Washington, Apr 14 : A new study by researchers at University of Toronto, has discovered that in utero or prenatal supplementation of folic acid may protect offspring from developing colorectal cancer.
It is known that folic acid supplementation results in lowering the rates of neural tube defects and some childhood cancers, but too much folic acid may increase one's risk of developing colorectal cancer as well.
"This study provides important insights into the critical role of timing of folic acid intervention in colorectal cancer development and progression. Folic acid may prevent 'new' cancers in the colorectum," said Karen K. Sie, a graduate medical student at the University of Toronto.
In an earlier research it was shown that folic acid supplementation could promote the progression of the earliest precursor to colorectal cancer.
In the current study, the researchers placed female rats on a control diet or folic acid supplemented diet three weeks prior to breeding, and they stayed on this diet throughout pregnancy and lactation. The male pups from each group were then fed a control or folic acid supplemented diet at weaning.
After five to six weeks, the pups were injected with a colorectal cancer causing chemical, and, at 34 weeks, researchers measured tumour incidence, multiplicity and burden as well as plasma folate, homocysteine and liver folate concentrations.
It was discovered that pups from mothers on the control diet had almost a three-fold increased risk of developing colorectal cancer compared with those from rats on folic acid supplementation.
While maternal folic acid supplementation significantly decreased the risk of offspring developing colorectal cancer, postnatal folic acid supplementation had no significant effect on the incidence of tumour development.
"With the continuing debate and controversy surrounding mandatory folic acid fortification and supplementation, it is critical to determine safe and effective doses and timing of folic acid intervention for colorectal cancer revention," said Sie.