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Pooled analyses of 13 prospective cohort studies on folate intake and colon cancer.
Kim, DH, Smith-Warner, SA, Spiegelman, D, Yaun, SS, Colditz, GA, Freudenheim, JL, Giovannucci, E, Goldbohm, RA, Graham, S, Harnack, L, et al
Cancer causes & control : CCC. 2010;(11):1919-30
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Abstract
OBJECTIVE Studies of folate intake and colorectal cancer risk have been inconsistent. We examined the relation with colon cancer risk in a series of 13 prospective studies. METHODS Study- and sex-specific relative risks (RRs) were estimated from the primary data using Cox proportional hazards models and then pooled using a random-effects model. RESULTS Among 725,134 participants, 5,720 incident colon cancers were diagnosed during follow-up. The pooled multivariate RRs (95% confidence interval [CI]) comparing the highest vs. lowest quintile of intake were 0.92 (95% CI 0.84-1.00, p-value, test for between-studies heterogeneity = 0.85) for dietary folate and 0.85 (95% CI 0.77-0.95, p-value, test for between-studies heterogeneity = 0.42) for total folate. Results for total folate intake were similar in analyses using absolute intake cutpoints (pooled multivariate RR = 0.87, 95% CI 0.78-0.98, comparing ≥ 560 mcg/days vs. <240 mcg/days, p-value, test for trend = 0.009). When analyzed as a continuous variable, a 2% risk reduction (95% CI 0-3%) was estimated for every 100 μg/day increase in total folate intake. CONCLUSION These data support the hypothesis that higher folate intake is modestly associated with reduced risk of colon cancer.
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A randomized trial on folic acid supplementation and risk of recurrent colorectal adenoma.
Wu, K, Platz, EA, Willett, WC, Fuchs, CS, Selhub, J, Rosner, BA, Hunter, DJ, Giovannucci, E
The American journal of clinical nutrition. 2009;(6):1623-31
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Abstract
BACKGROUND Evidence from observational studies suggests that inadequate folate status enhances colorectal carcinogenesis, but results from some randomized trials do not support this hypothesis. OBJECTIVE To assess the effect of folic acid supplementation on recurrent colorectal adenoma, we conducted a cost-efficient, double-blind, randomized trial among participants of 2 large prospective cohorts, the Health Professionals Follow-Up Study and the Nurses' Health Study. DESIGN Participants were randomly assigned to receive folic acid (1 mg/d) (n = 338) or placebo (n = 334) for 3-6.5 y. The primary endpoint was any new diagnosis of adenoma during the study period (May 1996-March 2004). Secondary outcomes were adenoma by site and stage and number of recurrent adenomas. Associations were also examined by plasma folate concentrations at baseline. RESULTS Incidence of at least one recurrent adenoma was not significantly associated with folic acid supplementation [relative risk (RR): 0.82; 95% CI: 0.59,1.13; P = 0.22]. Among participants with low plasma folate concentrations at baseline (7.5 ng/mL), supplemental folic acid had no significant effect (RR: 1.28; 95% CI: 0.82, 1.99; P = 0.27, P(interaction) = 0.01). Contrary to findings from another clinical trial, there was no evidence for an increased risk of advanced or multiple adenomas. CONCLUSIONS Our results do not support an overall protective effect of folic acid supplementation on adenoma recurrence. Folic acid supplementation may be beneficial among those with lower folate concentrations at baseline. This trial was registered at clinical trials.gov as NCT00512850.
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Folate intake and risk of Parkinson's disease.
Chen, H, Zhang, SM, Schwarzschild, MA, Hernán, MA, Logroscino, G, Willett, WC, Ascherio, A
American journal of epidemiology. 2004;(4):368-75
Abstract
In clinical studies, individuals with Parkinson's disease have had higher concentrations of plasma homocysteine than did controls, and experimental evidence suggests that folate deficiency or focal administration of homocysteine sensitizes dopaminergic neurons to the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. The authors thus prospectively investigated whether higher intake of folate, vitamin B(6), or vitamin B(12) was related to a lower risk of Parkinson's disease in the Health Professionals Follow-up Study (1986-2000) and the Nurses' Health Study (1980-1998). They documented Parkinson's disease diagnoses in 248 men and 167 women during the follow-up. Folate intake was not associated with the risk of Parkinson's disease; the relative risks for the highest compared with the lowest quintiles were 1.0 (95% confidence interval: 0.7, 1.5) in men and 1.3 (95% confidence interval: 0.8, 2.3) in women. Neither did they find significant associations in analyses stratified by age, smoking, alcohol consumption, or lactose intake. Intake of vitamin B(6) or vitamin B(12) also was not related to the risk of Parkinson's disease. The current study does not support the hypothesis that higher intake of folate or related B vitamins lowers the risk of Parkinson's disease.