Over the last decade there has been an increased interest in the role that flaxseed may play in reducing the onset of various forms of cancer. Flaxseed is a nutrient-dense food that contains three components that may help to lower cancer risk: the plant lignan secoisolariciresinol diglucoside (SDG), representing 1% of dry weight, the omega-3 polyunsaturated fatty acid alpha-linolenic acid (ALA), accounting for 20% of flaxseed dry weight, and soluble fibre representing 6% of dry weight. Flaxseed and its components have been shown to possess numerous anti-cancer properties (1).
Breast cancer is one of the most common cancers and the second most responsible for cancer mortality worldwide. Flaxseed has been widely studied in experimental animals and in a number of clinical trials for reduction of breast cancer. Flaxseed lignans are phytoestrogenic compounds. The predominant lignan in flaxseed is secoisolariciresinol diglucoside (SDG), with other lignans present, including pinoresinol, lariciresinol, and matairesinol. After ingestion, SDG is converted to mammalian lignans by bacteria in the colon. The first step in the conversion produces secoisolariciresinol (SECO), which is then converted to enterodiol and enterolactone. These lignans are structurally similar to estradiol, the major form of estrogen in the body, which allows their binding to estrogen receptors (2).
A new publication performed a comprehensive systematic review and meta-analyses of studies published in PubMed, and websites of institutions like Cancer Research UK and the WHO (3).
The meta-analysis found that observational studies showed that ground flaxseed (32 g/day) may decrease the risk of breast cancer. In patients with breast cancer, flaxseed intake of 25 g/day was associated with anti-tumour effects, including increased tumour apoptotic index (tumour cell death), decreased expression of HER2 (an oncogene associated with development and progression of breast cancer), and decreased tumour cell proliferation (4).
Two clinical trials concluded that 28 postmenopausal women, who followed a diet including 10 or 25 g of ground flaxseed for 7 or 16 weeks, witnessed an increased level of excretion of 2OHE1 in their urine, without an increase in the excretion of 16OHE1. These results indicate that flaxseed can have some protective effects in postmenopausal women (5).
Flaxseed does not appear to interact with drug therapies for breast cancer and may in fact provide an additional protective effect when consumed concurrently with treatment. Flaxseed, flaxseed oil or SDG consumption in conjunction with tamoxifen, a standard breast cancer pharmaceutical has been shown in animal models to decrease tumour size to a greater extent than tamoxifen treatment alone (4).
Flaxseed is the richest plant source of the essential omega-3 fatty acid ALA. Similar to lignans, ALA has been found to suppress the growth, size and proliferation, and increase the death of, breast cancer cells in an animal model (5). Additional protective mechanisms of ALA include modulating the expression and function of numerous receptors, transcription factors and signaling molecules involved in reducing tumorigenesis (6).
Overall, this review indicated that in experimental studies, diets including 5 or 10% of flaxseed (approximately 25–30 g of flaxseed daily in humans) inhibited the growth of the ER+ in human breast cancer cells injected in mice. The same happened with the growth of the ER−. Flaxseed also reduced the metastasis of ER− breast tumor.
During clinical trials, flaxseed has shown the potential to reduce the growth of tumors in patients with breast cancer, mainly postmenopausal women, and decrease the risk of this type of cancer.
References
- Lowcock EC, et al. Cancer Causes Control 2013;24:813-816.
- Adolphe JL, et al. Br J Nutr 2010;103:929-938.
- Calado A, Neves PM, Santos T, Ravasco P. See comment in PubMed Commons belowFront Nutr. 2018 Feb 7;5:4. doi: 10.3389/fnut.2018.00004.
- Flower G, et al. Integr Cancer Ther 2013;13:181-192.
- Buck K, et al. Am J Clin Nutr 2010;92:141-153.
- Velentzis LS, et al. Br J Cancer 2009;100:1492-1498.