Folate has important roles in DNA synthesis and repair. Folate deficiency is thought to contribute to increased risk of cancer through increased DNA strand breaks, impaired DNA repair, and increased mutagenesis. However, folic acid has been found to be associated with increased breast cancer risk in some studies. Now a new study has reported that folic acid supplementation promotes tumor progression in animal model of breast cancer.

Folic acid supplements normally are unnecessary in the U.S.

Some studies have linked adequate folic acid to a decrease in neuroblastomas, leukemia, some brain tumors, and colon cancer. Approximately 10% of the U.S. population overall (and a higher percentage of the poor) is estimated to have a level of folate deficiency sufficient to cause chromosome breaks. It is unclear how folic acid supplementation influences breast cancer risk in populations with low levels of folate deficiency. However, based on laboratory evidence, folic acid supplementation and food fortification may prevent the initiation of breast cancer in normal tissues.

Food sources of folate

The following foods are good sources of folate, as well as being associated with reduced risk of breast cancer:

Beans, dry
Bell peppers
Broccoli
Cabbage
Cauliflower
Celery

Collard greens
Lettuce, romaine
Liver, chicken or turkey
Mustard greens
Parsley
Squash

Note that both green tea and black tea reduce intestinal absorption of folate and should not be consumed simultaneously with high-folate foods by those wishing to increase their folate levels.

Latest research finds folate promotes mammary tumor growth and metastasis

The study referenced at the beginning of this news story was designed to investigate whether folic acid supplementation can promote the progression of established precancerous or cancerous mammary lesions. This is a critically important issue, according to the authors, since breast cancer patients and survivors in the U.S. and Canada are typically exposed to high levels of folic acid due to folic acid fortification of foods and widespread supplement use.

To conduct the study, the authors used mammary tumor-prone Sprague-Dawley rats who were administered a carcinogen at puberty. When the initial tumor reached a predetermined size, the animals were divided into groups to receive various levels of folic acid or a control diet for up to 12 weeks. Mammary tumor growth was monitored weekly. At the end of the study period, all mammary tumors were analyzed. The effect of folic acid on the expression of proteins involved in tumor proliferation, apoptosis (programmed cell death), and mammary tumorigenesis was determined in representative tumors.

The authors did not find a linear correlation between the dosage of folic acid received and its tumor-promoting effects in the animals. However, folic acid supplementation was clearly found to promote the progression of the mammary tumors (including significantly higher tumor weight and volume compared with rats on the control diet). The most significant and consistent mammary tumor-promoting effect was observed in rats given the lowest dosage of folic acid tested. Folic acid was also associated with an increased expression of HER2. The authors conclude that folic acid supplementation may promote the progression of established mammary tumors, a finding that needs further clarification in breast cancer patients and survivors.