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1. Coffee, tea, and caffeine intake and amyotrophic lateral sclerosis mortality in a pooled analysis of eight prospective cohort studies.

Author

Petimar, J, O'Reilly, É, Adami, H-O, van den Brandt, P A, Buring, J, English, D R, Freedman, D M, Giles, G G, Håkansson, N, Kurth, T, Larsson, Susanna C., Robien, K, Schouten, L J, Weiderpass, E, Wolk, Alicja, Smith-Warner, S A, Petimar, J, O'Reilly, É, Adami, H-O, van den Brandt, P A, Buring, J, English, D R, Freedman, D M, Giles, G G, Håkansson, N, Kurth, T, Larsson, Susanna C., Robien, K, Schouten, L J, Weiderpass, E, Wolk, Alicja, and Smith-Warner, S A

Abstract

BACKGROUND AND PURPOSE: Caffeine is associated with a lower risk of some neurological diseases, but few prospective studies have investigated caffeine intake and risk of amyotrophic lateral sclerosis (ALS) mortality. We therefore determined associations between coffee, tea and caffeine intake, and risk of ALS mortality. METHODS: We conducted pooled analyses of eight international, prospective cohort studies, including 351 565 individuals (120 688 men and 230 877 women). We assessed coffee, tea and caffeine intake using validated food-frequency questionnaires administered at baseline. We used Cox regression to estimate study- and sex-specific risk ratios and 95% confidence intervals (CI) for ALS mortality, which were then pooled using a random-effects model. We conducted analyses using cohort-specific tertiles, absolute common cut-points and continuous measures of all exposures. RESULTS: During follow-up, 545 ALS deaths were documented. We did not observe statistically significant associations between coffee, tea or caffeine intake and risk of ALS mortality. The pooled multivariable risk ratio (MVRR) for ≥3 cups per day vs. >0 to <1 cup per day was 1.04 (95% CI, 0.74-1.47) for coffee and 1.17 (95% CI, 0.77-1.79) for tea. The pooled MVRR comparing the highest with the lowest tertile of caffeine intake (mg/day) was 0.99 (95% CI, 0.80-1.23). No statistically significant results were observed when exposures were modeled as tertiles or continuously. CONCLUSIONS: Our results do not support associations between coffee, tea or total caffeine intake and risk of ALS mortality.

Published
2019
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2. Coffee, tea, and caffeine intake and amyotrophic lateral sclerosis mortality in a pooled analysis of eight prospective cohort studies

Author

Petimar, J., Petimar, J., O'Reilly, E., Adami, H. -O., van den Brandt, P. A., Buring, J., English, D. R., Freedman, D. M., Giles, G. G., Hakansson, N., Kurth, T., Larsson, S. C., Robien, K., Schouten, L. J., Weiderpass, E., Wolk, A., Smith-Warner, S. A., Petimar, J., Petimar, J., O'Reilly, E., Adami, H. -O., van den Brandt, P. A., Buring, J., English, D. R., Freedman, D. M., Giles, G. G., Hakansson, N., Kurth, T., Larsson, S. C., Robien, K., Schouten, L. J., Weiderpass, E., Wolk, A., and Smith-Warner, S. A.

Abstract

Background and purposeCaffeine is associated with a lower risk of some neurological diseases, but few prospective studies have investigated caffeine intake and risk of amyotrophic lateral sclerosis (ALS) mortality. We therefore determined associations between coffee, tea and caffeine intake, and risk of ALS mortality.MethodsWe conducted pooled analyses of eight international, prospective cohort studies, including 351565 individuals (120688 men and 230877 women). We assessed coffee, tea and caffeine intake using validated food-frequency questionnaires administered at baseline. We used Cox regression to estimate study- and sex-specific risk ratios and 95% confidence intervals (CI) for ALS mortality, which were then pooled using a random-effects model. We conducted analyses using cohort-specific tertiles, absolute common cut-points and continuous measures of all exposures.ResultsDuring follow-up, 545 ALS deaths were documented. We did not observe statistically significant associations between coffee, tea or caffeine intake and risk of ALS mortality. The pooled multivariable risk ratio (MVRR) for 3 cups per day vs. >0 toConclusionsOur results do not support associations between coffee, tea or total caffeine intake and risk of ALS mortality.

Published
2019

3. Coffee, tea, and caffeine intake and amyotrophic lateral sclerosis mortality in a pooled analysis of eight prospective cohort studies

Author

Petimar, J., O'Reilly, E., Adami, H. -O., van den Brandt, P. A., Buring, J., English, D. R., Freedman, D. M., Giles, G. G., Hakansson, N., Kurth, T., Larsson, S. C., Robien, K., Schouten, L. J., Weiderpass, E., Wolk, A., Smith-Warner, S. A., Petimar, J., O'Reilly, E., Adami, H. -O., van den Brandt, P. A., Buring, J., English, D. R., Freedman, D. M., Giles, G. G., Hakansson, N., Kurth, T., Larsson, S. C., Robien, K., Schouten, L. J., Weiderpass, E., Wolk, A., and Smith-Warner, S. A.

Abstract

Background and purposeCaffeine is associated with a lower risk of some neurological diseases, but few prospective studies have investigated caffeine intake and risk of amyotrophic lateral sclerosis (ALS) mortality. We therefore determined associations between coffee, tea and caffeine intake, and risk of ALS mortality.MethodsWe conducted pooled analyses of eight international, prospective cohort studies, including 351565 individuals (120688 men and 230877 women). We assessed coffee, tea and caffeine intake using validated food-frequency questionnaires administered at baseline. We used Cox regression to estimate study- and sex-specific risk ratios and 95% confidence intervals (CI) for ALS mortality, which were then pooled using a random-effects model. We conducted analyses using cohort-specific tertiles, absolute common cut-points and continuous measures of all exposures.ResultsDuring follow-up, 545 ALS deaths were documented. We did not observe statistically significant associations between coffee, tea or caffeine intake and risk of ALS mortality. The pooled multivariable risk ratio (MVRR) for 3 cups per day vs. >0 toConclusionsOur results do not support associations between coffee, tea or total caffeine intake and risk of ALS mortality.

Published
2019

4. Menopausal hormone use and ovarian cancer risk: individual participant meta-analysis of 52 epidemiological studies

Author

Gapstur, S. M., Patel, A. V., Banks, E., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Beral, V., Bull, D., Cairns, B., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Hermon, C., Key, T., Moser, K., Reeves, G., Sitas, F., Collins, R., Peto, R., Gonzalez, C. A., Lee, N., Marchbanks, P., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Goodman, M. T., Lidegaard, O., Kjaer, S. K., Morch, L. S., Tjonneland, A., Byers, T., Rohan, T., Mosgaard, B., Vessey, M., Yeates, D., Freudenheim, J. L., Titus, L. J., Chang-Claude, J., Kaaks, R., Anderson, K. E., Lazovich, D., Robien, K., Hampton, J., Newcomb, P. A., Rossing, M. A., Thomas, D. B., Weiss, N. S., Lokkegaard, E., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tamimi, R. M., Tworoger, S. S., Franceschi, S., La Vecchia, C., Negri, E., Adami, H. O., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., Brinton, L. A., Freedman, D. M., Hartge, P., Hsing, A. W., Jnr, J. V. Lacey, Lissowska, J., Hoover, R. N., Schairer, C., Babb, C., Urban, M., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., Moysich, K., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Lurie, G., Carney, M. E., Wilkens, L. R., Werner Hartman, Linda, Manjer, Jonas, Olsson, Håkan, Kumle, M., Grisso, J. A., Morgan, M., Wheeler, J. E., Edwards, R. P., Kelley, J. L., Modugno, F., Onland-Moret, N. C., Peeters, P. H. M., Casagrande, J., Pike, M. C., Wu, A. H., Canfell, K., Miller, A. B., Gram, I. T., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., Risch, H. A., Gapstur, S. M., Patel, A. V., Banks, E., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Beral, V., Bull, D., Cairns, B., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Hermon, C., Key, T., Moser, K., Reeves, G., Sitas, F., Collins, R., Peto, R., Gonzalez, C. A., Lee, N., Marchbanks, P., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Goodman, M. T., Lidegaard, O., Kjaer, S. K., Morch, L. S., Tjonneland, A., Byers, T., Rohan, T., Mosgaard, B., Vessey, M., Yeates, D., Freudenheim, J. L., Titus, L. J., Chang-Claude, J., Kaaks, R., Anderson, K. E., Lazovich, D., Robien, K., Hampton, J., Newcomb, P. A., Rossing, M. A., Thomas, D. B., Weiss, N. S., Lokkegaard, E., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tamimi, R. M., Tworoger, S. S., Franceschi, S., La Vecchia, C., Negri, E., Adami, H. O., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., Brinton, L. A., Freedman, D. M., Hartge, P., Hsing, A. W., Jnr, J. V. Lacey, Lissowska, J., Hoover, R. N., Schairer, C., Babb, C., Urban, M., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., Moysich, K., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Lurie, G., Carney, M. E., Wilkens, L. R., Werner Hartman, Linda, Manjer, Jonas, Olsson, Håkan, Kumle, M., Grisso, J. A., Morgan, M., Wheeler, J. E., Edwards, R. P., Kelley, J. L., Modugno, F., Onland-Moret, N. C., Peeters, P. H. M., Casagrande, J., Pike, M. C., Wu, A. H., Canfell, K., Miller, A. B., Gram, I. T., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., and Risch, H. A.

Abstract

Background Half the epidemiological studies with information about menopausal hormone therapy and ovarian cancer risk remain unpublished, and some retrospective studies could have been biased by selective participation or recall. We aimed to assess with minimal bias the effects of hormone therapy on ovarian cancer risk. Methods Individual participant datasets from 52 epidemiological studies were analysed centrally. The principal analyses involved the prospective studies (with last hormone therapy use extrapolated forwards for up to 4 years). Sensitivity analyses included the retrospective studies. Adjusted Poisson regressions yielded relative risks (RRs) versus never-use. Findings During prospective follow-up, 12 110 postmenopausal women, 55% (6601) of whom had used hormone therapy, developed ovarian cancer. Among women last recorded as current users, risk was increased even with <5 years of use (RR 1.43, 95% CI 1.31-1.56; p<0.0001). Combining current-or-recent use (any duration, but stopped <5 years before diagnosis) resulted in an RR of 1.37 (95% CI 1.29-1.46; p<0.0001); this risk was similar in European and American prospective studies and for oestrogen-only and oestrogen-progestagen preparations, but differed across the four main tumour types (heterogeneity p<0.0001), being definitely increased only for the two most common types, serous (RR 1.53, 95% CI 1.40-1.66; p<0.0001) and endometrioid (1.42, 1.20-1.67; p<0.0001). Risk declined the longer ago use had ceased, although about 10 years after stopping long-duration hormone therapy use there was still an excess of serous or endometrioid tumours (RR 1.25, 95% CI 1.07-1.46, p=0.005). Interpretation The increased risk may well be largely or wholly causal; if it is, women who use hormone therapy for 5 years from around age 50 years have about one extra ovarian cancer per 1000 users and, if its prognosis is typical, about one extra ovarian cancer death per 1700 users.

Published
2015

5. Ovarian Cancer and Body Size : Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies

Author

Beral, V., Hermon, C., Peto, R., Reeves, G., Brinton, L., Marchbanks, P., Negri, E., Ness, R., Peeters, P. H. M., Vessey, M., Calle, E. E., Gapstur, S. M., Patel, A. V., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Allen, N., Bull, D., Callaghan, K., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Key, T., Moser, K., Collins, R., Doll, R., Gonzalez, C. A., Lee, N., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Tjonneland, A., Titus-Ernstoff, L., Byers, T., Rohan, T., Mosgaard, B. J., Yeates, D., Freudenheim, J. L., Chang-Claude, J., Kaaks, R., Anderson, K. E., Folsom, A., Robien, K., Rossing, M. A., Thomas, D. B., Weiss, N. S., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tworoger, S. S., Franceschi, S., La Vecchia, C., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., de Gonzalez, A. Berrington, Freedman, D. M., Hartge, P., Hsing, A. W., Lacey, J. V., Jr., Hoover, R. N., Schairer, C., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Kelsey, J., Paffenbarger, R., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Goodman, M. T., Lurie, G., Carney, M. E., Wilkens, L. R., Hartman, L., Manjer, J., Olsson, H., Grisso, J. A., Morgan, M., Wheeler, J. E., Casagrande, J., Pike, M. C., Ross, R. K., Wu, A. H., Miller, A. B., Kumle, M., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., Risch, H. A., Beral, V., Hermon, C., Peto, R., Reeves, G., Brinton, L., Marchbanks, P., Negri, E., Ness, R., Peeters, P. H. M., Vessey, M., Calle, E. E., Gapstur, S. M., Patel, A. V., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Allen, N., Bull, D., Callaghan, K., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Key, T., Moser, K., Collins, R., Doll, R., Gonzalez, C. A., Lee, N., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Tjonneland, A., Titus-Ernstoff, L., Byers, T., Rohan, T., Mosgaard, B. J., Yeates, D., Freudenheim, J. L., Chang-Claude, J., Kaaks, R., Anderson, K. E., Folsom, A., Robien, K., Rossing, M. A., Thomas, D. B., Weiss, N. S., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tworoger, S. S., Franceschi, S., La Vecchia, C., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., de Gonzalez, A. Berrington, Freedman, D. M., Hartge, P., Hsing, A. W., Lacey, J. V., Jr., Hoover, R. N., Schairer, C., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Kelsey, J., Paffenbarger, R., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Goodman, M. T., Lurie, G., Carney, M. E., Wilkens, L. R., Hartman, L., Manjer, J., Olsson, H., Grisso, J. A., Morgan, M., Wheeler, J. E., Casagrande, J., Pike, M. C., Ross, R. K., Wu, A. H., Miller, A. B., Kumle, M., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., and Risch, H. A.

Abstract

Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with

Published
2012
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6. Ovarian Cancer and Body Size: Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies

Author

Beral, V., Hermon, C., Peto, R., Reeves, G., Brinton, L., Marchbanks, P., Negri, E., Ness, R., Peeters, P. H. M., Vessey, M., Calle, E. E., Gapstur, S. M., Patel, A. V., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Allen, N., Bull, D., Callaghan, K., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Key, T., Moser, K., Collins, R., Doll, R., Gonzalez, C. A., Lee, N., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Tjonneland, A., Titus-Ernstoff, L., Byers, T., Rohan, T., Mosgaard, B. J., Yeates, D., Freudenheim, J. L., Chang-Claude, J., Kaaks, R., Anderson, K. E., Folsom, A., Robien, K., Rossing, M. A., Thomas, D. B., Weiss, N. S., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tworoger, S. S., Franceschi, S., La Vecchia, C., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., de Gonzalez, A. Berrington, Freedman, D. M., Hartge, P., Hsing, A. W., Lacey Jr, J. V., Hoover, R. N., Schairer, C., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Kelsey, J., Paffenbarger, R., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Goodman, M. T., Lurie, G., Carney, M. E., Wilkens, L. R., Werner Hartman, Linda, Manjer, Jonas, Olsson, Håkan, Grisso, J. A., Morgan, M., Wheeler, J. E., Casagrande, J., Pike, M. C., Ross, R. K., Wu, A. H., Miller, A. B., Kumle, M., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., Risch, H. A., Beral, V., Hermon, C., Peto, R., Reeves, G., Brinton, L., Marchbanks, P., Negri, E., Ness, R., Peeters, P. H. M., Vessey, M., Calle, E. E., Gapstur, S. M., Patel, A. V., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Allen, N., Bull, D., Callaghan, K., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Key, T., Moser, K., Collins, R., Doll, R., Gonzalez, C. A., Lee, N., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Tjonneland, A., Titus-Ernstoff, L., Byers, T., Rohan, T., Mosgaard, B. J., Yeates, D., Freudenheim, J. L., Chang-Claude, J., Kaaks, R., Anderson, K. E., Folsom, A., Robien, K., Rossing, M. A., Thomas, D. B., Weiss, N. S., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tworoger, S. S., Franceschi, S., La Vecchia, C., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., de Gonzalez, A. Berrington, Freedman, D. M., Hartge, P., Hsing, A. W., Lacey Jr, J. V., Hoover, R. N., Schairer, C., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Kelsey, J., Paffenbarger, R., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Goodman, M. T., Lurie, G., Carney, M. E., Wilkens, L. R., Werner Hartman, Linda, Manjer, Jonas, Olsson, Håkan, Grisso, J. A., Morgan, M., Wheeler, J. E., Casagrande, J., Pike, M. C., Ross, R. K., Wu, A. H., Miller, A. B., Kumle, M., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., and Risch, H. A.

Abstract

Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ov

Published
2012

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