Added Folic acid linked to lower colorectal cancer rates.

[Nun Giver]

http://www.nutraingredients-usa.com/Research/Folate-fortification-linked-to-lower-colon-cancer-risk

Per work sponsored by American Cancer Society.

1. Gastroenterology. 2011 Jul;141(1):98-105, 105.e1. Epub 2011 Apr 14.

High levels of folate from supplements and fortification are not associated with
increased risk of colorectal cancer.

Stevens VL, McCullough ML, Sun J, Jacobs EJ, Campbell PT, Gapstur SM.

Epidemiology Research Program,
American Cancer Society,
Atlanta, Georgia
30303-1002, USA. ***@cancer.org

Comment in
Gastroenterology. 2011 Jul;141(1):16-20.

BACKGROUND & AIMS:
Folate intake has been inversely associated with
colorectal cancer risk in several prospective epidemiologic studies. However, no study fully assessed the influence of the high levels of folate that are
frequently consumed in the United States as a result of mandatory folate
fortification, which was fully implemented in 1998, and the recent increase in
use of folate-containing supplements. There is evidence that consumption of high levels of folic acid, the form of folate used for fortification and in
supplements, has different effects on biochemical pathways than natural folates
and might promote carcinogenesis.

METHODS:
We investigated the association between folate intake and colorectal
cancer among 43,512 men and 56,011 women in the Cancer Prevention Study II
(CPS-II) Nutrition Cohort; 1023 were diagnosed with colorectal cancer between
1999 and 2007, a period entirely after folate fortification began. Cox
proportional hazards regression was used to calculate multivariate hazards ratios (RR) and 95% confidence interval (CI).

RESULTS:
Intake of high levels of natural folate (RRQ5vsQ1=0.86; 95% CI:
0.70-1.06; P trend=.12) or folic acid (RRQ5vsQ1=0.84; 95% CI: 0.68-1.03; P
trend=.06) were not significantly associated with risk of colorectal cancer.
Total folate intake was significantly associated with lower risk (RRQ5vsQ1=0.81; 95% CI: 0.66-0.99; P trend=.047).

CONCLUSIONS:
Intake of high levels of total folate reduces risk of colorectal
cancer; there is no evidence that dietary fortification or supplementation with
this vitamin increases colorectal cancer risk.


PMID: 21586288 [PubMed - indexed for MEDLINE]

Trig

[Nun Giver]

Or perhaps additional folic acid is bad for men?

Nutr Cancer. 2011;63(3):357-66.

Nutrients in folate-mediated,
one-carbon metabolism and the risk of rectal tumors
in men and women.

Curtin K, Samowitz WS, Ulrich CM, Wolff RK,
Herrick JS, Caan BJ, Slattery ML.

Department of Internal Medicine,
University of Utah Health Sciences Center, Salt
Lake City, Utah 84132, USA.

In an investigation of rectal tumors characterized by CpG island methylator
phenotype (CIMP), KRAS2 mutation, and TP53 mutation, we examined associations
with dietary and supplemental folate, riboflavin, vitamins B(6) and B(12), and
methionine, nutrients involved in folate-mediated 1-carbon metabolism. We also
examined folate intake and common MTHFR polymorphisms in relation to CIMP. Data
from a population-based study of 951 cases (750 with tumor markers) and 1,205
controls were evaluated using multiple logistic regression models and generalized
estimating equations. Reduced risk of methylated tumors was suggested in women
with the upper tertile of folate intake (≥0.42 mg/day) vs. the lower tertile: OR
= 0.6, 95%CI = 0.3-1.2. In men, a significant 3-fold increased risk of CIMP+
tumor was observed for the upper tertile of folate (≥0.75 mg/day) vs. the lower
tertile (<0.44 mg/day): OR = 3.2, 95%CI = 1.5-6.7. These men consumed a greater
proportion of folic acid fortified foods relative to natural, primarily
plant-based sources (52% vs. 48%) than women with CIMP+ tumors (22% vs. 78%).
MTHFR 1298A>C influenced folate in male CIMP+ risk (P interaction < 0.01). Our
findings suggest folate supplementation effects may differ between genders,
perhaps due to variation in MTHFR and/or endogenous/exogenous hormones, and may
be important in the initiation and progression of methylated rectal tumors in
men.

PMCID: PMC3127576
PMID: 21462086 [PubMed - indexed for MEDLINE]

[Nun Giver]

Or maybe it only the prostate that has an elevated risk.

Quote: Prostate cancer was the only cancer type found to be
increased after folic acid supplementation (meta-analyses of six RCTs).
Prospective studies of cancer development in populations where food is fortified
with folic acid could indicate whether fortification similar to supplementation
moderately increases prostate cancer risk.

PMCID: PMC3278486
PMID: 22240654

http://www.ncbi.nlm.nih.gov/pubmed/22240654

The full read is available without charge.

[Nun Giver]

1. Br J Pharmacol. 2012 Apr 27. doi: 10.1111/j.1476-5381.2012.02002.x. [Epub ahead
of print]

Epigenetic mechanisms in anti-cancer actions of bioactive food components-the
implications in cancer prevention.

Stefanska B, Karlic H, Varga F, Fabianowska-Majewska K, Haslberger AG.
<snip>

The hallmarks of carcinogenesis are aberrations in gene expression and protein
function caused by both genetic and epigenetic modifications. Epigenetics refers
to the changes in gene expression programming that alter the phenotype in absence
of a change in DNA sequence. Epigenetic modifications, which include amongst
others DNA methylation, covalent modifications of histone tails, and regulation
by non-coding RNAs, play a significant role in normal development and genome
stability. The changes are dynamic and serve as an adaptation mechanism to a wide
variety of environmental and social factors including diet. A number of studies
provide evidence that some natural bioactive compounds found in food and herbs
can modulate gene expression by targeting different elements of the epigenetic
machinery. Nutrients that are components of one carbon metabolism such as folate,
riboflavin, pyridoxine, cobalamin, choline, betaine, and methionine, affect DNA
methylation by regulating levels of S-adenosyl-L-methionine, a methyl group
donor, and S-adenosyl-L-homocysteine which is an inhibitor of enzymes catalyzing
the DNA methylation reaction. Other natural compounds target histone
modifications and levels of non-coding RNAs such as vitamin D that recruits
histone acetylases or resveratrol that activates the deacetylase sirtuin and
regulates oncogenic and tumour suppressor micro-RNAs. Since epigenetic
abnormalities have been shown to be both causative and contributing factors in
different health conditions including cancer, natural compounds that are direct
or indirect regulators of the epigenome constitute an excellent approach in
cancer prevention and potentially in anti-cancer therapy.

<snip>

PMID: 22536923 [PubMed - as supplied by publisher]