High intakes of table sugar (sucrose) and surgary foods is associated with increased risk of breast cancer and reduced survival. This is partially because excess sugar consumption is more common in women who are obese and/or have type 2 diabetes, both of which are conditions that promote breast cancer.
However, even lean women who do not have diabetes and are not insulin resistant are more likely to develop breast cancer if they consume a significant proportion of their calories in the form of sugar.
Now a new study has reported that sugar promotes tumor development in three mouse models of breast cancer, including HER2 overexpressing (HER2+), metastatic (stage IV), and triple negative (ER-/PR-/HER2-) disease.

Sugar and breast cancer

Sucrose is converted to glucose by enzymes in the digestive tract. All of our cells require energy in the form of glucose. While it is true that breast cancer cells typically consume glucose at a much higher rate than normal cells, the idea that breast cancer is "fed by sugar" is at best a partial explanation for the association between sugar consumption and breast cancer risk. This is because cancer cells can obtain glucose from a variety of foods in the diet, not just sugar.
Sugar acts in other ways to promote breast cancer, not just as a fuel for cell metabolism and growth. For example, girls who are frequent consumers of sugar-sweetened beverages are more likely to experience early menarche (first period) at a relatively young age. Sweetened soda consumption has been shown to increase the level of circulating estradiol, the most important estrogen, in premenopausal women. High sugar consumption is associated with increased breast density. Early menarche, elevated circulating estradiol, and high breast density are all known breast cancer risk factors.

Latest research finds sugar promotes tumors in animal models of BC

The study referenced at the beginning of this news story was designed to investigate the effects of dietary sugar (sucrose) in the development of primary and metastatic breast tumors. As part of the study, the authors focused on the underlying molecular mechanism, primarily the 12-LOX pathway. Bioactive lipids, especially cyclooxygenases and lipoxygenases (LOXs) metabolites of arachidonic acid, are known to be involved in inflammation and cancer.
The study incorporated three different mouse models of breast cancer. The mice were administered sucrose-enriched diets containing 125 g/kg sucrose, which is equivalent to the average sugar consumption in the U.S. (70 lb. per person per year), or normal mouse diets (controls). Primary tumors and lung metastasis were measured. The levels of 12- LOX protein expression and its arachidonate metabolite, 12-HETE, were also assessed in tumor tissues from the mice, as well as in human breast cancer cells.
The sucrose-enriched diet was found to markedly reduce time to tumor development in MMTV-ErbB2/neu mice. Such mice normally produce HER2+ mammary tumors spontaneously by age four months. The number of tumors also increased by 77% in mice on the sucrose-enriched diet.
The sucrose diet was also found to promote the development of mammary tumors in the second group: mice bearing 4T1 mouse cancer cells. This is a model of metastatic disease: tumors in such mice can spontaneously metastasize from the primary tumor in the mammary gland to multiple distant sites. The average tumor in the sucrose group weighed 534.0 mg compared to 389.4 mg in control animals. In addition, the sucrose diet promoted lung metastasis: the sucrose group developed an average of 13.0 lung nodules per mouse compare to 6.6 in the control group.
The third group of mice were injected with human triple negative MDA-MB-231 cells at the start of feeding with the sucrose-enriched diet. Tumor weight was 2.2-fold higher in mice in the sucrose group.
The tumor-promoting effects of sucrose were associated with up-regulation of 12-LOX protein expression and 12-HETE production in tumor tissues across all three mouse models of breast cancer. When the authors examined the effects of glucose treatment in cultured MDA-MB-231 cells, they found that 12-LOX and 12-HETE were induced in the cells. They also demonstrated that 12-HETE promoted the growth, invasion and migration of the MDA-MB-231 cells. In addition, glucose stimulated proliferation of MDA-MB-231 cells cultured in 3-D matrigel. This effect was extinguished by the presence of the 12-LOX inhibitor Baicalein.
The authors conclude that added sugar promotes the development of breast cancer, in part through up-regulating expression of 12-LOX and production of 12-HETE. Dietary sugar induced 12-LOX signaling might play an important role in breast cancer that is associated with a high-carbohydrate diet.
See our webpages on sugar and glycemic load for more information. Please also see our article on how to optimize your breast cancer diet for information on what to eat during all stages of treatment and recovery.