Dietary intake of selected nutrients and persistence of HPV infection in men

Imagem de Miniatura
Arquivos
art_LOPES_Dietary_intake_of_selected_nutrients_and_persistence_of_2017.PDF (546.08 KB)
Citações na Scopus
15
Tipo de produção
article
Data de publicação
2017
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Autores
LOPES, Raissa do Vale C.
TEIXEIRA, Juliana A.
MARCHIONI, Dirce
GIULIANO, Anna R.
FISBERG, Regina M.
Citação
INTERNATIONAL JOURNAL OF CANCER, v.141, n.4, p.757-765, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Human papillomavirus (HPV) infection is a common sexually transmitted disease. Although often transitory, persistent oncogenic HPV infection may progress to a precursor lesion and, if not treated, can further increase the risk of cancer. The purpose of this study was to investigate the relation between dietary intake and HPV persistent infection in men of a Brazilian cohort. The study population consisted of 1,248 men from the Brazilian cohort of the HIM (HPV in Men) Study, ages 18 to 70 years, who completed a quantitative food frequency questionnaire. U Mann-Whitney test was used to assess differences in median nutrient intake of selected nutrients. The association of dietary intake and persistent HPV infection was assessed in multivariate logistic models. The prevalence of any HPV infection at baseline was 66.6%. Of 1,248 participants analyzed, 1,211 (97.0%) were HPV positive at one or more times during the 4 years of follow-up and 781 (62.6%) were persistently HPV positive. Men with nonpersistent oncogenic HPV infections had higher median intake of retinol (p=0.008), vitamin A (p<0.001) and folate (DFE; p=0.003) and lower median intake of energy (p=0.005) and lycopene (p=0.008) in comparison to men with persistent oncogenic infections. No significant association was found between selected nutrients and persistent oncogenic HPV infection. For nononcogenic persistent infections, only vitamin B12 intake was significantly associated (p=0.003, test for trend). No association was observed between dietary intake and persistent oncogenic-type HPV infection; however, vitamin B12 intake was inversely associated with nononcogenic HPV persistence. What's new? Can diet influence the persistence of HPV infection? Certain B vitamins, for instance, can promote viral integration, while other nutrients hinder it. This is the first study to investigate whether diet contributes to persistent oncogenic HPV-infection in men. Looking at a Brazilian cohort of men age 18-70, these authors tested the men for HPV over a period of 4 years. At each meeting, they gave them a questionnaire, asking about their diet. Persistent nononcogenic HPV infection was associated with B12 consumption, they found, but they could link none of the nutrients to persistent oncogenic HPV infection.
Palavras-chave
diet, HPV, men, food frequency questionnaire
URI
https://observatorio.fm.usp.br/handle/OPI/21279
Referências
  1. Bailey LB, 1999, J NUTR, V129, P779
  2. Borutinskaite VV, 2006, ANN NY ACAD SCI, V1091, P346, DOI 10.1196/annals.1378.079
  3. Bruni L, 2015, HUMAN PAPILLOMAVIRUS
  4. Cesar CLG, 2005, SAUDE CONDICAO VIDA
  5. Chih HJ, 2013, NUTR CANCER, V65, P317, DOI 10.1080/01635581.2013.757630
  6. Choi SW, 2000, J NUTR, V130, P129
  7. DisDomenico F, 2012, BIOCHIM BIOPHYS ACTA, V1822, P737
  8. Fisberg RM, 2008, REV SAUDE PUBL, V42, P550, DOI [10.1590/S0034-89102008000300023, 10.1590/s0034-89102008005000020]
  9. Gadducci A, 2011, GYNECOL ENDOCRINOL, V27, P597, DOI 10.3109/09513590.2011.558953
  10. Garcia-Closas R, 2005, INT J CANCER, V117, P629, DOI 10.1002/ijc.21193
  11. Giuliano AR, 2008, CANCER EPIDEM BIOMAR, V17, P2036, DOI 10.1158/1055-9965.EPI-08-0151
  12. Giuliano AR, 2008, CANCER EPIDEM BIOMAR, V17, P805, DOI 10.1158/1055-9965.EPI-07-0741
  13. Giuliano AR, 2007, GYNECOL ONCOL, V107, pS24, DOI 10.1016/j.ygyno.2007.07.075
  14. Giuliano AR, 2011, LANCET, V377, P932, DOI 10.1016/S0140-6736(10)62342-2
  15. Giuliano AR, 2009, INT J CANCER, V124, P1251, DOI 10.1002/ijc.24097
  16. Giuliano AR, 2003, J INFECT DIS, V188, P1508, DOI 10.1086/379197
  17. Guenther PM, 1998, DESIGN OPERATION CON, P42
  18. Harttig U, 2011, EUR J CLIN NUTR, V65, pS87, DOI 10.1038/ejcn.2011.92
  19. Haubrock J, 2011, J NUTR, V141, P914, DOI 10.3945/jn.109.120394
  20. Hill RJ, 2001, BRIT J NUTR, V85, P415, DOI 10.1079/BJN2000281
  21. Ho GYF, 1998, NEW ENGL J MED, V338, P423, DOI 10.1056/NEJM199802123380703
  22. Luong KVQ, 2010, CRIT REV ONCOL HEMAT, V73, P192, DOI 10.1016/j.critrevonc.2009.04.008
  23. Lajous M, 2005, CANCER EPIDEM BIOMAR, V14, P1710, DOI 10.1158/1055-9965.EPI-04-0926
  24. Moscicki AB, 2001, JAMA-J AM MED ASSOC, V285, P2995, DOI 10.1001/jama.285.23.2995
  25. Narisawa-Saito M, 2007, CANCER SCI, V98, P1505, DOI 10.1111/j.1349-7006.2007.00546.x
  26. Potischman N, 1996, CANCER CAUSE CONTROL, V7, P113, DOI 10.1007/BF00115643
  27. Reddy L, 2003, PHARMACOL THERAPEUT, V99, P1, DOI 10.1016/S0163-7258(03)00042-1
  28. Sedjo RL, 2002, CANCER EPIDEM BIOMAR, V11, P353
  29. Sedjo RL, 2002, CANCER EPIDEM BIOMAR, V11, P876
  30. SELHUB J, 1992, AM J CLIN NUTR, V55, P131
  31. Siegel EM, 2010, GYNECOL ONCOL, V118, P289, DOI 10.1016/j.ygyno.2010.05.022
  32. Teixeira JA, 2011, J AM DIET ASSOC, V111, P1045, DOI 10.1016/j.jada.2011.04.006
  33. Tooze JA, 2004, AM J CLIN NUTR, V79, P795
  34. Trabulsi J, 2001, AM J PHYSIOL-ENDOC M, V281, pE891
  35. World Health Organization, 1990, WHO TECHN REP SER, V797
  36. Willett WC, 1997, AM J CLIN NUTR, V65, P1220

Coleções
Artigos e Materiais de Revistas Científicas - FM/MDR
Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - LIM/24
Artigos e Materiais de Revistas Científicas - ODS/03