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2. Lifestyle changes in middle age and risk of cancer: evidence from the European Prospective Investigation into Cancer and Nutrition

Author

Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Hoff, G, Heath, A, Cross, A, Vineis, P, Dossus, L, Johansson, M, Freisling, H, Matta, K, Huybrechts, I, Chen, S, B. Borch, K, Sandanger, T, H. Nost, T, Dahm, C, Antoniussen, C, Tin Tin, S, Fournier, A, Marques, C, Artaud, F, Sanchez, M, Guevara, M, Santiuste, C, Agudo, A, Bajracharya, R, Katzke, V, Ricceri, F, Agnoli, C, Bergmann, M, Schulze, M, Panico, S, Masala, G, Tjonneland, A, Olsen, A, Stocks, T, Manjer, J, Aizpurua-Atxega, A, Weiderpass, E, Riboli, E, Gunter, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Hoff G., Heath A. K., Cross A. J., Vineis P., Dossus L., Johansson M., Freisling H., Matta K., Huybrechts I., Chen S. L. F., B. Borch K., Sandanger T. M., H. Nost T., Dahm C. C., Antoniussen C. S., Tin Tin S., Fournier A., Marques C., Artaud F., Sanchez M. -J., Guevara M., Santiuste C., Agudo A., Bajracharya R., Katzke V., Ricceri F., Agnoli C., Bergmann M. M., Schulze M. B., Panico S., Masala G., Tjonneland A., Olsen A., Stocks T., Manjer J., Aizpurua-Atxega A., Weiderpass E., Riboli E., Gunter M. J., Ferrari P., Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Hoff, G, Heath, A, Cross, A, Vineis, P, Dossus, L, Johansson, M, Freisling, H, Matta, K, Huybrechts, I, Chen, S, B. Borch, K, Sandanger, T, H. Nost, T, Dahm, C, Antoniussen, C, Tin Tin, S, Fournier, A, Marques, C, Artaud, F, Sanchez, M, Guevara, M, Santiuste, C, Agudo, A, Bajracharya, R, Katzke, V, Ricceri, F, Agnoli, C, Bergmann, M, Schulze, M, Panico, S, Masala, G, Tjonneland, A, Olsen, A, Stocks, T, Manjer, J, Aizpurua-Atxega, A, Weiderpass, E, Riboli, E, Gunter, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Hoff G., Heath A. K., Cross A. J., Vineis P., Dossus L., Johansson M., Freisling H., Matta K., Huybrechts I., Chen S. L. F., B. Borch K., Sandanger T. M., H. Nost T., Dahm C. C., Antoniussen C. S., Tin Tin S., Fournier A., Marques C., Artaud F., Sanchez M. -J., Guevara M., Santiuste C., Agudo A., Bajracharya R., Katzke V., Ricceri F., Agnoli C., Bergmann M. M., Schulze M. B., Panico S., Masala G., Tjonneland A., Olsen A., Stocks T., Manjer J., Aizpurua-Atxega A., Weiderpass E., Riboli E., Gunter M. J., and Ferrari P.

Abstract

In this study, we aimed to provide novel evidence on the impact of changing lifestyle habits on cancer risk. In the EPIC cohort, 295,865 middle-aged participants returned a lifestyle questionnaire at baseline and during follow-up. At both timepoints, we calculated a healthy lifestyle index (HLI) score based on cigarette smoking, alcohol consumption, body mass index and physical activity. HLI ranged from 0 (most unfavourable) to 16 (most favourable). We estimated the association between HLI change and risk of lifestyle-related cancers—including cancer of the breast, lung, colorectum, stomach, liver, cervix, oesophagus, bladder, and others—using Cox regression models. We reported hazard ratios (HR) with 95% confidence intervals (CI). Median time between the two questionnaires was 5.7 years, median age at follow-up questionnaire was 59 years. After the follow-up questionnaire, we observed 14,933 lifestyle-related cancers over a median follow-up of 7.8 years. Each unit increase in the HLI score was associated with 4% lower risk of lifestyle-related cancers (HR 0.96; 95%CI 0.95–0.97). Among participants in the top HLI third at baseline (HLI > 11), those in the bottom third at follow-up (HLI ≤ 9) had 21% higher risk of lifestyle-related cancers (HR 1.21; 95%CI 1.07–1.37) than those remaining in the top third. Among participants in the bottom HLI third at baseline, those in the top third at follow-up had 25% lower risk of lifestyle-related cancers (HR 0.75; 95%CI 0.65–0.86) than those remaining in the bottom third. These results indicate that lifestyle changes in middle age may have a significant impact on cancer risk.

Published
2024

13. Association between transportation noise exposure ans hypertension risk in the french E3N cohort

Author

Faure, E., primary, Houeto, A., additional, Boileau, A., additional, Perrin, C., additional, Gelot, A., additional, Correia, E., additional, Artaud, F., additional, Jamard, P., additional, Perez Munoz, A., additional, Mietlicki, F., additional, Quenez, M., additional, Gissinger, V., additional, Domergue, C., additional, Janillon, V., additional, Vincent, B., additional, Mohamed, F., additional, Godet, K., additional, Giorgis-Allemand, L., additional, Leduc, J., additional, Evrard, A.-S., additional, and Severi, G., additional

Published
2022
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15. Parkinson's disease polygenic risk score is not associated with impulse control disorders: A longitudinal study

Author

Corvol, Jean-Christophe, Elbaz, Alexis, Vidailhet, Marie, Brice, Alexis, Artaud, Fanny, Bourdain, Frédéric, Brandel, Jean-Philippe, Derkinderen, Pascal, Durif, Franck, Levy, Richard, Pico, Fernando, Rascol, Olivier, Bonnet, Anne-Marie, Bonnet, Cecilia, Brefel-Courbon, Christine, Cormier-Dequaire, Florence, Degos, Bertrand, Debilly, Bérangère, Galitsky, Monique, Grabli, David, Hartmann, Andreas, Klebe, Stephan, Kraemmer, Julia, Lacomblez, Lucette, Leder, Sara, Mangone, Graziella, Mariani, Louise-Laure, Marques, Ana-Raquel, Mesnage, Valérie, Muellner, Julia, Ory-Magne, Fabienne, Planté-Bordeneuve, Violaine, Roze, Emmanuel, Tir, Melissa, You, Hana, Benchetrit, Eve, Socha, Julie, Pineau, Fanny, Vidal, Tiphaine, Pomies, Elsa, Bayet, Virginie, Lesage, Suzanne, Tahiri, Khadija, Bertrand, Hélène, Mallet, Alain, Villeret, Coralie, Mazmanian, Merry, Manseur, Hakima, Hajji, Mostafa, Le Toullec, Benjamin, Brochard, Vanessa, Roy, Monica, Rieu, Isabelle, Bernard, Stéphane, Faurie-Grepon, Antoine, Ihle, J., Artaud, F., Bekadar, S., Mangone, G., Sambin, S., Mariani, LL, Bertrand, H., Rascol, O., Durif, F., Derkinderen, P., Scherzer, C., Elbaz, A., and Corvol, JC

Published
2020
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16. Development and validation of a lifestyle-based model for colorectal cancer risk prediction: the LiFeCRC score

Author

Aleksandrova, K. Reichmann, R. Kaaks, R. Jenab, M. Bueno-de-Mesquita, H.B. Dahm, C.C. Eriksen, A.K. Tjønneland, A. Artaud, F. Boutron-Ruault, M.-C. Severi, G. Hüsing, A. Trichopoulou, A. Karakatsani, A. Peppa, E. Panico, S. Masala, G. Grioni, S. Sacerdote, C. Tumino, R. Elias, S.G. May, A.M. Borch, K.B. Sandanger, T.M. Skeie, G. Sánchez, M.-J. Huerta, J.M. Sala, N. Gurrea, A.B. Quirós, J.R. Amiano, P. Berntsson, J. Drake, I. van Guelpen, B. Harlid, S. Key, T. Weiderpass, E. Aglago, E.K. Cross, A.J. Tsilidis, K.K. Riboli, E. Gunter, M.J.

Abstract

Background: Nutrition and lifestyle have been long established as risk factors for colorectal cancer (CRC). Modifiable lifestyle behaviours bear potential to minimize long-term CRC risk; however, translation of lifestyle information into individualized CRC risk assessment has not been implemented. Lifestyle-based risk models may aid the identification of high-risk individuals, guide referral to screening and motivate behaviour change. We therefore developed and validated a lifestyle-based CRC risk prediction algorithm in an asymptomatic European population. Methods: The model was based on data from 255,482 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study aged 19 to 70 years who were free of cancer at study baseline (1992–2000) and were followed up to 31 September 2010. The model was validated in a sample comprising 74,403 participants selected among five EPIC centres. Over a median follow-up time of 15 years, there were 3645 and 981 colorectal cancer cases in the derivation and validation samples, respectively. Variable selection algorithms in Cox proportional hazard regression and random survival forest (RSF) were used to identify the best predictors among plausible predictor variables. Measures of discrimination and calibration were calculated in derivation and validation samples. To facilitate model communication, a nomogram and a web-based application were developed. Results: The final selection model included age, waist circumference, height, smoking, alcohol consumption, physical activity, vegetables, dairy products, processed meat, and sugar and confectionary. The risk score demonstrated good discrimination overall and in sex-specific models. Harrell’s C-index was 0.710 in the derivation cohort and 0.714 in the validation cohort. The model was well calibrated and showed strong agreement between predicted and observed risk. Random survival forest analysis suggested high model robustness. Beyond age, lifestyle data led to improved model performance overall (continuous net reclassification improvement = 0.307 (95% CI 0.264–0.352)), and especially for young individuals below 45 years (continuous net reclassification improvement = 0.364 (95% CI 0.084–0.575)). Conclusions: LiFeCRC score based on age and lifestyle data accurately identifies individuals at risk for incident colorectal cancer in European populations and could contribute to improved prevention through motivating lifestyle change at an individual level. © 2020, The Author(s).

Published
2021

17. Development and validation of a lifestyle-based model for colorectal cancer risk prediction: the LiFeCRC score

Author

Aleksandrova, K, Reichmann, R, Kaaks, R, Jenab, M, Bueno-de-Mesquita, HB, Dahm, CC, Eriksen, AK, Tjonneland, A, Artaud, F, Boutron-Ruault, M-C, Severi, G, Husing, A, Trichopoulou, A, Karakatsani, A, Peppa, E, Panico, S, Masala, G, Grioni, S, Sacerdote, C, Tumino, R, Elias, SG, May, AM, Borch, KB, Sandanger, TM, Skeie, G, Sanchez, M-J, Huerta, JM, Sala, N, Gurrea, AB, Quiros, JR, Amiano, P, Berntsson, J, Drake, I, van Guelpen, B, Harlid, S, Key, T, Weiderpass, E, Aglago, EK, Cross, AJ, Tsilidis, KK, Riboli, E, Gunter, MJ, Aleksandrova, K, Reichmann, R, Kaaks, R, Jenab, M, Bueno-de-Mesquita, HB, Dahm, CC, Eriksen, AK, Tjonneland, A, Artaud, F, Boutron-Ruault, M-C, Severi, G, Husing, A, Trichopoulou, A, Karakatsani, A, Peppa, E, Panico, S, Masala, G, Grioni, S, Sacerdote, C, Tumino, R, Elias, SG, May, AM, Borch, KB, Sandanger, TM, Skeie, G, Sanchez, M-J, Huerta, JM, Sala, N, Gurrea, AB, Quiros, JR, Amiano, P, Berntsson, J, Drake, I, van Guelpen, B, Harlid, S, Key, T, Weiderpass, E, Aglago, EK, Cross, AJ, Tsilidis, KK, Riboli, E, and Gunter, MJ

Abstract

BACKGROUND: Nutrition and lifestyle have been long established as risk factors for colorectal cancer (CRC). Modifiable lifestyle behaviours bear potential to minimize long-term CRC risk; however, translation of lifestyle information into individualized CRC risk assessment has not been implemented. Lifestyle-based risk models may aid the identification of high-risk individuals, guide referral to screening and motivate behaviour change. We therefore developed and validated a lifestyle-based CRC risk prediction algorithm in an asymptomatic European population. METHODS: The model was based on data from 255,482 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study aged 19 to 70 years who were free of cancer at study baseline (1992-2000) and were followed up to 31 September 2010. The model was validated in a sample comprising 74,403 participants selected among five EPIC centres. Over a median follow-up time of 15 years, there were 3645 and 981 colorectal cancer cases in the derivation and validation samples, respectively. Variable selection algorithms in Cox proportional hazard regression and random survival forest (RSF) were used to identify the best predictors among plausible predictor variables. Measures of discrimination and calibration were calculated in derivation and validation samples. To facilitate model communication, a nomogram and a web-based application were developed. RESULTS: The final selection model included age, waist circumference, height, smoking, alcohol consumption, physical activity, vegetables, dairy products, processed meat, and sugar and confectionary. The risk score demonstrated good discrimination overall and in sex-specific models. Harrell's C-index was 0.710 in the derivation cohort and 0.714 in the validation cohort. The model was well calibrated and showed strong agreement between predicted and observed risk. Random survival forest analysis suggested high model robustness. Beyond age, lifestyle data l

Published
2021

18. Weight change in middle adulthood and risk of cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort

Author

Christakoudi, S, Pagoni, P, Ferrari, P, Cross, AJ, Tzoulaki, I, Muller, DC, Weiderpass, E, Freisling, H, Murphy, N, Dossus, L, Turzanski Fortner, R, Agudo, A, Overvad, K, Perez-Cornago, A, Key, TJ, Brennan, P, Johansson, M, Tjonneland, A, Halkjaer, J, Boutron-Ruault, M-C, Artaud, F, Severi, G, Kaaks, R, Schulze, MB, Bergmann, MM, Masala, G, Grioni, S, Simeon, V, Tumino, R, Sacerdote, C, Skeie, G, Rylander, C, Borch, KB, Quiros, JR, Rodriguez-Barranco, M, Chirlaque, M-D, Ardanaz, E, Amiano, P, Drake, I, Stocks, T, Haggstrom, C, Harlid, S, Ellingjord-Dale, M, Riboli, E, Tsilidis, KK, Christakoudi, S, Pagoni, P, Ferrari, P, Cross, AJ, Tzoulaki, I, Muller, DC, Weiderpass, E, Freisling, H, Murphy, N, Dossus, L, Turzanski Fortner, R, Agudo, A, Overvad, K, Perez-Cornago, A, Key, TJ, Brennan, P, Johansson, M, Tjonneland, A, Halkjaer, J, Boutron-Ruault, M-C, Artaud, F, Severi, G, Kaaks, R, Schulze, MB, Bergmann, MM, Masala, G, Grioni, S, Simeon, V, Tumino, R, Sacerdote, C, Skeie, G, Rylander, C, Borch, KB, Quiros, JR, Rodriguez-Barranco, M, Chirlaque, M-D, Ardanaz, E, Amiano, P, Drake, I, Stocks, T, Haggstrom, C, Harlid, S, Ellingjord-Dale, M, Riboli, E, and Tsilidis, KK

Abstract

Obesity is a risk factor for several major cancers. Associations of weight change in middle adulthood with cancer risk, however, are less clear. We examined the association of change in weight and body mass index (BMI) category during middle adulthood with 42 cancers, using multivariable Cox proportional hazards models in the European Prospective Investigation into Cancer and Nutrition cohort. Of 241 323 participants (31% men), 20% lost and 32% gained weight (>0.4 to 5.0 kg/year) during 6.9 years (average). During 8.0 years of follow-up after the second weight assessment, 20 960 incident cancers were ascertained. Independent of baseline BMI, weight gain (per one kg/year increment) was positively associated with cancer of the corpus uteri (hazard ratio [HR] = 1.14; 95% confidence interval: 1.05-1.23). Compared to stable weight (±0.4 kg/year), weight gain (>0.4 to 5.0 kg/year) was positively associated with cancers of the gallbladder and bile ducts (HR = 1.41; 1.01-1.96), postmenopausal breast (HR = 1.08; 1.00-1.16) and thyroid (HR = 1.40; 1.04-1.90). Compared to maintaining normal weight, maintaining overweight or obese BMI (World Health Organisation categories) was positively associated with most obesity-related cancers. Compared to maintaining the baseline BMI category, weight gain to a higher BMI category was positively associated with cancers of the postmenopausal breast (HR = 1.19; 1.06-1.33), ovary (HR = 1.40; 1.04-1.91), corpus uteri (HR = 1.42; 1.06-1.91), kidney (HR = 1.80; 1.20-2.68) and pancreas in men (HR = 1.81; 1.11-2.95). Losing weight to a lower BMI category, however, was inversely associated with cancers of the corpus uteri (HR = 0.40; 0.23-0.69) and colon (HR = 0.69; 0.52-0.92). Our findings support avoiding weight gain and encouraging weight loss in middle adulthood.

Published
2021

19. Parkinson's disease polygenic risk score is not associated with impulse control disorders: A longitudinal study

Author

Ihle, J., primary, Artaud, F., additional, Bekadar, S., additional, Mangone, G., additional, Sambin, S., additional, Mariani, LL, additional, Bertrand, H., additional, Rascol, O., additional, Durif, F., additional, Derkinderen, P., additional, Scherzer, C., additional, Elbaz, A., additional, Corvol, JC, additional, Corvol, Jean-Christophe, additional, Elbaz, Alexis, additional, Vidailhet, Marie, additional, Brice, Alexis, additional, Artaud, Fanny, additional, Bourdain, Frédéric, additional, Brandel, Jean-Philippe, additional, Derkinderen, Pascal, additional, Durif, Franck, additional, Levy, Richard, additional, Pico, Fernando, additional, Rascol, Olivier, additional, Bonnet, Anne-Marie, additional, Bonnet, Cecilia, additional, Brefel-Courbon, Christine, additional, Cormier-Dequaire, Florence, additional, Degos, Bertrand, additional, Debilly, Bérangère, additional, Galitsky, Monique, additional, Grabli, David, additional, Hartmann, Andreas, additional, Klebe, Stephan, additional, Kraemmer, Julia, additional, Lacomblez, Lucette, additional, Leder, Sara, additional, Mangone, Graziella, additional, Mariani, Louise-Laure, additional, Marques, Ana-Raquel, additional, Mesnage, Valérie, additional, Muellner, Julia, additional, Ory-Magne, Fabienne, additional, Planté-Bordeneuve, Violaine, additional, Roze, Emmanuel, additional, Tir, Melissa, additional, You, Hana, additional, Benchetrit, Eve, additional, Socha, Julie, additional, Pineau, Fanny, additional, Vidal, Tiphaine, additional, Pomies, Elsa, additional, Bayet, Virginie, additional, Lesage, Suzanne, additional, Tahiri, Khadija, additional, Bertrand, Hélène, additional, Mallet, Alain, additional, Villeret, Coralie, additional, Mazmanian, Merry, additional, Manseur, Hakima, additional, Hajji, Mostafa, additional, Le Toullec, Benjamin, additional, Brochard, Vanessa, additional, Roy, Monica, additional, Rieu, Isabelle, additional, Bernard, Stéphane, additional, and Faurie-Grepon, Antoine, additional

Published
2020
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21. Socioeconomic position, lifestyle habits and biomarkers of epigenetic aging: a multi-cohort analysis

Author

Fiorito, G., Mccrory, C., Robinson, O., Carmeli, C., Rosales, C. O., Zhang, Y., Colicino, E., Dugue, P. -A., Artaud, F., Mckay, G. J., Jeong, A., Mishra, P. P., Nost, T. H., Krogh, V., Panico, S., Sacerdote, C., Tumino, R., Palli, D., Matullo, G., Guarrera, S., Gandini, M., Bochud, M., Dermitzakis, E., Muka, T., Schwartz, J., Vokonas, P. S., Just, A., Hodge, A. M., Giles, G. G., Southey, M. C., Hurme, M. A., Young, I., Mcknight, A. J., Kunze, S., Waldenberger, M., Peters, A., Schwettmann, L., Lund, E., Baccarelli, A., Milne, R. L., Kenny, R. A., Elbaz, A., Brenner, H., Kee, F., Voortman, T., Probst-Hensch, N., Lehtimaki, T., Elliot, P., Stringhini, S., Vineis, P., Polidoro, S., Alberts, J., Alenius, H., Avendano, M., Baltar, V., Bartley, M., Barros, H., Bellone, M., Berger, E., Blane, D., Candiani, G., Carra, L., Castagne, R., Chadeau-Hyam, M., Cima, S., Clavel-Chapelon, F., Costa, G., Courtin, E., Delpierre, C., D'Errico, A., Dermitzakis, M., Elovainio, M., Elliott, P., Fagherazzi, G., Fraga, S., Gares, V., Gerbouin-Rerolle, P., Giles, G., Goldberg, M., Greco, D., Guessous, I., Haba-Rubio, J., Heinzer, R., Hodge, A., Joost, S., Karimi, M., Kelly-Irving, M., Kahonen, M., Karisola, P., Khenissi, L., Kivimaki, M., Laine, J., Lang, T., Laurent, A., Layte, R., Lepage, B., Lorsch, D., Macguire, F., Machell, G., Mackenbach, J., Marmot, M., de Mestral, C., Miller, C., Milne, R., Muennig, P., Nusselder, W., Petrovic, D., Pilapil, L., Preisig, M., Pulkki-Raback, L., Raitakari, O., Ribeiro, A. I., Ricceri, F., Recalcati, P., Reinhard, E., Valverde, J. R., Saba, S., Santegoets, F., Satolli, R., Simmons, T., Severi, G., Shipley, M. J., Tabak, A., Terhi, V., Tieulent, J., Vaccarella, S., Vigna-Taglianti, F., Vollenweider, P., Vuilleumier, N., Zins, M., Medical Research Council (MRC), Commission of the European Communities, BIOS Consortium, Lifepath consortium, Epidemiology, Dermitzakis, Emmanouil, and Stringhini, Silvia

Subjects
Male, Aging, Geriatrics & Gerontology, Disease, epigenetic clocks, Bioinformatics, 0601 Biochemistry and Cell Biology, DISEASE, Epigenesis, Genetic, Cohort Studies, 0302 clinical medicine, Risk Factors, DNA METHYLATION, media_common, 0303 health sciences, education, Lifepath consortium, VDP::Medisinske Fag: 700::Helsefag: 800::Samfunnsmedisin, sosialmedisin: 801, CARDIOVASCULAR RISK, Aged, Aging/genetics, Aging/psychology, DNA Methylation, Educational Status, Female, Humans, Life Style, Mutation, Social Class, biological aging, socioeconomic position, Longevity, ASSOCIATION, Biological aging, Education, Epigenetic clocks, Socioeconomic position, 3. Good health, WIDE METHYLATION, Aging/genetics/psychology, DNA methylation, Biomarker (medicine), HEALTH, BIOS Consortium, Life Sciences & Biomedicine, Research Paper, Cohort study, VDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk genetikk: 714, media_common.quotation_subject, CANCER-RISK, 610 Medicine & health, VDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710::Medical genetics: 714, Biology, PERIPHERAL-BLOOD, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Genetic, 360 Social problems & social services, 1112 Oncology and Carcinogenesis, Epigenetics, ddc:613, 030304 developmental biology, Science & Technology, Mechanism (biology), MUTATIONS, dNaM, Socioeconomic Position, Biological Aging, Epigenetic Clocks, Cell Biology, 0606 Physiology, DRIFT, VDP::Medical disciplines: 700::Health sciences: 800::Community medicine, Social medicine: 801, 030217 neurology & neurosurgery, Epigenesis
Abstract

Source at https://doi.org/10.18632/aging.101900. Differences in health status by socioeconomic position (SEP) tend to be more evident at older ages, suggesting the involvement of a biological mechanism responsive to the accumulation of deleterious exposures across the lifespan. DNA methylation (DNAm) has been proposed as a biomarker of biological aging that conserves memory of endogenous and exogenous stress during life. We examined the association of education level, as an indicator of SEP, and lifestyle-related variables with four biomarkers of age-dependent DNAm dysregulation: the total number of stochastic epigenetic mutations (SEMs) and three epigenetic clocks (Horvath, Hannum and Levine), in 18 cohorts spanning 12 countries. The four biological aging biomarkers were associated with education and different sets of risk factors independently, and the magnitude of the effects differed depending on the biomarker and the predictor. On average, the effect of low education on epigenetic aging was comparable with those of other lifestyle-related risk factors (obesity, alcohol intake), with the exception of smoking, which had a significantly stronger effect. Our study shows that low education is an independent predictor of accelerated biological (epigenetic) aging and that epigenetic clocks appear to be good candidates for disentangling the biological pathways underlying social inequalities in healthy aging and longevity.

Published
2019
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22. Timing of eating across ten European countries - Results from the European Prospective Investigation into Cancer and Nutrition (EPIC) calibration study

Author

Huseinovic, E. Winkvist, A. Freisling, H. Slimani, N. Boeing, H. Buckland, G. Schwingshackl, L. Olsen, A. Tjonneland, A. Stepien, M. Boutron-Ruault, M.-C. Mancini, F. Artaud, F. Kühn, T. Katzke, V. Trichopoulou, A. Naska, A. Orfanos, P. Tumino, R. Masala, G. Krogh, V. Santucci De Magistris, M. Ocké, M.C. Brustad, M. Jensen, T.E. Skeie, G. Rodríguez-Barranco, M. Huerta, J.M. Ardanaz, E. Quirós, J.R. Jakszyn, P. Sonestedt, E. Ericson, U. Wennberg, M. Key, T.J. Aune, D. Riboli, E. Weiderpass, E. Bertéus Forslund, H.

Abstract

Objective To examine timing of eating across ten European countries.Design Cross-sectional analysis of the European Prospective Investigation into Cancer and Nutrition (EPIC) calibration study using standardized 24 h diet recalls collected during 1995-2000. Eleven predefined food consumption occasions were assessed during the recall interview. We present time of consumption of meals and snacks as well as the later:earlier energy intake ratio, with earlier and later intakes defined as 06.00-14.00 and 15.00-24.00 hours, respectively. Type III tests were used to examine associations of sociodemographic, lifestyle and health variables with timing of energy intake.Setting Ten Western European countries.Subjects In total, 22 985 women and 13 035 men aged 35-74 years (n 36 020).Results A south-north gradient was observed for timing of eating, with later consumption of meals and snacks in Mediterranean countries compared with Central and Northern European countries. However, the energy load was reversed, with the later:earlier energy intake ratio ranging from 0·68 (France) to 1·39 (Norway) among women, and from 0·71 (Greece) to 1·35 (the Netherlands) among men. Among women, country, age, education, marital status, smoking, day of recall and season were all independently associated with timing of energy intake (all P

Published
2019

24. Socioeconomic position, lifestyle habits and biomarkers of epigenetic aging: a multi-cohort analysis.

Author

Kee F., Rosales C.O., Zhang Y., Colicino E., Dugue P.-A., Artaud F., McKay G.J., Jeong A., Mishra P.P., Elbaz A., Brenner H., Carmeli C., Voortman T., Probst-Hensch N., Lehtimaki T., Elliot P., Stringhini S., Vineis P., Polidoro S., Fiorito G., McCrory C., Robinson O., Nost T.H., Krogh V., Panico S., Sacerdote C., Tumino R., Palli D., Matullo G., Guarrera S., Gandini M., Bochud M., Dermitzakis E., Muka T., Schwartz J., Vokonas P.S., Just A., Hodge A.M., Giles G.G., Southey M.C., Hurme M.A., Young I., McKnight A.J., Kunze S., Waldenberger M., Peters A., Schwettmann L., Lund E., Baccarelli A., Milne R.L., Kenny R.A., Kee F., Rosales C.O., Zhang Y., Colicino E., Dugue P.-A., Artaud F., McKay G.J., Jeong A., Mishra P.P., Elbaz A., Brenner H., Carmeli C., Voortman T., Probst-Hensch N., Lehtimaki T., Elliot P., Stringhini S., Vineis P., Polidoro S., Fiorito G., McCrory C., Robinson O., Nost T.H., Krogh V., Panico S., Sacerdote C., Tumino R., Palli D., Matullo G., Guarrera S., Gandini M., Bochud M., Dermitzakis E., Muka T., Schwartz J., Vokonas P.S., Just A., Hodge A.M., Giles G.G., Southey M.C., Hurme M.A., Young I., McKnight A.J., Kunze S., Waldenberger M., Peters A., Schwettmann L., Lund E., Baccarelli A., Milne R.L., and Kenny R.A.

Abstract

Differences in health status by socioeconomic position (SEP) tend to be more evident at older ages, suggesting the involvement of a biological mechanism responsive to the accumulation of deleterious exposures across the lifespan. DNA methylation (DNAm) has been proposed as a biomarker of biological aging that conserves memory of endogenous and exogenous stress during life.We examined the association of education level, as an indicator of SEP, and lifestyle-related variables with four biomarkers of age-dependent DNAm dysregulation: the total number of stochastic epigenetic mutations (SEMs) and three epigenetic clocks (Horvath, Hannum and Levine), in 18 cohorts spanning 12 countries.The four biological aging biomarkers were associated with education and different sets of risk factors independently, and the magnitude of the effects differed depending on the biomarker and the predictor. On average, the effect of low education on epigenetic aging was comparable with those of other lifestyle-related risk factors (obesity, alcohol intake), with the exception of smoking, which had a significantly stronger effect.Our study shows that low education is an independent predictor of accelerated biological (epigenetic) aging and that epigenetic clocks appear to be good candidates for disentangling the biological pathways underlying social inequalities in healthy aging and longevity.

Published
2019

25. Socioeconomic position, lifestyle habits and biomarkers of epigenetic aging: a multi-cohort analysis

Author

Fiorito, G, McCrory, C, Robinson, O, Carmeli, C, Rosales, CO, Zhang, Y, Colicino, E, Dugue, P-A, Artaud, F, Mckay, GJ, Jeong, A, Mishra, PP, Nost, TH, Krogh, V, Panico, S, Sacerdote, C, Tumino, R, Palli, D, Matullo, G, Guarrera, S, Gandini, M, Bochud, M, Dermitzakis, E, Muka, T, Schwartz, J, Vokonas, PS, Just, A, Hodge, AM, Giles, GG, Southey, MC, Hurme, MA, Young, I, McKnight, AJ, Kunze, S, Waldenberger, M, Peters, A, Schwettmann, L, Lund, E, Baccarelli, A, Milne, RL, Kenny, RA, Elbaz, A, Brenner, H, Kee, F, Voortman, T, Probst-Hensch, N, Lehtimaki, T, Elliot, P, Stringhini, S, Vineis, P, Polidoro, S, Alberts, J, Alenius, H, Avendano, M, Baltar, V, Bartley, M, Barros, H, Bellone, M, Berger, E, Blane, D, Candiani, G, Carra, L, Castagne, R, Chadeau-Hyam, M, Cima, S, Clavel-Chapelon, F, Costa, G, Courtin, E, Delpierre, C, D'Errico, A, Manolis, Dermitzakis, Elovainio, M, Elliott, P, Fagherazzi, G, Fraga, S, Gares, V, Gerbouin-Rerolle, P, Giles, G, Goldberg, M, Greco, D, Guessous, I, Haba-Rubio, J, Heinzer, R, Hodge, A, Joost, S, Karimi, M, Kelly-Irving, M, Kahonen, M, Karisola, P, Khenissi, L, Kivimaki, M, Laine, J, Lang, T, Laurent, A, Layte, R, Lepage, B, Lorsch, D, MacGuire, F, Machell, G, Mackenbach, J, Marmot, M, de Mestral, C, Miller, C, Milne, R, Muennig, P, Nusselder, W, Petrovic, D, Lourdes, Pilapil, Preisig, M, Pulkki-Raback, L, Raitakari, O, Ribeiro, AI, Ricceri, F, Recalcati, P, Reinhard, E, Valverde, JR, Saba, S, Santegoets, F, Satolli, R, Simmons, T, Severi, G, Shipley, MJ, Tabak, A, Terhi, V, Tieulent, J, Vaccarella, S, Vigna-Taglianti, F, Vollenweider, P, Vuilleumier, N, Zins, M, Fiorito, G, McCrory, C, Robinson, O, Carmeli, C, Rosales, CO, Zhang, Y, Colicino, E, Dugue, P-A, Artaud, F, Mckay, GJ, Jeong, A, Mishra, PP, Nost, TH, Krogh, V, Panico, S, Sacerdote, C, Tumino, R, Palli, D, Matullo, G, Guarrera, S, Gandini, M, Bochud, M, Dermitzakis, E, Muka, T, Schwartz, J, Vokonas, PS, Just, A, Hodge, AM, Giles, GG, Southey, MC, Hurme, MA, Young, I, McKnight, AJ, Kunze, S, Waldenberger, M, Peters, A, Schwettmann, L, Lund, E, Baccarelli, A, Milne, RL, Kenny, RA, Elbaz, A, Brenner, H, Kee, F, Voortman, T, Probst-Hensch, N, Lehtimaki, T, Elliot, P, Stringhini, S, Vineis, P, Polidoro, S, Alberts, J, Alenius, H, Avendano, M, Baltar, V, Bartley, M, Barros, H, Bellone, M, Berger, E, Blane, D, Candiani, G, Carra, L, Castagne, R, Chadeau-Hyam, M, Cima, S, Clavel-Chapelon, F, Costa, G, Courtin, E, Delpierre, C, D'Errico, A, Manolis, Dermitzakis, Elovainio, M, Elliott, P, Fagherazzi, G, Fraga, S, Gares, V, Gerbouin-Rerolle, P, Giles, G, Goldberg, M, Greco, D, Guessous, I, Haba-Rubio, J, Heinzer, R, Hodge, A, Joost, S, Karimi, M, Kelly-Irving, M, Kahonen, M, Karisola, P, Khenissi, L, Kivimaki, M, Laine, J, Lang, T, Laurent, A, Layte, R, Lepage, B, Lorsch, D, MacGuire, F, Machell, G, Mackenbach, J, Marmot, M, de Mestral, C, Miller, C, Milne, R, Muennig, P, Nusselder, W, Petrovic, D, Lourdes, Pilapil, Preisig, M, Pulkki-Raback, L, Raitakari, O, Ribeiro, AI, Ricceri, F, Recalcati, P, Reinhard, E, Valverde, JR, Saba, S, Santegoets, F, Satolli, R, Simmons, T, Severi, G, Shipley, MJ, Tabak, A, Terhi, V, Tieulent, J, Vaccarella, S, Vigna-Taglianti, F, Vollenweider, P, Vuilleumier, N, and Zins, M

Abstract

Differences in health status by socioeconomic position (SEP) tend to be more evident at older ages, suggesting the involvement of a biological mechanism responsive to the accumulation of deleterious exposures across the lifespan. DNA methylation (DNAm) has been proposed as a biomarker of biological aging that conserves memory of endogenous and exogenous stress during life.We examined the association of education level, as an indicator of SEP, and lifestyle-related variables with four biomarkers of age-dependent DNAm dysregulation: the total number of stochastic epigenetic mutations (SEMs) and three epigenetic clocks (Horvath, Hannum and Levine), in 18 cohorts spanning 12 countries.The four biological aging biomarkers were associated with education and different sets of risk factors independently, and the magnitude of the effects differed depending on the biomarker and the predictor. On average, the effect of low education on epigenetic aging was comparable with those of other lifestyle-related risk factors (obesity, alcohol intake), with the exception of smoking, which had a significantly stronger effect.Our study shows that low education is an independent predictor of accelerated biological (epigenetic) aging and that epigenetic clocks appear to be good candidates for disentangling the biological pathways underlying social inequalities in healthy aging and longevity.

Published
2019

32. Scenario Development for FAST in the View of ITER and DEMO

Author

Crisanti F., Albanese R., Artaud F., Baiocchi B., Baruzzo M., Basiuk V., Bierwage A., Bilato R., Bolzonella T., Brambilla M., Briguglio S., Calabrò G., Cardinali A., Corrigan G., Cucchiaro A., Di Troia C., Farina D., Figini L., Fogaccia G., Giruzzi G., Granucci G., Imbeaux F., Johnson T., Lauro Taroni L., Maggiora R., Mantica P., Milanesio D., Parail V., Pericoli-Ridolfini V., Pizzuto A., Podda S., Ramogida G., Santinelli M., Schneider M., Tuccillo A., Valisa M., Villari R., Viola B., Vlad G., Wang X., and Zonca F.

Subjects
____
Abstract

____

Published
2010

49. Involvement of lateral habenula-dorsal raphe neurons in the differential regulation of striatal and nigral serotonergic transmission cats

Author

Jacques Glowinski, Reisine Td, Artaud F, and Philippe Soubrie

Subjects
Male, Serotonin, Caudate nucleus, Substance P, Serotonergic, Synaptic Transmission, chemistry.chemical_compound, Dorsal raphe nucleus, Thalamus, Basal ganglia, Animals, Neurons, Raphe, General Neuroscience, Serotonergic cell groups, Electric Conductivity, Articles, Corpus Striatum, Electric Stimulation, Substantia Nigra, Kinetics, nervous system, chemistry, Cats, Raphe Nuclei, Female, Neuroscience, Brain Stem, Picrotoxin
Abstract

The importance of the lateral habenula-dorsal raphe pathway in the control of in vivo [3H]serotonin release in the cat basal ganglia was examined using the push-pull cannula technique and an isotopic method for the estimation of [3H]serotonin continuously formed from [3H]tryptophan. [3H]Serotonin was measured in both caudate nuclei and substantiae nigra and, in some cases, in the dorsal raphe. Electrical stimulation of the lateral habenula decreased [3H]serotonin release in all structures studied. Blockade of the GABA inhibitory pathway to the lateral habenula by the local application of picrotoxin reduced [3H]serotonin release in both substantiae nigra and increased release of the 3H-amine in the dorsal raphe but was without effect on [3H]serotonin release in either caudate nucleus. This inhibition of nigral [3H]serotonin release was antagonized by simultaneous application of picrotoxin to the dorsal raphe. Substance P delivery to the dorsal raphe produced the same effects on [3H]serotonin release as described for picrotoxin application to the lateral habenula except that inhibition of nigral [3H]serotonin release was not prevented by local co-administration of picrotoxin. These results suggest that the lateral habenula can control serotonergic transmission in the basal ganglia and that this regulation may be different for those serotonergic neurons innervating the caudate nucleus versus those projecting to the substantia nigra.

Published
1982
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50. Effects of kelatorphan and other peptidase inhibitors on the in vitro and in vivo release of methionine-enkephalin-like material from the rat spinal cord.

Author

Bourgoin, S, Le Bars, D, Artaud, F, Clot, A M, Bouboutou, R, Fournie-Zaluski, M C, Roques, B P, Hamon, M, and Cesselin, F

Abstract

The effects of the novel mixed peptidase inhibitor, kelatorphan [N-(R)-3-(N-hydroxyaminocarbonyl-2-benzyl-1-oxopropyl)-L-alanine], were compared to those of a combination of the potent "enkephalinase" inhibitor thiorphan and the nonselective aminopeptidase inhibitor bestatin, on the catabolism of [3H]Met-enkephalin and on the release of endogenous Met-enkephalin by the rat spinal cord in vitro and in vivo. At 20 microM, kelatorphan almost prevented completely the degradation of exogenous [3H] Met-enkephalin by slices of the dorsal zone of the lumbar enlargement. Similarly, the addition of 20 microM kelatorphan to a [3H] Met-enkephalin-containing artificial cerebrospinal fluid superfusing the whole spinal cord of halothane-anesthetized rats efficiently protected the exogenous peptide from enzymatic degradation. In contrast, in the same in vitro and in vivo models, thiorphan (1 microM) or bestatin (20 microM) alone was inactive, and only their combination induced a significant protection of the exogenous peptide. In vitro and in vivo, kelatorphan (20 microM) increased markedly the spontaneous outflow of endogenous Met-enkephalin-like material as well as the peptide overflow due to K+-induced depolarization (in vitro and in vivo) or noxious stimulation (in vivo). Under similar conditions, thiorphan (1 microM) plus bestatin (20 microM) also enhanced the efflux of Met-enkephalin-like material, but generally to a lower extent than kelatorphan. Compared to thiorphan plus bestatin, kelatorphan exerts additional inhibitory effects on dipeptidylaminopeptidase activity and the present results could indicate that this enzyme also may be involved in the inactivation of extracellular Met-enkephalin at the spinal level in rats.

Published
1986

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