Study

Author

Allott, Emma H., primary, Ebot, Ericka M., additional, Gonzalez-Feliciano, Amparo G., additional, Markt, Sarah C., additional, Wilson, Kathryn M., additional, Ahearn, Thomas U., additional, Gerke, Travis A., additional, Downer, Mary K., additional, Stopsack, Konrad H., additional, Rider, Jennifer R., additional, Freedland, Stephen J., additional, Platz, Elizabeth A., additional, Stampfer, Meir J., additional, Giovannucci, Edward L., additional, Sweeney, Christopher J., additional, Finn, Stephen P., additional, and Mucci, Lorelei A., additional

Published
2018
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26. Dairy intake in relation to prostate cancer survival.

Author

Downer, Mary K, Batista, Julie L, Mucci, Lorelei A, Stampfer, Meir J, Epstein, Mara Meyer, Håkansson, Niclas, Wolk, Alicja, Johansson, Jan-Erik, Andrén, Ove, Fall, Katja, Andersson, Sven-Olof, Downer, Mary K, Batista, Julie L, Mucci, Lorelei A, Stampfer, Meir J, Epstein, Mara Meyer, Håkansson, Niclas, Wolk, Alicja, Johansson, Jan-Erik, Andrén, Ove, Fall, Katja, and Andersson, Sven-Olof

Abstract

Dairy intake has been associated with increased risk of advanced prostate cancer. Two US cohort studies reported increased prostate cancer-specific mortality with increased high-fat milk intake. We examined whether dairy and related nutrient intake were associated with prostate cancer progression in a Swedish patient population with high dairy consumption. We prospectively followed 525 men with newly diagnosed prostate cancer (diagnosed 1989-1994). We identified and confirmed deaths through February 2011 (n = 222 prostate cancer-specific, n = 268 from other causes). Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the associations between food or nutrient intake and prostate cancer-specific death. On average, patients consumed 5.0 servings/day of total dairy products at diagnosis. In the whole population, high-fat milk intake was not associated with prostate cancer-specific death (95% CI: 0.78, 2.10; p-trend = 0.32; multivariate-adjusted model). However, among patients diagnosed with localized prostate cancer, compared to men who consumed <1 servings/day of high-fat milk, those who drank ≥3 servings/day had an increased hazard of prostate cancer mortality (HR = 6.10; 95% CI: 2.14, 17.37; p-trend = 0.004; multivariate-adjusted model). Low-fat milk intake was associated with a borderline reduction in prostate cancer death among patients with localized prostate cancer. These associations were not observed among patients diagnosed with advanced stage prostate cancer. Our data suggest a positive association between high-fat milk intake and prostate cancer progression among patients diagnosed with localized prostate cancer. Further studies are warranted to investigate this association and elucidate the mechanisms by which high-fat milk intake may promote prostate cancer progression.

Published
2017
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27. FTO genetic variants, dietary intake and body mass index: insights from 177 330 individuals

Author

Qi, Qibin, Kilpeläinen, Tuomas O., Downer, Mary K., Tanaka, Toshiko, Smith, Caren E., Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y., Renström, Frida, Lin, Xiaochen, Ängquist, Lars H., Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarunveer Singh, Boer, Jolanda M.A., Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H.M., Holloway, John W., Houston, Denise K., Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A., Jääskeläinen, Tiina, Lee, Nanette R., Lehtimäki, Terho, Lemaitre, Rozenn N., Lu, Wei, Luben, Robert N., Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L., Ngwa, Julius S., Perusse, Louis, van Rooij, Frank J.A., Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K., Zhu, Jingwen, Borecki, Ingrid B., Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V., Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G., Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K., Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T., Uitterlinden, André G., Zillikens, M. Carola, Franco, Oscar H., Shyong Tai, E., Ou Shu, Xiao, Siscovick, David S., Toft, Ulla, Verschuren, W.M. Monique, Vollenweider, Peter, Wareham, Nicholas J., Witteman, Jacqueline C.M., Zheng, Wei, Ridker, Paul M., Kang, Jae H., Liang, Liming, Jensen, Majken K., Curhan, Gary C., Pasquale, Louis R., Hunter, David J., Mohlke, Karen L., Uusitupa, Matti, Cupples, L. Adrienne, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I., Franks, Paul W., Sørensen, Thorkild I.A., Hu, Frank B., Loos, Ruth J. F., Nettleton, Jennifer A., Qi, Lu, Qi, Qibin, Kilpeläinen, Tuomas O., Downer, Mary K., Tanaka, Toshiko, Smith, Caren E., Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y., Renström, Frida, Lin, Xiaochen, Ängquist, Lars H., Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarunveer Singh, Boer, Jolanda M.A., Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H.M., Holloway, John W., Houston, Denise K., Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A., Jääskeläinen, Tiina, Lee, Nanette R., Lehtimäki, Terho, Lemaitre, Rozenn N., Lu, Wei, Luben, Robert N., Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L., Ngwa, Julius S., Perusse, Louis, van Rooij, Frank J.A., Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K., Zhu, Jingwen, Borecki, Ingrid B., Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V., Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G., Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K., Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T., Uitterlinden, André G., Zillikens, M. Carola, Franco, Oscar H., Shyong Tai, E., Ou Shu, Xiao, Siscovick, David S., Toft, Ulla, Verschuren, W.M. Monique, Vollenweider, Peter, Wareham, Nicholas J., Witteman, Jacqueline C.M., Zheng, Wei, Ridker, Paul M., Kang, Jae H., Liang, Liming, Jensen, Majken K., Curhan, Gary C., Pasquale, Louis R., Hunter, David J., Mohlke, Karen L., Uusitupa, Matti, Cupples, L. Adrienne, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I., Franks, Paul W., Sørensen, Thorkild I.A., Hu, Frank B., Loos, Ruth J. F., Nettleton, Jennifer A., and Qi, Lu

Abstract

FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177 330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide polymorphism) and total energy and macronutrient intake and (ii) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in Whites (effect per allele = 0.34 [0.31, 0.37] kg/m2, P = 1.9 × 10−105), and all participants (0.30 [0.30, 0.35] kg/m2, P = 3.6 × 10−107). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele = 0.08 [0.06, 0.10] %, P = 2.4 × 10−16), and relative weak associations with lower total energy intake (−6.4 [−10.1, −2.6] kcal/day, P = 0.001) and lower dietary carbohydrate intake (−0.07 [−0.11, −0.02] %, P = 0.004). The associations with protein (P = 7.5 × 10−9) and total energy (P = 0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity

Published
2017

30. Should We Fear Folate?

Author

Downer, Mary K., primary, Van Blarigan, Erin L., additional, Peisch, Sam F., additional, and Stampfer, Meir J., additional

Published
2016
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32. Dietary intake, FTO genetic variants and adiposity:a combined analysis of over 16,000 children and adolescents

Author

Qi, Qibin, Downer, Mary K, Oskari Kilpeläinen, Tuomas, Taal, H Rob, Barton, Sheila J, Ntalla, Ioanna, Standl, Marie, Boraska, Vesna, Huikari, Ville, Kiefte-de Jong, Jessica C, Körner, Antje, Lakka, Timo A, Liu, Gaifen, Magnusson, Jessica, Okuda, Masayuki, Raitakari, Olli, Richmond, Rebecca, Scott, Robert A, Bailey, Mark E S, Scheuermann, Kathrin, Holloway, John W, Inskip, Hazel, Isasi, Carmen R, Mossavar-Rahmani, Yasmin, Jaddoe, Vincent W V, Laitinen, Jaana, Lindi, Virpi, Melén, Erik, Pitsiladis, Yannis, Pitkänen, Niina, Snieder, Harold, Heinrich, Joachim, Timpson, Nicholas J, Wang, Tao, Yuji, Hinoda, Zeggini, Eleftheria, Dedoussis, George V, Kaplan, Robert C, Wylie-Rosett, Judith, Loos, Ruth J F, Hu, Frank B, Qi, Lu, Qi, Qibin, Downer, Mary K, Oskari Kilpeläinen, Tuomas, Taal, H Rob, Barton, Sheila J, Ntalla, Ioanna, Standl, Marie, Boraska, Vesna, Huikari, Ville, Kiefte-de Jong, Jessica C, Körner, Antje, Lakka, Timo A, Liu, Gaifen, Magnusson, Jessica, Okuda, Masayuki, Raitakari, Olli, Richmond, Rebecca, Scott, Robert A, Bailey, Mark E S, Scheuermann, Kathrin, Holloway, John W, Inskip, Hazel, Isasi, Carmen R, Mossavar-Rahmani, Yasmin, Jaddoe, Vincent W V, Laitinen, Jaana, Lindi, Virpi, Melén, Erik, Pitsiladis, Yannis, Pitkänen, Niina, Snieder, Harold, Heinrich, Joachim, Timpson, Nicholas J, Wang, Tao, Yuji, Hinoda, Zeggini, Eleftheria, Dedoussis, George V, Kaplan, Robert C, Wylie-Rosett, Judith, Loos, Ruth J F, Hu, Frank B, and Qi, Lu

Abstract

The FTO gene harbors variation with the strongest effect on adiposity and obesity risk. Previous data support a role for FTO variation in influencing food intake. We conducted a combined analysis of 16,094 boys and girls aged 1–18 years from 14 studies to examine the following: 1) the association between the FTO rs9939609 variant (or a proxy) and total energy and macronutrient intake; and 2) the interaction between the FTO variant and dietary intake, and the effect on BMI. We found that the BMI-increasing allele (minor allele) of the FTO variant was associated with increased total energy intake (effect per allele = 14.3 kcal/day [95% CI 5.9, 22.7 kcal/day], P = 6.5 × 10−4), but not with protein, carbohydrate, or fat intake. We also found that protein intake modified the association between the FTO variant and BMI (interactive effect per allele = 0.08 SD [0.03, 0.12 SD], P for interaction = 7.2 × 10−4): the association between FTO genotype and BMI was much stronger in individuals with high protein intake (effect per allele = 0.10 SD [0.07, 0.13 SD], P = 8.2 × 10−10) than in those with low intake (effect per allele = 0.04 SD [0.01, 0.07 SD], P = 0.02). Our results suggest that the FTO variant that confers a predisposition to higher BMI is associated with higher total energy intake, and that lower dietary protein intake attenuates the association between FTO genotype and adiposity in children and adolescents.

Published
2015

33. FTO genetic variants, dietary intake and body mass index:insights from 177 330 individuals

Author

Qi, Qibin, Oskari Kilpeläinen, Tuomas, Downer, Mary K, Tanaka, Toshiko, Smith, Caren E, Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y, Renström, Frida, Lin, Xiaochen, Angquist, Lars H, Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarun Veer Singh, Boer, Jolanda M A, Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H M, Holloway, John W, Houston, Denise K, Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A, Jääskeläinen, Tiina, Lee, Nanette R, Lehtimäki, Terho, Lemaitre, Rozenn N, Lu, Wei, Luben, Robert N, Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L, Ngwa, Julius S, Perusse, Louis, van Rooij, Frank J A, Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K, Zhu, Jingwen, Borecki, Ingrid B, Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V, Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G, Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K, Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T, Uitterlinden, André G, Carola Zillikens, M, Franco, Oscar H, Shyong Tai, E, Ou Shu, Xiao, Siscovick, David S, Toft, Ulla, Monique Verschuren, W M, Vollenweider, Peter, Wareham, Nicholas J, Witteman, Jacqueline C M, Zheng, Wei, Ridker, Paul M, Kang, Jae H, Liang, Liming, Jensen, Majken K, Curhan, Gary C, Pasquale, Louis R, Hunter, David J, Mohlke, Karen L, Uusitupa, Matti, Adrienne Cupples, L, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I, Franks, Paul W, Sørensen, Thorkild I A, Hu, Frank B, Loos, Ruth J F, Nettleton, Jennifer A, Qi, Lu, Qi, Qibin, Oskari Kilpeläinen, Tuomas, Downer, Mary K, Tanaka, Toshiko, Smith, Caren E, Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y, Renström, Frida, Lin, Xiaochen, Angquist, Lars H, Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarun Veer Singh, Boer, Jolanda M A, Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H M, Holloway, John W, Houston, Denise K, Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A, Jääskeläinen, Tiina, Lee, Nanette R, Lehtimäki, Terho, Lemaitre, Rozenn N, Lu, Wei, Luben, Robert N, Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L, Ngwa, Julius S, Perusse, Louis, van Rooij, Frank J A, Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K, Zhu, Jingwen, Borecki, Ingrid B, Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V, Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G, Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K, Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T, Uitterlinden, André G, Carola Zillikens, M, Franco, Oscar H, Shyong Tai, E, Ou Shu, Xiao, Siscovick, David S, Toft, Ulla, Monique Verschuren, W M, Vollenweider, Peter, Wareham, Nicholas J, Witteman, Jacqueline C M, Zheng, Wei, Ridker, Paul M, Kang, Jae H, Liang, Liming, Jensen, Majken K, Curhan, Gary C, Pasquale, Louis R, Hunter, David J, Mohlke, Karen L, Uusitupa, Matti, Adrienne Cupples, L, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I, Franks, Paul W, Sørensen, Thorkild I A, Hu, Frank B, Loos, Ruth J F, Nettleton, Jennifer A, and Qi, Lu

Abstract

FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177 330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide polymorphism) and total energy and macronutrient intake and (ii) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in Whites (effect per allele = 0.34 [0.31, 0.37] kg/m(2), P = 1.9 × 10(-105)), and all participants (0.30 [0.30, 0.35] kg/m(2), P = 3.6 × 10(-107)). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele = 0.08 [0.06, 0.10] %, P = 2.4 × 10(-16)), and relative weak associations with lower total energy intake (-6.4 [-10.1, -2.6] kcal/day, P = 0.001) and lower dietary carbohydrate intake (-0.07 [-0.11, -0.02] %, P = 0.004). The associations with protein (P = 7.5 × 10(-9)) and total energy (P = 0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity.

Published
2014

34. Mercury exposure and risk of cardiovascular disease: a nested case-control study in the PREDIMED (PREvention with MEDiterranean Diet) study.

Author

Downer, Mary K., Martínez-González, Miguel A., Gea, Alfredo, Stampfer, Meir, Warnberg, Julia, Ruiz-Canela, Miguel, Salas-Salvadó, Jordi, Corella, Dolores, Ros, Emilio, Fitó, Montse, Estruch, Ramon, Arós, Fernando, Fiol, Miquel, Lapetra, José, Serra-Majem, Lluís, Bullo, Monica, Sorli, Jose V., Muñoz, Miguel A., García-Rodriguez, Antonio, and Gutierrez-Bedmar, Mario

Subjects
PHYSIOLOGICAL effects of mercury, CARDIOVASCULAR diseases risk factors, UNSATURATED fatty acids, NUCLEAR activation analysis, MEDICAL records, LOGISTIC regression analysis, CARDIOVASCULAR disease prevention, ORGANIC compound analysis, CARDIOVASCULAR diseases, COMPARATIVE studies, FOOD contamination, LONGITUDINAL method, RESEARCH methodology, MEDICAL cooperation, MULTIVARIATE analysis, NAILS (Anatomy), NUTRITION policy, NUTRITIONAL requirements, ORGANIC compounds, POLLUTANTS, PROBABILITY theory, RESEARCH, RISK assessment, STATISTICAL sampling, SEAFOOD, TIME, EVALUATION research, RANDOMIZED controlled trials, CASE-control method, BODY burden, MEDITERRANEAN diet, ODDS ratio
Abstract

Background: Substantial evidence suggests that consuming 1-2 servings of fish per week, particularly oily fish (e.g., salmon, herring, sardines) is beneficial for cardiovascular health due to its high n-3 polyunsaturated fatty acid content. However, there is some concern that the mercury content in fish may increase cardiovascular disease risk, but this relationship remains unclear.Methods: The PREDIMED trial included 7477 participants who were at high risk for cardiovascular disease at baseline. In this study, we evaluated associations between mercury exposure, fish consumption and cardiovascular disease. We randomly selected 147 of the 288 cases diagnosed with cardiovascular disease during follow-up and matched them on age and sex to 267 controls. Instrumental neutron activation analysis was used to assess toenail mercury concentration. In-person interviews, medical record reviews and validated questionnaires were used to assess fish consumption and other covariates. Information was collected at baseline and updated yearly during follow-up. We used conditional logistic regression to evaluate associations in the total nested case-control study, and unconditional logistic regression for population subsets.Results: Mean (±SD) toenail mercury concentrations (μg per gram) did not significantly differ between cases (0.63 (±0.53)) and controls (0.67 (±0.49)). Mercury concentration was not associated with cardiovascular disease in any analysis, and neither was fish consumption or n-3 fatty acids. The fully-adjusted relative risks for the highest versus lowest quartile of mercury concentration were 0.71 (95% Confidence Interval [CI], 0.34, 1.14; ptrend = 0.37) for the nested case-control study, 0.74 (95% CI, 0.32, 1.76; ptrend = 0.43) within the Mediterranean diet intervention group, and 0.50 (95% CI, 0.13, 1.96; ptrend = 0.41) within the control arm of the trial. Associations remained null when mercury was jointly assessed with fish consumption at baseline and during follow-up. Results were similar in different sensitivity analyses.Conclusions: We found no evidence that mercury exposure from regular fish consumption increases cardiovascular disease risk in a population of Spanish adults with high cardiovascular disease risk and high fish consumption. This implies that the mercury content in fish does not detract from the already established cardiovascular benefits of fish consumption.Trial Registration: ISRCTN35739639 . [ABSTRACT FROM AUTHOR]

Published
2017
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35. Dietary Intake, FTO Genetic Variants, and Adiposity: A Combined Analysis of Over 16,000 Children and Adolescents.

Author

Qibin Qi, Downer, Mary K., Kilpeläinen, Tuomas O., Taal, H. Rob, Barton, Sheila J., Ntalla, Ioanna, Standl, Marie, Boraska, Vesna, Huikari, Ville, Kiefte-de Jong, Jessica C., Körner, Antje, Lakka, Timo A., Gaifen Liu, Magnusson, Jessica, Masayuki Okuda, Raitakari, Olli, Richmond, Rebecca, Scott, Robert A., Bailey, Mark E. S., and Scheuermann, Kathrin

Subjects
*OBESITY genetics, *GENETICS of childhood obesity, *FOOD consumption research, *METABOLIC disorders, *OBESITY risk factors, *GENETICS
Abstract

The FTO gene harbors variation with the strongest effect on adiposity and obesity risk. Previous data support a role for FTO variation in influencing food intake. We conducted a combined analysis of 16,094 boys and girls aged 1-18 years from 14 studies to examine the following: 1) the association between the FTO rs9939609 variant (or a proxy) and total energy and macronutrient intake; and 2) the interaction between the FTO variant and dietary intake, and the effect on BMI. We found that the BMI-increasing allele (minor allele) of the FTO variant was associated with increased total energy intake (effect per allele = 14.3 kcal/day [95%CI 5.9, 22.7 kcal/day], P = 6 x 5 10-4), but not with protein, carbohydrate, or fat intake. We also found that protein intake modified the association between the FTO variant and BMI (interactive effect per allele = 0.08 SD [0.03, 0.12 SD], P for interaction = 7.2 x 10-4): the association between FTO genotype and BMI was much stronger in individuals with high protein intake (effect per allele = 0.10 SD [0.07, 0.13 SD], P = 8.2 x 10-10)) than in those with low intake (effect per allele = 0.04 SD [0.01, 0.07 SD], P = 0.02). Our results suggest that the FTO variant that confers a predisposition to higher BMI is associated with higher total energy intake, and that lower dietary protein intake attenuates the association between FTO genotype and adiposity in children and adolescents. [ABSTRACT FROM AUTHOR]

Published
2015
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36. Letters to the Editor.

Author

Cote, David J., Downer, Mary K., Zoltick, Emilie S., Smith, Timothy R., and Stampfer, Meir J.

Published
2017

38. Circulating inflammation markers and prostate cancer

Author

Ugge, Henrik, Downer, Mary K., Carlsson, Jessica, Bowden, Michaela, Davidsson, Sabina, Mucci, Lorelai A., Fall, Katja, Andersson, Sven-Olof, Andrén, Ove, Ugge, Henrik, Downer, Mary K., Carlsson, Jessica, Bowden, Michaela, Davidsson, Sabina, Mucci, Lorelai A., Fall, Katja, Andersson, Sven-Olof, and Andrén, Ove

39. FTO genetic variants, dietary intake and body mass index: insights from 177 330 individuals

Author

Qi, Qibin, Kilpeläinen, Tuomas O., Downer, Mary K., Tanaka, Toshiko, Smith, Caren E., Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y., Renström, Frida, Lin, Xiaochen, Ängquist, Lars H., Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarunveer Singh, Boer, Jolanda M.A., Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H.M., Holloway, John W., Houston, Denise K., Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A., Jääskeläinen, Tiina, Lee, Nanette R., Lehtimäki, Terho, Lemaitre, Rozenn N., Lu, Wei, Luben, Robert N., Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L., Ngwa, Julius S., Perusse, Louis, van Rooij, Frank J.A., Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K., Zhu, Jingwen, Borecki, Ingrid B., Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V., Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G., Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K., Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T., Uitterlinden, André G., Zillikens, M. Carola, Franco, Oscar H., Shyong Tai, E., Ou Shu, Xiao, Siscovick, David S., Toft, Ulla, Verschuren, W.M. Monique, Vollenweider, Peter, Wareham, Nicholas J., Witteman, Jacqueline C.M., Zheng, Wei, Ridker, Paul M., Kang, Jae H., Liang, Liming, Jensen, Majken K., Curhan, Gary C., Pasquale, Louis R., Hunter, David J., Mohlke, Karen L., Uusitupa, Matti, Cupples, L. Adrienne, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I., Franks, Paul W., Sørensen, Thorkild I.A., Hu, Frank B., Loos, Ruth J. F., Nettleton, Jennifer A., Qi, Lu, Qi, Qibin, Kilpeläinen, Tuomas O., Downer, Mary K., Tanaka, Toshiko, Smith, Caren E., Sluijs, Ivonne, Sonestedt, Emily, Chu, Audrey Y., Renström, Frida, Lin, Xiaochen, Ängquist, Lars H., Huang, Jinyan, Liu, Zhonghua, Li, Yanping, Asif Ali, Muhammad, Xu, Min, Ahluwalia, Tarunveer Singh, Boer, Jolanda M.A., Chen, Peng, Daimon, Makoto, Eriksson, Johan, Perola, Markus, Friedlander, Yechiel, Gao, Yu-Tang, Heppe, Denise H.M., Holloway, John W., Houston, Denise K., Kanoni, Stavroula, Kim, Yu-Mi, Laaksonen, Maarit A., Jääskeläinen, Tiina, Lee, Nanette R., Lehtimäki, Terho, Lemaitre, Rozenn N., Lu, Wei, Luben, Robert N., Manichaikul, Ani, Männistö, Satu, Marques-Vidal, Pedro, Monda, Keri L., Ngwa, Julius S., Perusse, Louis, van Rooij, Frank J.A., Xiang, Yong-Bing, Wen, Wanqing, Wojczynski, Mary K., Zhu, Jingwen, Borecki, Ingrid B., Bouchard, Claude, Cai, Qiuyin, Cooper, Cyrus, Dedoussis, George V., Deloukas, Panos, Ferrucci, Luigi, Forouhi, Nita G., Hansen, Torben, Christiansen, Lene, Hofman, Albert, Johansson, Ingegerd, Jørgensen, Torben, Karasawa, Shigeru, Khaw, Kay-Tee, Kim, Mi-Kyung, Kristiansson, Kati, Li, Huaixing, Lin, Xu, Liu, Yongmei, Lohman, Kurt K., Long, Jirong, Mikkilä, Vera, Mozaffarian, Dariush, North, Kari, Pedersen, Oluf, Raitakari, Olli, Rissanen, Harri, Tuomilehto, Jaakko, van der Schouw, Yvonne T., Uitterlinden, André G., Zillikens, M. Carola, Franco, Oscar H., Shyong Tai, E., Ou Shu, Xiao, Siscovick, David S., Toft, Ulla, Verschuren, W.M. Monique, Vollenweider, Peter, Wareham, Nicholas J., Witteman, Jacqueline C.M., Zheng, Wei, Ridker, Paul M., Kang, Jae H., Liang, Liming, Jensen, Majken K., Curhan, Gary C., Pasquale, Louis R., Hunter, David J., Mohlke, Karen L., Uusitupa, Matti, Cupples, L. Adrienne, Rankinen, Tuomo, Orho-Melander, Marju, Wang, Tao, Chasman, Daniel I., Franks, Paul W., Sørensen, Thorkild I.A., Hu, Frank B., Loos, Ruth J. F., Nettleton, Jennifer A., and Qi, Lu

Abstract

FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177 330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide polymorphism) and total energy and macronutrient intake and (ii) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in Whites (effect per allele = 0.34 [0.31, 0.37] kg/m2, P = 1.9 × 10−105), and all participants (0.30 [0.30, 0.35] kg/m2, P = 3.6 × 10−107). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele = 0.08 [0.06, 0.10] %, P = 2.4 × 10−16), and relative weak associations with lower total energy intake (−6.4 [−10.1, −2.6] kcal/day, P = 0.001) and lower dietary carbohydrate intake (−0.07 [−0.11, −0.02] %, P = 0.004). The associations with protein (P = 7.5 × 10−9) and total energy (P = 0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity

40. Aspirin and Alcohol in Relation to Lethal Prostate Cancer

Author

Downer, Mary K.

Subjects
Health Sciences, Epidemiology, Health Sciences, Nutrition, Statistics
Abstract

Problem: Prostate cancer is the most commonly diagnosed cancer and second-leading cancer cause of death among U.S. men. However, most prostate cancers are indolent. Thus, it is necessary to identify risk factors for lethal (metastatic or fatal) prostate cancer. This dissertation investigates the role of aspirin use and alcohol intake in relation to prostate cancer. Methods: Data from two large, longitudinal studies of U.S. adult males – the Physicians’ Health Study (PHS) and Health Professionals Follow-up Study (HPFS) – were used. PHS began in 1981 as a randomized trial of aspirin and beta carotene among 22,071 U.S. male physicians. HPFS began in 1986 when investigators enrolled 51,529 U.S. male health professionals. In both cohorts, regular questionnaires ascertained medical diagnoses, medications, diet, and lifestyle factors. Cox proportional hazards regression was used to investigate all associations. Results: In the general study population, compared to never use, current aspirin use was associated with decreased risk of lethal prostate cancer (Hazard Ratio [HR], 95% Confidence Intervals [CI]: PHS: = 0.80, 0.66-0.96; HPFS: 0.80, 0.66-0.96). Findings were similar when assessing post-diagnosis aspirin use among patients. Total pre-diagnosis alcohol intake was associated with a decreased risk of lethal prostate cancer in HPFS (0.84, 0.71-0.99). Among patients, compared to none, any red wine after diagnosis was associated with a decreased risk of lethal prostate cancer (0.50, 0.29-0.86) and overall mortality (0.74, 0.57-0.97). Conclusions: Recommending aspirin use to men with and without prostate cancer may help prevent lethal prostate cancer. Moderate alcohol intake did not increase risk of lethal prostate cancer, suggesting it may be part of a healthy diet among older men. Red wine may be beneficial. In all analyses, we were unable to differentiate a late effect from reverse causation.

Published
2018

41. FTO genetic variants, dietary intake and body mass index: insights from 177,330 individuals.

Author

Qi Q, Kilpeläinen TO, Downer MK, Tanaka T, Smith CE, Sluijs I, Sonestedt E, Chu AY, Renström F, Lin X, Ängquist LH, Huang J, Liu Z, Li Y, Asif Ali M, Xu M, Ahluwalia TS, Boer JM, Chen P, Daimon M, Eriksson J, Perola M, Friedlander Y, Gao YT, Heppe DH, Holloway JW, Houston DK, Kanoni S, Kim YM, Laaksonen MA, Jääskeläinen T, Lee NR, Lehtimäki T, Lemaitre RN, Lu W, Luben RN, Manichaikul A, Männistö S, Marques-Vidal P, Monda KL, Ngwa JS, Perusse L, van Rooij FJ, Xiang YB, Wen W, Wojczynski MK, Zhu J, Borecki IB, Bouchard C, Cai Q, Cooper C, Dedoussis GV, Deloukas P, Ferrucci L, Forouhi NG, Hansen T, Christiansen L, Hofman A, Johansson I, Jørgensen T, Karasawa S, Khaw KT, Kim MK, Kristiansson K, Li H, Lin X, Liu Y, Lohman KK, Long J, Mikkilä V, Mozaffarian D, North K, Pedersen O, Raitakari O, Rissanen H, Tuomilehto J, van der Schouw YT, Uitterlinden AG, Zillikens MC, Franco OH, Shyong Tai E, Ou Shu X, Siscovick DS, Toft U, Verschuren WM, Vollenweider P, Wareham NJ, Witteman JC, Zheng W, Ridker PM, Kang JH, Liang L, Jensen MK, Curhan GC, Pasquale LR, Hunter DJ, Mohlke KL, Uusitupa M, Cupples LA, Rankinen T, Orho-Melander M, Wang T, Chasman DI, Franks PW, Sørensen TI, Hu FB, Loos RJ, Nettleton JA, and Qi L

Subjects
Adult, Black or African American, Aged, Alleles, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Asian People, Body Mass Index, Dietary Carbohydrates administration & dosage, Dietary Fats administration & dosage, Female, Gene Frequency, Humans, Male, Middle Aged, Obesity metabolism, Obesity pathology, White People, Dietary Proteins administration & dosage, Energy Intake genetics, Obesity ethnology, Obesity genetics, Polymorphism, Single Nucleotide, Proteins genetics
Abstract

FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177,330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide polymorphism) and total energy and macronutrient intake and (ii) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in Whites (effect per allele = 0.34 [0.31, 0.37] kg/m(2), P = 1.9 × 10(-105)), and all participants (0.30 [0.30, 0.35] kg/m(2), P = 3.6 × 10(-107)). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele = 0.08 [0.06, 0.10] %, P = 2.4 × 10(-16)), and relative weak associations with lower total energy intake (-6.4 [-10.1, -2.6] kcal/day, P = 0.001) and lower dietary carbohydrate intake (-0.07 [-0.11, -0.02] %, P = 0.004). The associations with protein (P = 7.5 × 10(-9)) and total energy (P = 0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity., (© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Published
2014
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