Folate deficiency and cervical dysplasia
C. E. Butterworth Jr, K. D. Hatch, M. Macaluso, P. Cole, H. E. Sauberlich, S. J. Soong, M. Borst and V. V. Baker
Department of Nutrition Sciences, School of Medicine, University of Alabama, Birmingham 35294-3360.
OBJECTIVE--To test the hypothesis that nutritional deficiency affects the
incidence of cervical dysplasia in young women. DESIGN AND
SETTING--Case-control study. Participants were derived from community
family-planning clinics and referrals to a colposcopy center.
PARTICIPANTS--A total of 726 subjects were screened, yielding 294 cases of
dysplasia and 170 controls defined by coexistent cytologic and colposcopic
evidence. MAIN OUTCOME MEASURES--Planned prior to data collection. Odds
ratios were computed using logistic regression models to evaluate
association between cervical dysplasia and sociodemographic, sexual, and
reproductive factors; smoking; oral contraceptive use; human papillomavirus
(HPV) infection; and 12 nutritional indices determined by blind analysis of
nonfasting blood specimens. RESULTS--The number of sexual partners, parity,
oral contraceptive use, and HPV-16 infection were significantly associated
with cervical dysplasia. Plasma nutrient levels were generally not
associated with risk. However, red blood cell folate levels at or below 660
nmol/L interacted with HPV-16 infection. The adjusted odds ratio for HPV-16
was 1.1 among women with folate levels above 660 nmol/L but 5.1 (95%
confidence interval, 2.3 to 11) among women with lower levels. Interactions
of red blood cell folate levels with cigarette smoking and parity were also
present but were not statistically significant. CONCLUSION--Low red blood
cell folate levels enhance the effect of other risk factors for cervical
dysplasia and, in particular, that of HPV-16 infection.
Nutritional biomarkers associated with gynecological conditions among US women with or at risk of HIV infection
Tohill et al.
Am. J. Clin. Nutr. 2007;85:1327-1334.
ABSTRACT
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Chronic cigarette smoking is associated with diminished folate status, altered folate form distribution, and increased genetic damage in the buccal mucosa of healthy adults.
Gabriel et al.
Am. J. Clin. Nutr. 2006;83:835-841.
ABSTRACT
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Interaction among Folate, Riboflavin, Genotype, and Cancer, with Reference to Colorectal and Cervical Cancer
Powers
J. Nutr. 2005;135:2960S-2966S.
ABSTRACT
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Folate: A Key to Optimizing Health and Reducing Disease Risk in the Elderly
Rampersaud et al.
J. Am. Coll. Nutr. 2003;22:1-8.
ABSTRACT
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Vitamin A, Carotenoids, and Risk of Persistent Oncogenic Human Papillomavirus Infection
Sedjo et al.
Cancer Epidemiol. Biomarkers Prev. 2002;11:876-884.
ABSTRACT
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Proceedings of the Trans-HHS Workshop: Diet, DNA Methylation Processes and Health
Ross and Poirier
J. Nutr. 2002;132:2329S-2332.
FULL TEXT
Human Papillomavirus Persistence and Nutrients Involved in the Methylation Pathway among a Cohort of Young Women
Sedjo et al.
Cancer Epidemiol. Biomarkers Prev. 2002;11:353-359.
ABSTRACT
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Association of Methylenetetrahydrofolate Reductase Polymorphism C677T and Dietary Folate with the Risk of Cervical Dysplasia
Goodman et al.
Cancer Epidemiol. Biomarkers Prev. 2001;10:1275-1280.
ABSTRACT
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Impact of Extracellular Folate Levels on Global Gene Expression
Jhaveri et al.
Mol. Pharmacol. 2001;60:1288-1295.
ABSTRACT
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Low Serum and Red Blood Cell Folate Are Moderately, but Nonsignificantly Associated with Increased Risk of Invasive Cervical Cancer in U.S. Women
Weinstein et al.
J. Nutr. 2001;131:2040-2048.
ABSTRACT
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The Risk of Cervical Cancer in Relation to Serum Concentrations of Folate, Vitamin B12, and Homocysteine
Alberg et al.
Cancer Epidemiol. Biomarkers Prev. 2000;9:761-764.
ABSTRACT
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Development of Difluoromethylornithine (DFMO) as a Chemoprevention Agent
Meyskens and Gerner
Clin. Cancer Res. 1999;5:945-951.
ABSTRACT
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Hereditary Factors in Gynecologic Cancer
Lynch et al.
The Oncologist 1998;3:319-338.
ABSTRACT
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